A method and system for neuroprotection based on AMPK-pak2 pathway regulation

Abstract

The application relates to the field of medical health, and discloses a nerve protection method and system based on AMPK-Pak2 channel regulation, which comprises the following steps: establishing a channel-damage relationship graph by using the AMPK activity level, the Pak2 function state and the nerve function score of a nerve injury patient; matching AMPK-Pak2 targeted drugs of the nerve injury patient according to AMPK-Pak2 channel regulation abnormality typing, and positioning the nerve injury area to set the AMPK-Pak2 channel regulation mode of the nerve injury patient; calculating the nerve protection efficiency index of the nerve injury patient to generate an adaptive adjustment instruction of the AMPK-Pak2 channel regulation mode; identifying the treatment response state of the nerve injury patient by using the neuron apoptosis rate and the nerve function score; and outputting a treatment execution scheme of the nerve injury patient based on the treatment response state and in combination with the AMPK-Pak2 channel regulation mode and the adaptive adjustment instruction. The application can target the regulation of key signal channels in cells and improve the overall recovery effect of nerve function.

Description

TECHNICAL FIELD

[0001] The application relates to a nerve protection method and system based on AMPK-Pak2 pathway regulation, and belongs to the medical health field. BACKGROUND

[0002] Nerve protection refers to a process of protecting the nervous system from injury, delaying degeneration or promoting repair through drug, treatment or lifestyle intervention measures, mainly functions to reduce nerve injury and promote nerve function recovery, is one of the key means in the treatment of nervous system diseases, and is widely used in the diagnosis and treatment of cerebral apoplexy, brain trauma, neurodegenerative diseases and the like. In recent years, with the deepening of neuroscientific research, the development of biomedical technology and the increasing demand of patients for improvement of nerve function, the application scenarios are continuously expanded, and the exploration of nerve regulation, neurotrophic drug intervention, stem cell transplantation assisted nerve repair and the like provides more possibilities for protection of damaged nerves.

[0003] However, traditional nerve protection mainly relies on basic physical stimulation, such as conventional electrical stimulation. Although this method can alleviate the surface symptoms of nerve injury to a certain extent, the physical stimulation cannot target the regulation of key signal pathways in cells, resulting in that some patients are affected by insufficient activation of the nerve protection mechanism, and the overall recovery effect of nerve function is affected.

[0004] Therefore, a solution is urgently needed to target the regulation of key signal pathways in cells and improve the overall recovery effect of nerve function. SUMMARY

[0005] The application provides a nerve protection method and system based on AMPK-Pak2 pathway regulation, which mainly aims to target the regulation of key signal pathways in cells and improve the overall recovery effect of nerve function.

[0006] To achieve the above-mentioned purpose, the application provides a nerve protection method based on AMPK-Pak2 pathway regulation, which comprises the following steps:

[0007] Detecting the AMPK activity level and Pak2 function state of a nerve injury patient, and synchronously acquiring a nerve function score of the nerve injury patient, and establishing a pathway-injury relationship graph of the nerve injury patient by using the AMPK activity level, the Pak2 function state and the nerve function score;

[0008] Based on the pathway-injury relationship graph, determining an AMPK-Pak2 pathway regulation abnormality type of the nerve injury patient, matching an AMPK-Pak2 targeted drug of the nerve injury patient according to the AMPK-Pak2 pathway regulation abnormality type, and positioning a nerve injury area of the nerve injury patient;

[0009] According to the AMPK-Pak2 targeted drug and the nerve injury area, an AMPK-Pak2 pathway regulation mode of the nerve injury patient is set, and based on the AMPK-Pak2 pathway regulation mode, a local AMPK-Pak2 activity state of the nerve injury patient is monitored in real time;

[0010] Based on the local AMPK-Pak2 activity state, a nerve protection efficiency index of the nerve injury patient is calculated, and according to the nerve protection efficiency index, an adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode is generated;

[0011] The neuron apoptosis rate of the nerve injury patient is calculated, and according to the neuron apoptosis rate and the nerve function score, a treatment response state of the nerve injury patient is identified;

[0012] Based on the treatment response state, and in combination with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction, a treatment execution scheme of the nerve injury patient is output.

[0013] Optionally, the path-injury relationship graph of the nerve injury patient is established by using the AMPK activity level, the Pak2 function state and the nerve function score, including:

[0014] The pathological process stage corresponding to the AMPK activity level, the Pak2 function state and the nerve function score is analyzed;

[0015] Based on the pathological process stage, a characteristic linkage fluctuation section of the AMPK activity level, the Pak2 function state and the nerve function score is identified;

[0016] The path-injury correlation level of the characteristic linkage fluctuation section is analyzed;

[0017] The index integration rule corresponding to the path-injury correlation level is formulated;

[0018] Based on the index integration rule, the path-injury relationship graph of the nerve injury patient is constructed.

[0019] Optionally, the AMPK-Pak2 pathway regulation abnormality type of the nerve injury patient is determined based on the path-injury relationship graph, including:

[0020] The external imbalance performance and the internal action law of the path-injury relationship graph are extracted;

[0021] In combination with the external imbalance performance and the internal action law, a multi-dimensional regulation feature vector of the nerve injury patient is established;

[0022] Collect actual regulation data of the AMPK-Pak2 pathway in the pathway-damage relationship diagram;

[0023] Based on the actual regulation data, calculate a feature deviation index of the multi-dimensional regulation feature vector;

[0024] According to the multi-dimensional regulation feature vector and the feature deviation index, screen out a potential abnormal regulation category from a preset pathway regulation abnormality category library;

[0025] Analyze the clinical pathological characteristics of the neural injury patient, and perform a correlation test of the potential abnormal regulation category and the clinical pathological characteristics to obtain a correlation test result;

[0026] According to the correlation test result, determine a typing determination rule of the AMPK-Pak2 pathway;

[0027] Determine the AMPK-Pak2 pathway regulation abnormality typing of the neural injury patient through the typing determination rule.

[0028] Optionally, the matching of the AMPK-Pak2 targeted drug of the neural injury patient according to the AMPK-Pak2 pathway regulation abnormality typing comprises:

[0029] Extract a key regulation parameter corresponding to the AMPK-Pak2 pathway regulation abnormality typing;

[0030] Based on the key regulation parameter, screen out a candidate targeted drug from a preset targeted drug library;

[0031] Calculate the efficacy matching degree of the candidate targeted drug;

[0032] Detect the effective action duration of the candidate targeted drug;

[0033] According to the efficacy matching degree and the effective action duration, match the AMPK-Pak2 targeted drug of the neural injury patient.

[0034] Optionally, the setting of the AMPK-Pak2 pathway regulation mode of the neural injury patient according to the AMPK-Pak2 targeted drug and the neural injury area comprises:

[0035] Obtain anatomical image data and pathological staging data of the neural injury area;

[0036] Based on the anatomical image data, calculate a drug accumulation coefficient of the neural injury area;

[0037] Analyze the drug delivery characteristics of the AMPK-Pak2 targeted drug;

[0038] determine a drug administration parameter of the patient with the neural injury according to the drug accumulation coefficient and the drug delivery characteristic;

[0039] plan an AMPK-Pak2 pathway regulation timing of the patient with the neural injury by using the pathological staging data;

[0040] define a pathway activity fluctuation threshold of the patient with the neural injury by the AMPK-Pak2 pathway regulation timing;

[0041] set an AMPK-Pak2 pathway regulation mode of the patient with the neural injury in combination with the drug administration parameter, the AMPK-Pak2 pathway regulation timing and the pathway activity fluctuation threshold.

[0042] Optionally, the local AMPK-Pak2 activity state of the patient with the neural injury is monitored in real time based on the AMPK-Pak2 pathway regulation mode, including:

[0043] AMPK-Pak2 activity signals of a lesion local part of the patient with the neural injury are collected based on the AMPK-Pak2 pathway regulation mode;

[0044] spatiotemporal activity gradient characteristics in the AMPK-Pak2 activity signals are analyzed;

[0045] the AMPK-Pak2 activity sensitive area of the lesion local part is defined by using the spatiotemporal activity gradient characteristics;

[0046] a multi-modal sensing array of the patient with the neural injury is configured in the AMPK-Pak2 activity sensitive area;

[0047] a spatiotemporal synchronous network of the multi-modal sensing array is constructed, and multi-modal activity data of the multi-modal sensing array in the spatiotemporal synchronous network are collected;

[0048] activity anomaly characteristics of the AMPK-Pak2 activity sensitive area are extracted from the multi-modal activity data;

[0049] an activity detection module of the AMPK-Pak2 activity sensitive area is constructed according to the activity anomaly characteristics;

[0050] the AMPK-Pak2 activity state of the patient with the neural injury is monitored in real time based on the activity detection module.

[0051] Optionally, the neural protection efficiency index of the patient with the neural injury is calculated based on the local AMPK-Pak2 activity state, including:

[0052] dynamic activity parameters of the local AMPK-Pak2 activity state are extracted;

[0053] a parameter performance threshold value defining each of the dynamic activity parameters;

[0054] identifying a nerve repair progress of the nerve injury patient and a progress adaptation coefficient thereof;

[0055] calculating a real-time progress deviation value of the nerve repair progress based on the progress adaptation coefficient;

[0056] in combination with the parameter performance threshold value, the progress adaptation coefficient and the real-time progress deviation value, a neuroprotection performance index of the nerve injury patient is calculated.

[0057] Optionally, the generating of the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotection performance index comprises:

[0058] collecting patient clinical data and prognosis analysis reports under the AMPK-Pak2 pathway regulation mode;

[0059] setting a dynamic calibration threshold value of the neuroprotection performance index according to the patient clinical data and the prognosis analysis reports;

[0060] labeling a risk level of the neuroprotection performance index based on the dynamic calibration threshold value;

[0061] mapping the risk level to a hierarchical regulation instruction of the AMPK-Pak2 pathway regulation mode;

[0062] dynamically generating an adaptive adjustment parameter corresponding to the hierarchical regulation instruction based on the risk level;

[0063] defining a synergistic regulation variable of the AMPK-Pak2 pathway regulation mode according to the adaptive adjustment parameter;

[0064] generating the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode in combination with the adaptive adjustment parameter and the synergistic regulation variable.

