18 results about "Cognitive defects" patented technology

The invention discloses a nerve regulation system for cognitive impairment, and the system comprises a cognitive behavior evaluation module which is used for recognizing a cognitive defect field which needs to be improved by a target object; the image data acquisition module is used for acquiring and preprocessing task state nuclear magnetic data and T1 weighted structure images of a target object; the brain region activation analysis module is used for determining a neural regulation potential target spot according to the preprocessed task state nuclear magnetic data; the brain network analysis module