[0065] Optionally, the identifying of the treatment response state of the nerve injury patient according to the neuron apoptosis rate and the neurological function score comprises:

[0066] performing a standardization conversion processing of the neuron apoptosis rate to obtain a cell survival evaluation vector;

[0067] extracting a motor function score, a sensory function score and an autonomic nervous function score in the neurological function score to generate a functional recovery parameter vector;

[0068] analyze a dynamic change trend of the neuron apoptosis rate to extract an apoptosis trend feature vector under the dynamic change trend;

[0069] generate a cell survival feature vector of the nerve injury patient based on the apoptosis trend feature vector and the cell survival evaluation vector;

[0070] calculate a functional recovery efficiency index and a stability index of the nerve injury patient according to the nerve function score;

[0071] determine a functional recovery evaluation vector of the nerve injury patient based on the functional recovery efficiency index and the stability index;

[0072] construct a treatment response feature matrix of the nerve injury patient in combination with the cell survival evaluation vector, the functional recovery parameter vector, the cell survival feature vector and the functional recovery evaluation vector;

[0073] identify a treatment response state of the nerve injury patient based on the treatment response feature matrix.

[0074] To solve the above problems, the application further provides a nerve protection system based on AMPK-Pak2 pathway regulation, which comprises:

[0075] a graph construction module, which is used for detecting an AMPK activity level and a Pak2 function state of a nerve injury patient, synchronously acquiring a nerve function score of the nerve injury patient, and establishing a pathway-injury relationship graph of the nerve injury patient by using the AMPK activity level, the Pak2 function state and the nerve function score;

[0076] a typing matching module, which is used for determining an AMPK-Pak2 pathway regulation abnormality typing of the nerve injury patient based on the pathway-injury relationship graph, matching an AMPK-Pak2 targeted drug of the nerve injury patient according to the AMPK-Pak2 pathway regulation abnormality typing, and locating a nerve injury area of the nerve injury patient;

[0077] a regulation generation module, which is used for setting an AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drug and the nerve injury area, and monitoring a local AMPK-Pak2 activity state of the nerve injury patient in real time based on the AMPK-Pak2 pathway regulation mode;

[0078] an efficacy evaluation module, which is used for calculating a nerve protection efficacy index of the nerve injury patient based on the local AMPK-Pak2 activity state, and generating an adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the nerve protection efficacy index.

[0079] a response analysis module, configured to calculate a neuron apoptosis rate of the patient with the nerve injury, and identify a treatment response state of the patient with the nerve injury according to the neuron apoptosis rate and the neurological function score;

[0080] a scheme output module, configured to output a treatment execution scheme of the patient with the nerve injury based on the treatment response state and in combination with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction.

[0081] Compared with the problems described in the background art, the embodiment of the present application can capture the path regulation dynamics and the nerve function recovery of the patient in real time by detecting the AMPK activity level and the Pak2 function state of the nerve injury patient and synchronously acquiring the nerve function score of the nerve injury patient, and providing data support for accurately judging the nerve protection effect based on the AMPK-Pak2 pathway regulation; further, the embodiment of the present application can integrate scattered pathway molecule data and nerve function recovery data by establishing the pathway-injury relationship graph of the nerve injury patient by using the AMPK activity level, the Pak2 function state and the nerve function score, and form a multi-dimensional and linked analysis system to provide a structured framework for real-time capturing of the dynamic correlation between the AMPK-Pak2 pathway regulation state and the nerve injury repair process; the embodiment of the present application can ensure that the pathway function can be accurately targeted for repair according to the abnormal type in the nerve protection based on the AMPK-Pak2 pathway regulation, realize the efficient reversal of nerve injury, and improve the targeting and specificity of the nerve protection intervention by determining the AMPK-Pak2 pathway regulation abnormality type of the nerve injury patient based on the pathway-injury relationship graph; further, the embodiment of the present application can adapt to the abnormal characteristics of different types of pathways, form a targeted and synergistic nerve protection system, ensure efficient intervention on complex pathway regulation abnormality scenarios, and improve the nerve protection effect based on the AMPK-Pak2 pathway regulation by matching the AMPK-Pak2 targeted drugs of the nerve injury patient according to the AMPK-Pak2 pathway regulation abnormality type and positioning the nerve injury area of the nerve injury patient; the embodiment of the present application can break through the limitations of single drug treatment, improve the accuracy of correcting the pathway abnormalities, and enhance the effectiveness and safety of the AMPK-Pak2 pathway regulation mode for nerve injury treatment by setting the AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drugs and the nerve injury area; further, the embodiment of the present application can dynamically quantify the real-time matching degree of the pathway regulation effect and the nerve function recovery target by monitoring the local AMPK-Pak2 activity state of the nerve injury patient in real time based on the AMPK-Pak2 pathway regulation mode, improve the precision intervention ability and treatment safety of the AMPK-Pak2 pathway regulation in complex nerve injury scenarios; the embodiment of the present application can quantitatively evaluate the actual effect of the nerve protection measure, optimize the formulation and adjustment of the nerve protection scheme, and improve the targeting and effectiveness of the nerve protection in the nerve injury repair process by calculating the nerve protection efficiency index of the nerve injury patient based on the local AMPK-Pak2 activity state.Further, the embodiment of the present application can dynamically quantify the real-time matching state of the AMPK-Pak2 pathway regulation operation and the physiological safety boundary of nerve injury repair by generating the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotective efficacy index, thereby improving the precise regulation capability and neuroprotective effectiveness of the AMPK-Pak2 pathway regulation mode in a complex nerve injury environment; the embodiment of the present application can improve the accuracy of the treatment effect evaluation of the nerve injury patient by calculating the neuron apoptosis rate of the nerve injury patient and identifying the treatment response state of the nerve injury patient according to the neuron apoptosis rate and the neurological function score, and can also provide a precise basis for adjusting the neuroprotective strategy by judging the treatment response type in real time, thereby improving the efficiency of neurological function recovery and the pertinence of neuroprotection; finally, the embodiment of the present application can output the treatment execution scheme of the nerve injury patient based on the treatment response state and in combination with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction, which can not only significantly improve the comprehensiveness of neurological function recovery and reduce the residual defects of neurological function, but also can dynamically adjust the regulation strategy according to the treatment response characteristics of the patient, the nerve repair process and the like, thereby effectively improving the precision and clinical effectiveness of neuroprotective treatment, and can also optimize the treatment process by treatment response state evaluation and adaptive regulation, thereby reducing the risk of over-treatment, improving the activation efficiency of the neuroprotective mechanism and enhancing the long-term recovery effect of the patient. Therefore, the neuroprotective method and system based on AMPK-Pak2 pathway regulation provided by the embodiment of the present application can target the regulation of key signal pathways in cells and improve the overall recovery effect of neurological function. BRIEF DESCRIPTION OF DRAWINGS

[0082] Figure 1 A flowchart of a neuroprotective method based on AMPK-Pak2 pathway regulation provided by an embodiment of the present application is shown in FIG. 1.

[0083] Figure 2 An AMPK-Pak2 pathway diagram of a neuroprotective method based on AMPK-Pak2 pathway regulation provided by an embodiment of the present application is shown in FIG. 2.

[0084] Figure 3 A functional module diagram of a neuroprotective system based on AMPK-Pak2 pathway regulation provided by an embodiment of the present application is shown in FIG. 3.

[0085] The object implementation, functional features and advantages of the present application will be further described with reference to the embodiments and the accompanying drawings. DETAILED DESCRIPTION

[0086] It should be understood that the specific embodiments described herein are merely intended to explain the present application, and are not intended to limit the present application.

[0087] The embodiment of the present application provides a nerve protection method based on AMPK-Pak2 pathway regulation. The execution subject of the nerve protection method based on AMPK-Pak2 pathway regulation includes but is not limited to at least one of electronic devices such as a server, a terminal and the like which can be configured to execute the method provided by the embodiment of the present application. In other words, the nerve protection method based on AMPK-Pak2 pathway regulation can be executed by software or hardware installed in a terminal device or a server device. The server includes but is not limited to a single server, a server cluster, a cloud server or a cloud server cluster and the like.

[0088] Referring to Figure 1 As shown in the figure, it is a flowchart of a nerve protection method based on AMPK-Pak2 pathway regulation provided by an embodiment of the present application. In the embodiment, the nerve protection method based on AMPK-Pak2 pathway regulation includes:

[0089] S1, detecting the AMPK activity level and the Pak2 function state of a nerve injury patient, and synchronously acquiring a nerve function score of the nerve injury patient, and using the AMPK activity level, the Pak2 function state and the nerve function score to establish a pathway-injury relationship diagram of the nerve injury patient.

[0090] The embodiment of the present application can capture the pathway regulation dynamics and the nerve function recovery of the patient in real time by detecting the AMPK activity level and the Pak2 function state of the nerve injury patient and synchronously acquiring the nerve function score of the nerve injury patient, and provides data support for accurately judging the nerve protection effect based on AMPK-Pak2 pathway regulation. The nerve injury patient refers to a clinical individual whose nerve conduction function is damaged due to peripheral / central axon rupture, compression, ischemia or metabolic injury. The AMPK activity level refers to the activation degree and the function level of AMPK (adenosine acid activated protein kinase) in the body of the nerve injury patient, including Thr172 phosphorylation level, kinase activity, ACCSer79 phosphorylation level of the downstream target, and the like. The Pak2 function state refers to the integrated state of phosphorylation modification, subcellular localization and substrate cleavage function of p21 activated kinase 2 (Pak2). The nerve function score refers to a score obtained by quantitatively evaluating the recovery of motor function, sensory function, language function, cognitive function and the like of the nerve injury patient through a specific evaluation scale (such as a modified Rankin scale, a U.S. National Institutes of Health Stroke Scale and the like).

[0091] Optionally, the AMPK activity level and the Pak2 function state of the nerve injury patient can be detected by Western blot (protein blotting method).

[0092] Further, by using the AMPK activity level, the Pak2 function state and the neural function score, the embodiment of the present application establishes the pathway-injury relationship diagram of the neural injury patient, can integrate scattered pathway molecule data and neural function recovery data, forms a multi-dimensional and linked analysis system, provides a structured framework for real-time capturing of the dynamic correlation between the AMPK-Pak2 pathway regulation state and the neural injury repair process, and the pathway-injury relationship diagram refers to a visual chart constructed by data correlation analysis, taking the AMPK-Pak2 pathway related molecule data such as the AMPK activity level and the Pak2 function state as the horizontal axis core element, and taking the neural injury and repair condition reflected by the neural function score as the vertical axis core index.

[0093] As an embodiment of the present application, the use of the AMPK activity level, the Pak2 function state and the neural function score to establish the pathway-injury relationship diagram of the neural injury patient comprises:

[0094] Analyzing the pathological process stage corresponding to the AMPK activity level, the Pak2 function state and the neural function score;

[0095] Based on the pathological process stage, identifying the characteristic linkage fluctuation section of the AMPK activity level, the Pak2 function state and the neural function score;

[0096] Analyzing the pathway-injury correlation level of the characteristic linkage fluctuation section;

[0097] Formulating the index integration rule corresponding to the pathway-injury correlation level;

[0098] Based on the index integration rule, constructing the pathway-injury relationship diagram of the neural injury patient.

[0099] The pathological process staging refers to dividing the whole process of a patient with nerve injury from injury occurrence to stable function into continuous stages with clear time limits and typical pathological characteristics based on the biological law of nerve injury occurrence, development and outcome, which can be divided into acute injury period, subacute period and recovery period. For example, 0-72 hours after injury of a certain nerve patient, AMPK activity drops sharply, Pak2 is over-activated, and nerve function score decreases significantly, which can be determined as the acute injury period of the nerve patient. The characteristic linkage fluctuation segment refers to the statistically significant synergistic change interval of AMPK activity level, Pak2 function status and nerve function score at the same time in the pathological process staging. The synergistic change interval meets the following conditions: the change trend of the three indicators is consistent (such as simultaneous rise or showing a synergistic trend of "AMPK rise-Pak2 fall-nerve function score rise"), and the change amplitude reaches a preset threshold (such as AMPK activity change amplitude > 30%, Pak2 function change amplitude > 25%, nerve function score change amplitude > 20%), and the duration exceeds 1 / 3 of the pathological stage (such as the duration of the acute injury period characteristic linkage fluctuation segment needs to exceed 24 hours). For example, in the acute injury period, when the AMPK activity decreases by > 40%, the Pak2 function activation intensity is > 50%, and the nerve function score decreases by > 30 points, it is determined as the "acute injury correlation fluctuation segment". In the recovery period, when the AMPK activity rises to more than 80% of the normal level, the Pak2 function abnormal value is < 20%, and the nerve function score improves by > 20%, it is determined as the "recovery correlation fluctuation segment". The pathway-injury correlation level refers to quantifying the correlation between the AMPK-Pak2 pathway (reflected by AMPK activity level and Pak2 function status) and the degree of nerve injury (reflected by nerve function score) in the characteristic linkage fluctuation segment. When the correlation coefficient is > 0.7, it is a strong correlation; when the correlation coefficient is between 0.3 and 0.7, it is a moderate correlation; and when the correlation coefficient is < 0.3, it is a weak correlation. For example, when the ratio of AMPK activity change to Pak2 function change and the change of nerve function score shows a "positive correlation" (such as AMPK rise → Pak2 fall → score rise), and the correlation coefficient is > 0.7, it is defined as "strong correlation". When the correlation coefficient is between 0.3 and 0.7, it is "moderate correlation". When the correlation coefficient is < 0.3, it is "weak correlation".3, as "weak association", the index integration rule is to develop a rule set for converting the raw data of AMPK activity level, Pak2 function state and neurological function score into standardized data that can be used to construct the pathway-injury relationship graph according to the pathway-injury association level, wherein different association levels correspond to different rules: when the association is strong, the "weighted superposition rule" is adopted: the standardized values (0-100 points) of the three indicators are weighted and calculated according to the preset weight (such as AMPK 40%, Pak2 30%, and neurological function score 30%) to obtain the comprehensive association value; when the association is moderate, the "hierarchical matching rule" is adopted: first, the neurological function score is divided into several levels (such as 0-3 points, 4-7 points, and 8-10 points), and then the normal reference range of AMPK activity level and Pak2 function state is matched for each level to form a hierarchical data matrix; when the association is weak, the "abnormal marking rule" is adopted: the indicators deviating from the normal reference range are marked separately (such as using "↑" and "↓" to mark the increase or decrease of AMPK activity).

[0100] Optionally, the characteristic linkage fluctuation section of the AMPK activity level, the Pak2 function state and the neurological function score can be identified by a multivariate LSTM model, the pathway-injury association level of the characteristic linkage fluctuation section can be analyzed by Granger causality test, and the pathway-injury relationship graph of the neurological injury patient can be established based on Cypher query language.

[0101] S2, based on the pathway-injury relationship graph, determining the AMPK-Pak2 pathway regulation abnormality type of the neurological injury patient, matching the AMPK-Pak2 targeted drug of the neurological injury patient according to the AMPK-Pak2 pathway regulation abnormality type, and positioning the neurological injury area of the neurological injury patient.

[0102] The embodiment of the present application can ensure that in the nerve protection based on the AMPK-Pak2 pathway regulation, the pathway function can be accurately targeted for repair according to the abnormal type, the nerve injury can be efficiently reversed, the targeting and specificity of the nerve protection intervention can be improved, and the AMPK-Pak2 pathway regulation abnormality type refers to the specific form of the imbalance of the overall function of the signaling pathway composed of AMPK (adenosine acid activated protein kinase) and Pak2 (p21 activated kinase 2) due to the deviation of the function, expression or interaction of key molecules from the normal physiological state under pathological conditions such as neurological injury, including AMPK activity deficiency type, Pak2 function deficiency type and coordination disorder type, etc.

[0103] As an embodiment of the present application, the determination of the AMPK-Pak2 pathway abnormality type of the neural injury patient based on the pathway-injury relationship graph comprises:

[0104] extracting the external imbalance performance and the internal action rule of the pathway-injury relationship graph;

[0105] establishing a multi-dimensional regulation characteristic vector of the neural injury patient in combination with the external imbalance performance and the internal action rule;

[0106] collecting actual regulation data of the AMPK-Pak2 pathway in the pathway-injury relationship graph;

[0107] calculating a characteristic deviation index of the multi-dimensional regulation characteristic vector based on the actual regulation data;

[0108] screening a potential abnormal regulation category from a preset pathway abnormality category library according to the multi-dimensional regulation characteristic vector and the characteristic deviation index;

[0109] analyzing the clinical pathological characteristics of the neural injury patient, and performing a correlation test of the potential abnormal regulation category and the clinical pathological characteristics to obtain a correlation test result;

[0110] determining a type determination rule of the AMPK-Pak2 pathway according to the correlation test result;

[0111] determining the AMPK-Pak2 pathway abnormality type of the neural injury patient through the type determination rule.

[0112] The external imbalance performance refers to the observable and quantifiable external characteristic changes related to the nerve injury state of the AMPK-Pak2 pathway function, such as the deviation of the AMPK-Pak2 activity ratio from the healthy range, the decline rate of the nerve function score, the abnormal increase of the neuron metabolic rate in the injury area, etc. The internal action law refers to the internal mechanism and dynamic change law of the pathway function regulation between AMPK and Pak2 molecules through interaction (such as phosphorylation / dephosphorylation, binding / dissociation). The multi-dimensional regulation feature vector refers to the multi-dimensional data vector formed after quantifying the key features related to the pathway regulation by fusing the external imbalance performance and the internal action law, including AMPK activity, Pak2 activity, AMPK inhibition rate of Pak2, nerve function score, inflammatory factor concentration, etc. The AMPK-Pak2 pathway refers to the signal transduction pathway formed by the interaction of AMPK (adenosine acid activated protein kinase) and Pak2 (p21 activated kinase 2) as core molecules and upstream and downstream signal molecules (such as LKB1, Cofilin, etc.). The actual regulation data refers to the quantitative data reflecting the real-time functional state of the AMPK-Pak2 pathway extracted from the pathway-injury relationship diagram, including molecular activity, interaction strength and related nerve function parameters, etc. The feature deviation index refers to the quantitative index representing the deviation of the multi-dimensional regulation feature vector from the normal state based on the difference between the actual regulation data and the healthy population benchmark data, which is obtained by standardization calculation.5is considered to be significantly abnormal, the abnormal regulation category library refers to a standardized database containing known types of AMPK-Pak2 pathway regulation abnormalities, including AMPK hyperactivity type (AMPK activity > 120%, inhibiting excessive Pak2), Pak2 inhibition type (Pak2 activity < 30%, unable to mediate axon regeneration), bidirectional disorder type (AMPK activity < 50% and Pak2 activity > 100%), feedback imbalance type (Pak2 negative feedback on AMPK < 20%) and the like, the potential abnormal regulation category refers to an abnormal type preliminarily matched with the multidimensional regulation feature vector and the feature deviation index of the patient to be analyzed, which is screened from the abnormal regulation category library, for example, if the patient's feature deviation index is mainly caused by low AMPK activity (40%) and high Pak2 activity (90%), the "bidirectional disorder type" is screened from the category library as the potential abnormal regulation category, the clinical pathological feature refers to an objective pathological index directly related to nerve injury obtained by imaging, pathological and other detection means, reflecting the anatomical and histological characteristics of the injury, including injury volume, neuron survival rate, axon breakage density, astrocyte proliferation degree and the like, the correlation test result refers to a quantitative result of the correlation between the potential abnormal regulation category and the clinical pathological feature, which is calculated by statistical methods such as Pearson correlation analysis, the typing determination rule refers to a standardized determination standard for determining the potential abnormal regulation category as the final typing, which is formulated based on the correlation test result, containing feature threshold, correlation strength threshold and other key parameters, for example, if the potential category is "bidirectional disorder type", and the following conditions are met: ① feature deviation index > 1.5; ② correlation coefficient with injury volume > 0.6; ③ neuron survival rate < 50%, then the AMPK-Pak2 pathway regulation abnormality is determined to be of the bidirectional disorder type.

[0113] Optionally, the feature deviation index of the multidimensional regulation feature vector can be calculated by using the Euclidean distance formula, and the potential abnormal regulation category can be matched by using the K nearest neighbor algorithm.

[0114] Further, the embodiment of the present application can adapt to the abnormal characteristics of different pathways by matching the AMPK-Pak2 targeted drugs for the nerve injury patients and locating the nerve injury area of the nerve injury patients according to the AMPK-Pak2 pathway regulation abnormality typing, form a targeted and synergistic nerve protection system, ensure efficient intervention in complex pathway regulation abnormality scenarios, improve the nerve protection effect based on the AMPK-Pak2 pathway regulation, the AMPK-Pak2 targeted drugs refer to drugs designed for AMPK (adenosine acid activated protein kinase) or Pak2 (p21 activated kinase 2) molecules and their interaction pathways, which have specific regulation effect, can correct the pathway regulation abnormality by affecting the AMPK activity or Pak2 function, and then play a nerve protection role, the nerve injury area refers to a specific anatomical area in the nerve injury patient's body where the neuron structure is damaged, functionally abnormal or metabolically disordered, and directly related to the AMPK-Pak2 pathway regulation abnormality, which can be clearly defined by imaging examination (such as MRI, CT) or pathological detection.

[0115] As an embodiment of the present application, the AMPK-Pak2 pathway regulation abnormality typing and matching the AMPK-Pak2 targeted drugs for the nerve injury patients comprises:

[0116] extracting the key regulation parameters corresponding to the AMPK-Pak2 pathway regulation abnormality typing;

[0117] based on the key regulation parameters, screening candidate targeted drugs from a pre-set targeted drug library;

[0118] calculate the performance matching degree of the candidate targeted drugs;

[0119] detect the effective action duration of the candidate targeted drugs;

[0120] According to the performance matching degree and the effective action duration, match the AMPK-Pak2 targeted drugs for the nerve injury patients.

[0121] The key regulatory parameters refer to a parameter set that quantitatively characterizes the core features of AMPK-Pak2 pathway abnormality typing, including the percentage of AMPK activity deviating from the normal range, the fold of Pak2 functional abnormality, the synergistic regulation coefficient of upstream and downstream molecules in the pathway, and the time window required for regulation. The targeting drug library refers to a standardized database pre-constructed and storing information of various specific drugs targeting the AMPK-Pak2 pathway, including key information such as the action object, action mechanism, efficacy parameter, and clinical data of the drug. The candidate targeting drug refers to a drug that may have a correcting effect on AMPK-Pak2 pathway abnormality typing, which is preliminarily screened from the targeting drug library based on the key regulatory parameters. The efficacy matching degree refers to an index for quantitatively evaluating the matching degree of the candidate targeting drug and the AMPK-Pak2 pathway abnormality typing, wherein the scoring index of the efficacy matching degree includes: the matching degree of the drug action mechanism and the abnormality typing (weight 40%), the correcting ability of the efficacy parameter to the abnormal index (weight 30%), and the clinical efficiency of the same type of patients (weight 30%). For example, the matching degree of a certain drug to the bidirectional disorder type is 90%, the correcting ability score is 80 points, and the clinical efficiency is 75%. The matching degree score is: 90% x 40 + 80 x 30% + 75 x 30% = 82.5 points. The effective action time refers to the time interval during which the candidate targeting drug can maintain an effective concentration and continuously exert the correcting effect on the AMPK-Pak2 pathway abnormality after entering the body of the patient with neural injury. For example, the half-life of a certain Pak2 inhibitor is 10 hours, the effective concentration is reached 2 hours after administration, and the inhibitory activity can still be maintained at more than 70% within 24 hours (which can reduce the Pak2 function from 2.3 times to less than 1.2 times), so the effective action time is 24 hours.

[0122] Optionally, the effective action time of the candidate targeting drug can be detected by PET imaging, and the efficacy matching degree of the candidate targeting drug can be calculated by a weighted summation algorithm.

[0123] S3, based on the AMPK-Pak2 pathway regulation mode, real-time monitoring the local AMPK-Pak2 activity state of the patient with neural injury.

[0124] The embodiment of the present application can break through the limitations of single drug treatment, improve the precision correction efficiency of the abnormal pathway, enhance the effectiveness and safety of the AMPK-Pak2 pathway regulation mode for nerve injury treatment by setting the AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drug and the nerve injury area. The AMPK-Pak2 pathway regulation mode refers to a comprehensive implementation scheme for accurately delivering drugs to the injury area and regulating the function of the AMPK-Pak2 pathway according to the physicochemical properties (such as molecular structure, half-life, solubility) of the AMPK-Pak2 targeted drug and the anatomical features (such as location, range, and blood-brain barrier integrity) of the nerve injury area, including administration route, dose adjustment strategy, action time window, and synergistic auxiliary means.

[0125] As an embodiment of the present application, the AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drug and the nerve injury area includes:

[0126] Obtaining anatomical image data and pathological staging data of the nerve injury area;

[0127] Based on the anatomical image data, calculating the drug accumulation coefficient of the nerve injury area;

[0128] Analyzing the drug delivery characteristics of the AMPK-Pak2 targeted drug;

[0129] According to the drug accumulation coefficient and the drug delivery characteristics, determining the drug administration parameters of the nerve injury patient;

[0130] Using the pathological staging data, planning the AMPK-Pak2 pathway regulation timing of the nerve injury patient;

[0131] Defining the pathway activity fluctuation threshold of the nerve injury patient through the AMPK-Pak2 pathway regulation timing;

[0132] Setting the AMPK-Pak2 pathway regulation mode of the nerve injury patient in combination with the drug administration parameters, the AMPK-Pak2 pathway regulation timing, and the pathway activity fluctuation threshold.

[0133] The anatomical image data refers to the digital image and derived data obtained by medical imaging technology (such as MRI, CT, PET) for representing the anatomical structure characteristics of the nerve injury area, the pathological staging data refers to the quantitative data for dividing the pathological stage of the nerve injury area based on the occurrence and development law of the nerve injury, including the time range, histological characteristics and pathway function state of each stage, the drug accumulation coefficient refers to the parameter for quantifying the accumulation ability of the nerve injury area to the AMPK-Pak2 targeted drug, the calculation formula is: drug accumulation coefficient = (vessel density of injury area / vessel density of normal area) x weight 1 + (intercellular space diameter of injury area / intercellular space diameter of normal area) x weight 2, wherein, weight 1 and weight 2 can be set to 0.6 and 0.4 according to the pre-experiment data, for example, when the vessel density of the injury area is 60% of the normal and the intercellular space diameter is 1.2 times of the normal, the accumulation coefficient = 60% x 0.6 + 1.2 x 0.4 = 0.36 + 0.48 = 0.84 (i.e. 84%), the drug delivery characteristics refer to the inherent properties of the AMPK-Pak2 targeted drug itself affecting its delivery process in vivo, including the physicochemical properties and kinetic characteristics affecting drug absorption, distribution, penetration of tissue barriers, the drug delivery parameters refer to the key parameter set for making the drug reach an effective concentration in the injury area and exert a regulatory effect according to the drug accumulation coefficient and drug delivery characteristics of the nerve injury area, including the drug delivery dose, mode and auxiliary means parameters, when the accumulation coefficient > 0.8 and the penetration rate is high, the conventional dose is used for oral administration, when the accumulation coefficient is 0.5-0.8, the dose is increased by 20-30%, when < 0.5, the nano-carrier delivery is used, the AMPK-Pak2 pathway regulation timing refers to the time arrangement of the AMPK-Pak2 pathway regulation process planned based on the pathological staging data of the nerve injury area, including the regulation frequency, target activity and intervention node of each stage, for example, the timing of acute phase (0-72 hours) is "monitoring the pathway activity once every 6 hours, the regulation target is AMPK activity ≥ 50%, Pak2 activity ≤ 120%, the pathway activity fluctuation threshold refers to the allowed fluctuation range of AMPK and Pak2 activity set to ensure the stability of the pathway function and avoid excessive regulation or insufficient regulation in each stage of the AMPK-Pak2 pathway regulation timing.

[0134] Optionally, the pathway activity fluctuation threshold of the nerve injury patient can be defined by the 3σ rule, and the AMPK-Pak2 pathway regulation timing of the nerve injury patient can be planned by using survival analysis algorithm, such as Kaplan-Meier algorithm.

[0135] To realize the scientific regulation of the AMPK-Pak2 pathway of the nerve injury patient, refer to Figure 2As shown, it is an AMPK-Pak2 pathway schematic diagram of a nerve protection method based on AMPK-Pak2 pathway regulation provided by an embodiment of the present application, which fully presents the activation of AMPK, the activation of Pak2 and the downstream series of biological effects mediated by the two under the triggering of nerve injury signals, and can provide operational molecular mechanism support for setting the AMPK-Pak2 pathway regulation mode. For example, in the calculation of drug accumulation coefficient and the analysis of drug delivery characteristics, relying on the molecular localization and key action sites of AMPK and Pak2 in the diagram, the precise matching of drugs and pathway action mechanisms can be ensured.

[0136] Further, by means of the AMPK-Pak2 pathway regulation mode, the local AMPK-Pak2 activity state of the nerve injury patient can be monitored in real time, the real-time matching degree of the pathway regulation effect and the nerve function recovery target can be dynamically quantified, the precise intervention ability and treatment safety of the AMPK-Pak2 pathway regulation in the complex nerve injury scene can be improved, and the local AMPK-Pak2 activity state refers to the functional activity level of AMPK (adenosine acid activated protein kinase) and Pak2 (p21 activated kinase 2) and the synergistic action state of the two in the specific nerve injury area (such as the hippocampal area, the cervical segment of the spinal cord and other local anatomical positions) of the nerve injury patient.

[0137] As an embodiment of the present application, the real-time monitoring of the local AMPK-Pak2 activity state of the nerve injury patient based on the AMPK-Pak2 pathway regulation mode comprises:

[0138] Based on the AMPK-Pak2 pathway regulation mode, the AMPK-Pak2 activity signal of the lesion local of the nerve injury patient is collected;

[0139] The spatiotemporal activity gradient characteristics in the AMPK-Pak2 activity signal are analyzed;

[0140] The AMPK-Pak2 activity sensitive area of the lesion local is defined by using the spatiotemporal activity gradient characteristics;

[0141] The multi-mode sensing array of the nerve injury patient is configured in the AMPK-Pak2 activity sensitive area;

[0142] The spatiotemporal synchronous network of the multi-mode sensing array is constructed, and the multi-mode activity data of the multi-mode sensing array under the spatiotemporal synchronous network is collected;

[0143] The activity anomaly characteristics of the AMPK-Pak2 activity sensitive area are extracted from the multi-mode activity data;

[0144] According to the activity anomaly characteristics, an activity detection module of the AMPK-Pak2 activity sensitive zone is constructed;

[0145] Based on the activity detection module, the AMPK-Pak2 activity state of the patient with nerve injury is monitored in real time.

[0146] The lesion local part refers to a specific local area in a patient with nerve injury that has functional abnormalities or pathological changes due to nerve injury. For example, if a patient has lower limb numbness and weakness due to sciatic nerve injury, the area including the damaged sciatic nerve and the corresponding muscles, skin, and other tissues of the lower limb innervated by the sciatic nerve is the lesion local part. The AMPK-Pak2 activity signal refers to a signal that reflects the activity level and changes of AMPK (adenosine monophosphate-activated protein kinase) and Pak2 (p21-activated kinase 2) in the lesion local part of a patient with nerve injury. When energy supply is insufficient in cells after nerve injury, AMPK is activated, and the threonine 172 site of its alpha subunit is phosphorylated. This change in phosphorylation state triggers a series of signal cascade reactions, forming an activity signal that can be detected. At the same time, Pak2 may also be phosphorylated due to the regulation of upstream signal pathways, and the change in its phosphorylation level also constitutes part of the AMPK-Pak2 activity signal. The spatiotemporal activity gradient feature refers to the gradient change characteristics of the AMPK-Pak2 activity signal in the time and space dimensions. In the time dimension, it reflects the dynamic change trend of the AMPK-Pak2 activity level from the occurrence of nerve injury over time. For example, at different time points after injury, the activity may gradually increase, decrease, or show fluctuating changes. In the spatial dimension, it reflects the differences in AMPK-Pak2 activity levels at different positions in the lesion local part, forming a spatial gradient distribution. The AMPK-Pak2 activity sensitive area refers to an area where the AMPK-Pak2 activity changes significantly and has a key impact on nerve injury repair or pathological progression, as determined by the spatiotemporal activity gradient feature. The multi-modal sensing array refers to a system composed of various types of sensing modules such as electrochemical modules, optical modules, and mechanical modules, for sensing and detecting various physical, chemical, and biological signals related to AMPK-Pak2 activity in the AMPK-Pak2 activity sensitive area. The electrochemical module can indirectly reflect the activity of AMPK-Pak2 by detecting changes in ion concentration (such as calcium ions and hydrogen ions) or metabolic products (such as ATP and ADP) in the extracellular fluid. The optical module uses fluorescence labeling technology to perform optical imaging detection of the expression amount and phosphorylation state of AMPK-Pak2 protein in cells.The mechanical module can perceive the changes in the mechanical properties of cells or tissues, as the mechanical properties of cells and tissues (such as elasticity, stiffness, etc.) change with the changes in AMPK-Pak2 activity during the process of nerve injury and repair. The spatiotemporal synchronization network refers to a network architecture for coordinating the work of each module in the multi-modal sensing array, enabling it to collect data synchronously in time and space. The multi-modal activity data refers to a collection of data collected by the multi-modal sensing array from the AMPK-Pak2 activity-sensitive region under the spatiotemporal synchronization network, containing multiple types of information and related to AMPK-Pak2 activity. For example, the data collected by the electrochemical module, such as the change in ion concentration in the extracellular fluid over time, such as the gradual increase in calcium ion concentration from 1.0 mmol / L to 1.5 mmol / L within a few hours after nerve injury; the fluorescence intensity data obtained by the optical module, such as the fluorescence signal intensity representing the expression level of p-Pak2, which is enhanced by 2 times within a day after injury; the elastic modulus data measured by the mechanical module, showing that the elastic modulus of the tissue around the injury site decreases from 10 kPa to 8 kPa within a week after injury, etc. The activity abnormality feature refers to the feature information extracted from the multi-modal activity data, which can represent the deviation of AMPK-Pak2 activity from the normal state, including transient features, sustained features, and coupled features. The transient feature reflects the sudden abnormal change of activity in a short time; the sustained feature reflects the abnormal state maintained by the activity in a longer period of time; and the coupled feature describes the abnormal correlation between AMPK-Pak2 activity and other physiological and pathological process-related parameters. The activity detection module refers to a functional module composed of a hardware layer, an algorithm layer, and a feedback layer, which is used for real-time detection and analysis of the activity state of AMPK-Pak2 and outputs the detection results. The hardware layer integrates a low-power SoC chip, which is responsible for implementing edge computing, such as real-time calculation of the p-AMPK / p-Pak2 ratio to obtain the activity quantification index of AMPK-Pak2; the algorithm layer deploys a lightweight LSTM network, which uses the network to learn and predict the time series activity data, enabling the prediction of activity trends with a prediction window ≥ 30s; and the feedback layer pushes a hierarchical alarm to the clinical terminal through Bluetooth 5.2, such as a yellow warning: activity deviation from baseline by 20%, enabling the clinician to timely understand the changes in the AMPK-Pak2 activity state of the patient.

[0147] Optionally, the AMPK-Pak2 activity signal in the lesion of the patient with nerve injury can be collected by an implantable biological fluorescence sensor, and the spatiotemporal activity gradient feature in the AMPK-Pak2 activity signal can be analyzed by combining a sliding window dynamic time warping (DTW) algorithm and functional MRI.

[0148] S4, calculate a nerve protection efficiency index of the nerve injury patient based on the local AMPK-Pak2 activity state, and generate an adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the nerve protection efficiency index.

[0149] The embodiment of the present application can quantitatively evaluate the actual effect of the nerve protection measure, optimize the formulation and adjustment of the nerve protection scheme, and improve the pertinence and effectiveness of the nerve protection in the nerve injury repair process by calculating the nerve protection efficiency index of the nerve injury patient based on the local AMPK-Pak2 activity state. The nerve protection efficiency index refers to a comprehensive index for quantitatively evaluating the actual effect of the nerve protection intervention measure implemented for the patient in protecting nerve cells and promoting nerve repair and regeneration.

[0150] As an embodiment of the present application, the calculation of the nerve protection efficiency index of the nerve injury patient based on the local AMPK-Pak2 activity state comprises:

[0151] extracting dynamic activity parameters of the local AMPK-Pak2 activity state;

[0152] defining parameter efficiency threshold values of the dynamic activity parameters;

[0153] identifying a nerve repair process of the nerve injury patient and a process adaptation coefficient thereof;

[0154] calculating a real-time process deviation value of the nerve repair process based on the process adaptation coefficient;

[0155] combining the parameter efficiency threshold values, the process adaptation coefficient, and the real-time process deviation value to calculate the nerve protection efficiency index of the nerve injury patient.

[0156] The dynamic activity parameter refers to a set of quantitative indicators reflecting the real-time activity change characteristics of the local AMPK-Pak2 pathway of a patient with nerve injury, including the phosphorylation rate of AMPK (unit: pmol / min mg protein, such as an increase from 0.3 pmol / min mg protein to 0.8 pmol / min mg protein within 12 hours after injury of a certain patient), the fluctuation amplitude of the kinase activity of Pak2 (unit: %, such as a difference of 25% between the maximum value and the minimum value of the activity within a day), the interaction frequency of AMPK and Pak2 (unit: times / min, such as 3 molecular binding events detected per minute), etc. The parameter performance threshold refers to a critical value or interval of the dynamic activity parameter that can achieve effective nerve protection, which is determined based on the physiological activity range of the AMPK-Pak2 pathway in the nerve tissue of healthy people and clinical research, and is a benchmark for judging whether the activity parameter reaches the protection effect. For example, the performance threshold interval of the phosphorylation level of AMPK is 0.5-1.2 pmol / mg protein (95% confidence interval of the sciatic nerve tissue of healthy adults), and if the detection value of the patient is 0.6 pmol / mg protein, which is within the threshold interval, it indicates that the basic activity meets the standard. The nerve repair process refers to the specific process of the injured nerve tissue in terms of structural repair and functional recovery after nerve injury, which can be characterized by quantifiable stage indicators, including axon regeneration length, myelin repair coverage, nerve conduction velocity recovery rate, etc. The process adaptation coefficient refers to the ideal progress standard value that matches the nerve repair process, which is set in advance according to the type and degree of nerve injury and individual characteristics of the patient. For example, for a 25-year-old patient with mild sciatic nerve contusion, the process adaptation coefficient can be set as the ideal rate of axon regeneration 1.0 mm / d (based on clinical big data statistics of patients of the same age); for a 60-year-old patient with severe spinal cord injury, the adaptation coefficient of myelin repair can be set as a 5% weekly coverage increase. The real-time process deviation value is a quantitative indicator calculated by the ratio of the actual observed value of the nerve repair process to the process adaptation coefficient (ideal value). For example, for a 60-year-old patient with severe spinal cord injury, the process adaptation coefficient (ideal weekly coverage increase) of myelin repair is 5%, the actual weekly coverage increase is 7%, and the real-time process deviation value is 7% ÷ 5% = 1.4, i.e. the actual progress is 1.4 times the ideal progress, indicating that the actual repair progress is ahead of the ideal progress.

[0157] Optionally, the nerve repair process of the patient with nerve injury can be identified by MRI imaging technology, and the dynamic activity parameter of the local AMPK-Pak2 activity state can be extracted by biofluorescent labeling or phosphorylation detection technology.

[0158] As another embodiment of the present application, the nerve protection performance index of the patient with nerve injury is calculated by the following formula:

[0159]

[0160] wherein, represents the neuroprotective efficacy index, represents the jth dynamic activity parameter, represents the weight coefficient of the jth dynamic activity parameter, represents the balance coefficient, n represents the number of dynamic activity parameters, and j represents the index of the dynamic activity parameter category, represents the parameter efficacy threshold of the jth dynamic activity parameter, represents the actual nerve repair progress, represents the standard nerve repair progress, represents the progress adaptation coefficient, represents the efficacy decay coefficient.

[0161] It should be noted that in the present application, the above formula breaks through the limitations of traditional single index evaluation, organically combines dynamic activity parameters with nerve repair progress through mathematical models, and realizes the multi-scale evaluation from the molecular level to the organizational function level by reflecting the real-time activity state of the AMPK-Pak2 pathway, and by reflecting the deviation of the repair progress, and by balancing the contributions of both, the formula represents the dynamic activity integrated value, which is used to reflect the synergistic effect of multiple dynamic activity parameters, represents the real-time progress deviation value, wherein, is the standard ideal progress set according to the site of nerve injury, which can be measured 3 times per week by high-resolution ultrasound images (resolution ≥ 0.1 mm), and the average value is determined, is used to adjust the contribution ratio of activity parameters and repair progress, which can be dynamically adjusted according to the time node after injury, for example, the acute phase (<2 weeks) can be set =0.7 (focus on activity), and the recovery period is set =0.4 (focus on progress), is the decay coefficient of neuroprotective efficacy, which can be determined by collecting follow-up data (tracking time ≥ 6 months) of at least 200 cases of nerve injury patients, and fitting the relationship curve between the deviation value and the actual nerve function recovery score (such as FIM score) by least squares method.

[0162] Further, the embodiment of the present application can dynamically quantify the real-time matching state of the AMPK-Pak2 pathway regulation operation and the physiological safety boundary of nerve injury repair by generating the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotective efficacy index, thereby improving the precise regulation capability and neuroprotective effectiveness of the AMPK-Pak2 pathway regulation mode in a complex nerve injury environment. The adaptive adjustment instruction refers to an instruction set that can dynamically adjust the regulation parameters and is automatically generated according to the local AMPK-Pak2 activity state of the nerve injury patient and the changes in the nerve repair process.

[0163] As an embodiment of the present application, the generation of the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotective efficacy index comprises:

[0164] Collecting patient clinical data and prognosis analysis reports under the AMPK-Pak2 pathway regulation mode;

[0165] Setting a dynamic calibration threshold of the neuroprotective efficacy index according to the patient clinical data and the prognosis analysis reports;

[0166] Labeling the risk level of the neuroprotective efficacy index based on the dynamic calibration threshold;

[0167] Mapping the risk level to a hierarchical regulation instruction of the AMPK-Pak2 pathway regulation mode;

[0168] Dynamically generating adaptive adjustment parameters corresponding to the hierarchical regulation instruction based on the risk level;

[0169] Defining a synergistic regulation variable of the AMPK-Pak2 pathway regulation mode according to the adaptive adjustment parameters;

[0170] Generating the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode in combination with the adaptive adjustment parameters and the synergistic regulation variable.

[0171] The patient clinical data refers to the sum of various types of quantitative and qualitative information related to the patient's condition, treatment response and physical state collected during the treatment and monitoring of patients with nerve injury using AMPK-Pak2 pathway regulation, including AMPK / Pak2 activity level data, nerve electrophysiological signal data, inflammation marker data and imaging index data. The prognosis analysis report refers to a written report formed after predicting and evaluating the future trend of nerve function recovery, possible complications and neuroprotective effect of patients with nerve injury using AMPK-Pak2 pathway regulation. The dynamic calibration threshold refers to the critical value or interval set for the neuroprotective efficacy index that can be dynamically adjusted according to the patient's clinical data and prognosis analysis report as the patient's condition changes and the treatment progresses. For example, for an acute nerve injury patient, the initial dynamic calibration threshold may be set to a normal range of neuroprotective efficacy index 0.6-0.9. After 2 weeks of treatment, according to the clinical data showing good recovery, the prognosis analysis report predicts that the efficacy index can be further improved, and the dynamic calibration threshold can be adjusted to 0.7-1.0, to more strictly evaluate the subsequent neuroprotective effect, the risk level refers to the level of neuroprotective condition of the patient with nerve injury under the regulation mode of the AMPK-Pak2 pathway according to the position and trend of the neuroprotective efficacy index relative to the dynamic calibration threshold, including level I (low risk): the neuroprotective efficacy index is stable in the healthy benchmark range, marked as green; level II (medium risk): the neuroprotective efficacy index is continuously lower than the benchmark but does not reach the critical value, marked as yellow; level III (high risk): the neuroprotective efficacy index breaks through the threshold or drops sharply in a short period of time, marked as red and triggers an alarm, the hierarchical regulation instruction refers to the instruction level obtained according to the risk level, which is used to guide the specific operation of the regulation mode of the AMPK-Pak2 pathway, including level 1 (basic maintenance), level 2 (active enhancement), and level 3 (emergency activation), for example, when the risk level is I (low risk), the corresponding level 1 (basic maintenance) instruction is to maintain the current AMPK activator dose of 10 mg per day and the Pak2 inhibitor medication frequency of once per day; when the risk level is II (medium risk), the corresponding level 2 (active enhancement) instruction is to increase the AMPK activator dose to 15 mg per day, while increasing the Pak2 activity detection frequency by 2 times per week; when the risk level is III (high risk), the corresponding level 3 (emergency activation) instruction is to immediately inject AMPK potent activator intravenously, suspend the use of Pak2 inhibitor, and monitor the AMPK and Pak2 activity every 2 hours, the adaptive adjustment parameter refers to the quantitative parameter dynamically generated based on the risk level, which is used to specifically adjust the operation of each item in the regulation mode of the AMPK-Pak2 pathway, for example, under the risk level I (low risk), the adaptive adjustment parameter can be the dose fluctuation range of the AMPK activator ±1 mg / day, and the Pak2 inhibitor administration time deviation is allowed ±30 minutes; under the risk level II (medium risk), the parameter can be adjusted to increase the AMPK activator dose by 5-10 mg / day, and shorten the detection interval by 2-4 hours; under the risk level III (high risk), the parameter can be to urgently increase the AMPK activator dose by 10-20 mg / day, while starting the standby detection equipment, and increasing the detection accuracy to ±0.01 pmol / mg protein, the synergistic regulation variable refers to the variable defined according to the adaptive adjustment parameter, which is used to coordinate the mutual cooperation between the regulation measures (such as drug use, detection frequency, intervention timing, etc.) in the regulation mode of the AMPK-Pak2 pathway, for example, when the adaptive adjustment parameter is to increase the AMPK activator dose and increase the Pak2 activity detection frequency, the synergistic regulation variable can be the ratio of the amount of activator dose increase to the increase amplitude of detection frequency (such as 5 mg of dose increase per day, 1 time / day of detection frequency increase), and the time interval of the two adjustments (such as increasing the dose for 24 hours before increasing the detection frequency).

[0172] Optionally, the dynamic calibration threshold of the neuroprotective efficacy index can be set by a machine learning model, such as a random forest model, and the mapping of the risk level to the hierarchical regulation instruction for regulating the AMPK-Pak2 pathway can be implemented based on a decision tree method of a rule engine.

[0173] S5, calculate the neuron apoptosis rate of the patient with nerve injury, and identify the treatment response state of the patient with nerve injury according to the neuron apoptosis rate and the neurological function score.

[0174] The embodiment of the present application can improve the accuracy of the evaluation of the treatment effect of the patient with nerve injury by calculating the neuron apoptosis rate of the patient with nerve injury and identifying the treatment response state of the patient with nerve injury according to the neuron apoptosis rate and the neurological function score. At the same time, the real-time judgment of the treatment response type can provide accurate basis for adjusting the neuroprotective strategy, improve the efficiency of neurological function recovery and the pertinence of neuroprotection. The neuron apoptosis rate refers to the percentage of the number of apoptotic neurons in a specific injury area of the patient with nerve injury to the total number of neurons in the area. The specific calculation steps are as follows: the number of apoptotic neurons and the total number of neurons in the injury area are calculated by tissue section staining (such as TUNEL staining) or flow cytometry detection. The treatment response state refers to the overall state of the patient with nerve injury after receiving a specific treatment (such as AMPK-Pak2 pathway regulation), which is improved, stable or worsened, combined with the dynamic change of the neuron apoptosis rate and the neurological function score.

[0175] As an embodiment of the present application, the identification of the treatment response state of the patient with nerve injury according to the neuron apoptosis rate and the neurological function score comprises:

[0176] Performing standardization conversion processing on the neuron apoptosis rate to obtain a cell survival evaluation vector;

[0177] Extracting the motor function score, sensory function score and autonomic nervous function score in the neurological function score to generate a functional recovery parameter vector;

[0178] Analyzing the dynamic change trend of the neuron apoptosis rate to extract an apoptosis trend feature vector under the dynamic change trend;

[0179] Generating a cell survival feature vector of the patient with nerve injury based on the apoptosis trend feature vector and the cell survival evaluation vector;

[0180] According to the neurological function score, calculating the functional recovery efficiency index and the stability index of the patient with nerve injury;

[0181] determining a functional recovery evaluation vector of the patient with neural injury based on the functional recovery efficiency index and the stability index;

[0182] constructing a treatment response feature matrix of the patient with neural injury by combining the cell survival evaluation vector, the functional recovery parameter vector, the cell survival feature vector and the functional recovery evaluation vector;

[0183] identifying a treatment response state of the patient with neural injury based on the treatment response feature matrix.

[0184] The cell survival evaluation vector refers to a multidimensional vector for quantifying the survival state of neurons in the injury area of the patient with neural injury. The motor function score refers to an index for quantitatively scoring the motor ability (such as joint mobility, muscle strength, motion coordination, etc.) of the patient with neural injury by using a standardized neural function evaluation scale (such as the muscle strength grading scale, the Fugl-Meyer motor function score scale). The sensory function score refers to an index for quantifying the recovery condition of the somatic sensation (such as touch, pain, temperature, and proprioception, etc.) of the patient with neural injury by using a standardized evaluation tool (such as the pinprick sensation, light touch, and vibration sensation test scale). Usually, a 0-10 point system or a grading score (such as 0 points for no sensation and 10 points for normal sensation) is used. The autonomic nervous function score refers to an index for quantitatively evaluating the autonomic nervous system function (such as heart rate regulation, blood pressure control, sweating function, bladder and rectum function, etc.) of the patient with neural injury by using a composite score scale (such as the COMPASS-31 scale), with a score range of 0-100 points. The higher the score, the more severe the autonomic nervous dysfunction. The functional recovery parameter vector refers to a three-dimensional vector composed of the motor function score, the sensory function score, and the autonomic nervous function score, which is used to comprehensively represent the multidimensional recovery condition of the neural function of the patient with neural injury. Each element in the vector corresponds to a standardized value of a functional score. The dynamic change trend refers to the rising, falling, or stable change law of the neuron apoptosis rate within a continuous monitoring period (such as daily or weekly). The apoptosis trend feature vector refers to a feature vector extracted based on the dynamic change trend of the neuron apoptosis rate, which includes three dimensions of trend direction (rising / falling / stable, represented by 1 / (-1) / 0 respectively), average change amplitude (such as the absolute value of the percentage change per week), and change acceleration (the difference between the change amplitudes of two consecutive weeks). The cell survival feature vector refers to a comprehensive vector formed by fusing the cell survival evaluation vector and the apoptosis trend feature vector. The functional recovery efficiency index refers to a value obtained by weighting the absolute change amount and the change rate of the comprehensive neural function score in combination with the improvement degree of the neuron apoptosis rate. The specific formula is: functional recovery efficiency index E = (absolute change amount of comprehensive neural function score) * (change rate of comprehensive neural function score) * (improvement degree of neuron apoptosis rate). + wherein, a neurological function score of the t th week, a baseline score, a neuronal apoptosis rate of the t th week, a baseline apoptosis rate, t is a treatment time (week), , a weight, satisfying + = 1, the stability index refers to an index for measuring the degree of fluctuation of the neurological function score within a continuous monitoring period, obtained by calculating the ratio of the score standard deviation to the mean value, with a value range of 0-1, and the smaller the value, the smaller the score fluctuation and the more stable the functional recovery, the functional recovery evaluation vector refers to a two-dimensional vector composed of the functional recovery efficiency index and the stability index, used for comprehensive evaluation of the efficiency and stability of the neurological function recovery of the neurological injury patient, each element in the vector is a standardized value, with a value range of 0-1, the higher the efficiency index standardized value, the faster the recovery, and the lower the stability index standardized value, the more stable the recovery, the treatment response feature matrix refers to a matrix formed by splicing the cell survival evaluation vector, the functional recovery parameter vector, the cell survival feature vector and the functional recovery evaluation vector column by column, with the rows of the matrix corresponding to different evaluation time points and the columns corresponding to different feature vector dimensions.

[0185] Optionally, the standardized conversion processing of the neuronal apoptosis rate can be realized by using the Z-score standardization method, and the dynamic change trend of the neuronal apoptosis rate can be analyzed by using the ARIMA time series model.

[0186] S6, based on the treatment response state, and in combination with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction, output a treatment execution scheme for the neurological injury patient.

[0187] The treatment execution scheme of the neurologic impairment patient is formed by taking the treatment response state as the core basis, fusing specific measures of the AMPK-Pak2 pathway regulation mode and dynamic modification rules of the adaptive adjustment instruction, and forming a standardized treatment operation scheme, for example, the treatment response state of a certain neurologic impairment patient is "general response", the basic regulation module of the treatment execution scheme is "AMPK activator 25 mg per day, once a day; Pak2 inhibitor 10 mg per day, once a day; detect the pathway activity once every 8 hours"; the dynamic adjustment module stipulates "if the neuron apoptosis rate decreases by less than 2% for two consecutive days, the AMPK activator dose is increased to 30 mg per day, and the detection interval is changed to once every 6 hours"; and the phase transition standard is set as "when the neurological function score increases by more than 1 point for three consecutive days and the apoptosis rate decreases by more than 3% per week, the scheme corresponding to 'good response' is entered.

[0188] Exemplarily, 30 acute ischemic stroke patients (onset time <72 hours) were selected, all of which were confirmed to have basal ganglia infarction by MRI, the neurological function score (NIHSS) was 10-15, and they were randomly divided into three groups: the experimental group: the AMPK-Pak2 pathway synergistic regulation method was used; the control group 1: only AMPK activator (metformin, 1500 mg per day) was used; the control group 2: only Pak2 inhibitor (FRAX597, 20 mg per day) was used, and the curative effects were compared as follows:

[0189]

[0190] Conclusion: The neurological function recovery rate of the experimental group by AMPK-Pak2 pathway synergistic regulation is significantly higher than that of the control groups with single target point intervention (P<0.01), which verifies the advantages of the method in targeted regulation of key signal pathways and improvement of neural repair effect.

[0191] Compared with the problems described in the background art, the embodiment of the present application can capture the path regulation dynamics and the nerve function recovery of the patient in real time by detecting the AMPK activity level and the Pak2 function state of the nerve injury patient and synchronously acquiring the nerve function score of the nerve injury patient, and providing data support for accurately judging the nerve protection effect based on the AMPK-Pak2 pathway regulation; further, the embodiment of the present application can integrate scattered pathway molecule data and nerve function recovery data by establishing the pathway-injury relationship graph of the nerve injury patient by using the AMPK activity level, the Pak2 function state and the nerve function score, and form a multi-dimensional and linked analysis system to provide a structured framework for real-time capturing of the dynamic correlation between the AMPK-Pak2 pathway regulation state and the nerve injury repair process; the embodiment of the present application can ensure that the pathway function can be accurately targeted for repair according to the abnormal type in the nerve protection based on the AMPK-Pak2 pathway regulation, realize the efficient reversal of nerve injury, and improve the targeting and specificity of the nerve protection intervention by determining the AMPK-Pak2 pathway regulation abnormality type of the nerve injury patient based on the pathway-injury relationship graph; further, the embodiment of the present application can adapt to the abnormal characteristics of different types of pathways, form a targeted and synergistic nerve protection system, ensure efficient intervention on complex pathway regulation abnormality scenarios, and improve the nerve protection effect based on the AMPK-Pak2 pathway regulation by matching the AMPK-Pak2 targeted drugs of the nerve injury patient according to the AMPK-Pak2 pathway regulation abnormality type and positioning the nerve injury area of the nerve injury patient; the embodiment of the present application can break through the limitations of single drug treatment, improve the accuracy of correcting the pathway abnormalities, and enhance the effectiveness and safety of the AMPK-Pak2 pathway regulation mode for nerve injury treatment by setting the AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drugs and the nerve injury area; further, the embodiment of the present application can dynamically quantify the real-time matching degree of the pathway regulation effect and the nerve function recovery target by monitoring the local AMPK-Pak2 activity state of the nerve injury patient in real time based on the AMPK-Pak2 pathway regulation mode, improve the precision intervention ability and treatment safety of the AMPK-Pak2 pathway regulation in complex nerve injury scenarios; the embodiment of the present application can quantitatively evaluate the actual effect of the nerve protection measure, optimize the formulation and adjustment of the nerve protection scheme, and improve the targeting and effectiveness of the nerve protection in the nerve injury repair process by calculating the nerve protection efficiency index of the nerve injury patient based on the local AMPK-Pak2 activity state.Further, the embodiment of the present application can dynamically quantify the real-time matching state of the AMPK-Pak2 pathway regulation operation and the physiological safety boundary of nerve injury repair by generating the adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotective efficacy index, thereby improving the precise regulation capability and neuroprotective effectiveness of the AMPK-Pak2 pathway regulation mode in a complex nerve injury environment; the embodiment of the present application can improve the accuracy of the treatment effect evaluation of the nerve injury patient by calculating the neuron apoptosis rate of the nerve injury patient and identifying the treatment response state of the nerve injury patient according to the neuron apoptosis rate and the neurological function score, and can also provide a precise basis for adjusting the neuroprotective strategy by judging the treatment response type in real time, thereby improving the efficiency of neurological function recovery and the pertinence of neuroprotection; finally, the embodiment of the present application can output the treatment execution scheme of the nerve injury patient by combining the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction based on the treatment response state, which can not only significantly improve the comprehensiveness of neurological function recovery and reduce the residual defects of neurological function, but also can dynamically adjust the regulation strategy according to the treatment response characteristics of the patient, the nerve repair process and the like, thereby effectively improving the precision and clinical effectiveness of neuroprotective treatment, and can also evaluate the treatment response state and optimize the treatment process through adaptive regulation, thereby reducing the risk of over-treatment, improving the activation efficiency of the neuroprotective mechanism, and enhancing the long-term recovery effect of the patient. Therefore, the neuroprotective method and system based on the AMPK-Pak2 pathway regulation provided by the embodiment of the present application can target the regulation of key signaling pathways in cells, thereby improving the overall recovery effect of neurological function.

[0192] As shown in Figure 3 FIG. 1 is a functional module diagram of a neuroprotective system based on AMPK-Pak2 pathway regulation according to the embodiment of the present application.

[0193] The neuroprotective system based on AMPK-Pak2 pathway regulation 200 can be installed in an electronic device. According to the functions to be implemented, the neuroprotective system based on AMPK-Pak2 pathway regulation can include a graph construction module 201, a typing matching module 202, a regulation generation module 203, an efficacy evaluation module 204, a response analysis module 205 and a scheme output module 206. The modules of the present application can also be referred to as units, which refer to a series of computer program segments that can be executed by an electronic device processor and can complete a fixed function, and are stored in the memory of the electronic device.

[0194] In the embodiment of the present application, the functions of each module / unit are as follows:

[0195] The atlas construction module 201 is configured to detect the AMPK activity level and Pak2 function state of the patient with neural injury, and synchronously acquire the neural function score of the patient with neural injury, and establish a pathway-injury relationship graph of the patient with neural injury by using the AMPK activity level, the Pak2 function state and the neural function score.

[0196] The typing matching module 202 is configured to determine the AMPK-Pak2 pathway abnormality typing of the patient with neural injury based on the pathway-injury relationship graph, match the AMPK-Pak2 targeted drug of the patient with neural injury according to the AMPK-Pak2 pathway abnormality typing, and locate the neural injury area of the patient with neural injury.

[0197] The regulation generation module 203 is configured to set the AMPK-Pak2 pathway regulation mode of the patient with neural injury according to the AMPK-Pak2 targeted drug and the neural injury area, and monitor the local AMPK-Pak2 activity state of the patient with neural injury in real time based on the AMPK-Pak2 pathway regulation mode.

[0198] The efficacy evaluation module 204 is configured to calculate the neuroprotective efficacy index of the patient with neural injury based on the local AMPK-Pak2 activity state, and generate an adaptive adjustment instruction of the AMPK-Pak2 pathway regulation mode according to the neuroprotective efficacy index.

[0199] The response analysis module 205 is configured to calculate the neuron apoptosis rate of the patient with neural injury, and identify the treatment response state of the patient with neural injury according to the neuron apoptosis rate and the neural function score.

[0200] The scheme output module 206 is configured to output a treatment execution scheme of the patient with neural injury based on the treatment response state, and in combination with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction.

[0201] In detail, the modules in the neuroprotective system 200 based on AMPK-Pak2 pathway regulation in the embodiments of the present application use the same technical means as the neuroprotective method based on AMPK-Pak2 pathway regulation in the above-mentioned Figure 1 , and can produce the same technical effects, which will not be described here again.

[0202] It is obvious for those skilled in the art that the present application is not limited to the details of the above exemplary embodiments, and the present application can be implemented in other specific forms without departing from the spirit or essential characteristics of the present application.

[0203] Finally, it should be noted that in the above embodiments, each embodiment can be combined with or independent of each other, and deleting any one of them does not affect the technical implementation of the other embodiments. The above embodiments are only used to illustrate the technical solutions of the present application and are not limiting. Although the present application has been described in detail with reference to the preferred embodiments, those skilled in the art should understand that the technical solutions of the present application can be modified or replaced by equivalents without departing from the spirit and scope of the present application.

Claims

1. A neuroprotective method based on AMPK-Pak2 pathway regulation, characterized in that, The method includes: The activity level of AMPK and the functional status of Pak2 in patients with nerve injury were detected, and the neurological function scores of the patients with nerve injury were obtained simultaneously. Using the AMPK activity level, the functional status of Pak2, and the neurological function scores, a pathway-damage relationship map of the patients with nerve injury was established. Among them, AMPK is adenosine monophosphate activated protein kinase, and Pak2 is p21 activated kinase 2. Based on the pathway-damage relationship diagram, the abnormal AMPK-Pak2 pathway regulation of the patients with nerve damage is determined. According to the abnormal AMPK-Pak2 pathway regulation, the AMPK-Pak2 targeted drug of the patients with nerve damage is matched, and the nerve damage area of ​​the patients with nerve damage is located. Based on the AMPK-Pak2 targeted drug and the nerve injury area, the AMPK-Pak2 pathway regulation mode of the nerve injury patient is set, and the local AMPK-Pak2 activity status of the nerve injury patient is monitored in real time based on the AMPK-Pak2 pathway regulation mode. Based on the local AMPK-Pak2 activity state, the neuroprotective efficacy index of the nerve-injured patient is calculated, and an adaptive adjustment instruction for the AMPK-Pak2 pathway regulation mode is generated according to the neuroprotective efficacy index. Calculate the neuronal apoptosis rate of the patients with nerve injury, and identify the treatment response status of the patients with nerve injury based on the neuronal apoptosis rate and the neurological function score; Based on the treatment response state, and in conjunction with the AMPK-Pak2 pathway regulation method and the adaptive adjustment instruction, a treatment execution plan for the patient with nerve injury is output.

2. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The process of establishing a pathway-damage relationship map for patients with neurological injury using the AMPK activity level, Pak2 functional status, and neurological function score includes: The pathological stages corresponding to the AMPK activity level, Pak2 functional status, and neurological function scores were analyzed. Based on the pathological process stage, characteristic interconnected fluctuation segments of the AMPK activity level, the Pak2 functional status, and the neurological function score are identified. Analyze the pathway-damage correlation level of the aforementioned characteristic linkage fluctuation segment; Develop rules for integrating indicators corresponding to the pathway-damage association levels; Based on the aforementioned indicator integration rules, a pathway-damage relationship diagram is constructed for the patients with nerve injuries.

3. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The process of determining the AMPK-Pak2 pathway regulation abnormality classification in patients with nerve injury based on the pathway-damage relationship diagram includes: Extract the external imbalance manifestations and internal mechanisms of the pathway-damage relationship diagram; By combining the external manifestations of imbalance with the internal mechanisms, a multidimensional regulatory feature vector is established for the patients with nerve damage. Collect actual regulatory data of the AMPK-Pak2 pathway from the pathway-damage relationship diagram; Based on the actual control data, the feature deviation index of the multidimensional control feature vector is calculated; Based on the multidimensional regulation feature vector and the feature deviation index, potential abnormal regulation categories are selected from the preset abnormal pathway regulation category library; The clinicopathological features of the patients with the nerve injury were analyzed, and a correlation test was performed between the potential abnormal regulation category and the clinicopathological features to obtain the correlation test results. Based on the correlation test results, the classification rules for the AMPK-Pak2 pathway are determined. The classification rules are used to determine the abnormal AMPK-Pak2 pathway regulation in patients with nerve damage.

4. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The AMPK-Pak2-targeting drugs matched to patients with nerve damage based on the AMPK-Pak2 pathway regulation abnormality classification include: Extract the key regulatory parameters corresponding to the abnormal AMPK-Pak2 pathway regulation subtypes; Based on the aforementioned key regulatory parameters, candidate targeted drugs are screened from a pre-defined targeted drug library. Calculate the efficacy matching degree of the candidate targeted drugs; The effective duration of action of the candidate targeted drug was determined; Based on the efficacy matching and the effective duration of action, the AMPK-Pak2 targeted drug is matched to the patients with nerve injury.

5. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The method of regulating the AMPK-Pak2 pathway in patients with nerve injury, based on the AMPK-Pak2-targeting drug and the nerve injury area, includes: Acquire anatomical imaging data and pathological staging data of the nerve injury area; Based on the anatomical imaging data, the drug accumulation coefficient of the nerve injury area is calculated; Analyze the drug delivery characteristics of the AMPK-Pak2 targeted drug; Based on the drug accumulation coefficient and the drug delivery characteristics, the dosing parameters for the patients with nerve injury are determined; Using the pathological staging data, the timing of AMPK-Pak2 pathway regulation in patients with nerve injury was planned; By regulating the timing of the AMPK-Pak2 pathway, the threshold for pathway activity fluctuation in the patients with nerve injury is defined. By combining the drug administration parameters, the timing of AMPK-Pak2 pathway regulation, and the threshold of pathway activity fluctuation, the AMPK-Pak2 pathway regulation mode for patients with nerve injury is set.

6. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The method of real-time monitoring of local AMPK-Pak2 activity in patients with nerve injury based on the AMPK-Pak2 pathway regulation includes: Based on the AMPK-Pak2 pathway regulation mechanism, AMPK-Pak2 activity signals were collected at the lesion site of the patient with nerve injury. The spatiotemporal activity gradient features in the AMPK-Pak2 activity signal were analyzed. Using the spatiotemporal activity gradient features, the AMPK-Pak2 activity sensitive area of ​​the lesion is defined; A multimodal sensing array of the neurologically injured patient is configured in the AMPK-Pak2 active sensitive area; Construct a spatiotemporal synchronization network for the multimodal sensing array and collect multimodal activity data of the multimodal sensing array under the spatiotemporal synchronization network; Extract the activity anomaly features of the AMPK-Pak2 activity-sensitive region from the multimodal activity data; Based on the described abnormal activity characteristics, an activity detection module for the AMPK-Pak2 activity-sensitive region is constructed. Based on the activity detection module, the AMPK-Pak2 activity status of the patients with nerve damage can be monitored in real time.

7. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The calculation of the neuroprotective efficacy index for the patient with nerve injury based on the local AMPK-Pak2 activity status includes: Extract the dynamic activity parameters of the local AMPK-Pak2 activity state; Define the parameter effectiveness threshold for each of the aforementioned dynamic activity parameters; Identify the nerve repair process and its process fit coefficient in the patients with the aforementioned nerve injury; Based on the process adaptation coefficient, the real-time process deviation value of the neural repair process is calculated; The neuroprotective efficacy index of the patient with nerve injury is calculated by combining the parameter efficacy threshold, the process adaptation coefficient, and the real-time process deviation value.

8. The neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The step of generating adaptive adjustment instructions for the AMPK-Pak2 pathway regulation based on the neuroprotective efficacy index includes: Collect clinical data and prognostic analysis reports of patients under the AMPK-Pak2 pathway regulation mode; Based on the patient's clinical data and the prognostic analysis report, a dynamic calibration threshold for the neuroprotective efficacy index is set. Based on the dynamic calibration threshold, the risk level of the neuroprotective efficacy index is labeled; The risk level is mapped to a hierarchical control instruction of the AMPK-Pak2 pathway regulation mode; Based on the risk level, adaptive adjustment parameters corresponding to the hierarchical control instructions are dynamically generated; Based on the adaptive adjustment parameters, define the co-regulatory variables for the AMPK-Pak2 pathway regulation mechanism; By combining the adaptive adjustment parameters and the collaborative regulation variables, an adaptive adjustment command for the AMPK-Pak2 pathway regulation mode is generated.

9. A neuroprotective method based on AMPK-Pak2 pathway regulation as described in claim 1, characterized in that, The step of identifying the treatment response status of the patient with neurological injury based on the neuronal apoptosis rate and the neurological function score includes: Perform a standardized transformation of the neuronal apoptosis rate to obtain a cell survival evaluation vector; The motor function score, sensory function score, and autonomic nervous function score are extracted from the neurological function score to generate a functional recovery parameter vector; The dynamic trend of neuronal apoptosis rate was analyzed to extract the apoptosis trend feature vector under the dynamic trend. Based on the apoptosis trend feature vector and the cell survival evaluation vector, a cell survival feature vector of the neurological injury patient is generated; Based on the neurological function scores, the functional recovery efficiency index and stability index of the patients with neurological injuries were calculated. Based on the functional recovery efficiency index and the stability index, a functional recovery assessment vector for the patient with nerve injury is determined; By combining the cell survival evaluation vector, the functional recovery parameter vector, the cell survival feature vector, and the functional recovery assessment vector, a treatment response feature matrix for the patient with nerve injury is constructed. Based on the treatment response feature matrix, the treatment response status of the patient with nerve injury is identified.

10. A neuroprotective system based on AMPK-Pak2 pathway regulation, characterized in that, The system includes: The atlas construction module is used to detect the AMPK activity level and Pak2 functional status of patients with nerve injury, and simultaneously acquire the neurological function scores of patients with nerve injury. Using the AMPK activity level, the Pak2 functional status, and the neurological function scores, a pathway-damage relationship map of the patients with nerve injury is established; wherein, AMPK is adenosine monophosphate activated protein kinase, and Pak2 is p21 activated kinase 2. The subtyping matching module is used to determine the abnormal AMPK-Pak2 pathway regulation of the nerve injury patient based on the pathway-damage relationship diagram, match the AMPK-Pak2 targeted drug of the nerve injury patient according to the abnormal AMPK-Pak2 pathway regulation, and locate the nerve damage area of ​​the nerve injury patient. The regulation generation module is used to set the AMPK-Pak2 pathway regulation mode of the nerve injury patient according to the AMPK-Pak2 targeted drug and the nerve injury area, and to monitor the local AMPK-Pak2 activity status of the nerve injury patient in real time based on the AMPK-Pak2 pathway regulation mode. The efficacy assessment module is used to calculate the neuroprotective efficacy index of the patient with nerve injury based on the local AMPK-Pak2 activity state, and generate adaptive adjustment instructions for the AMPK-Pak2 pathway regulation mode based on the neuroprotective efficacy index. The response analysis module is used to calculate the neuronal apoptosis rate of the patient with nerve injury, and to identify the treatment response status of the patient with nerve injury based on the neuronal apoptosis rate and the neurological function score. The treatment plan output module is used to output the treatment execution plan for the patient with nerve injury based on the treatment response state, combined with the AMPK-Pak2 pathway regulation mode and the adaptive adjustment instruction.

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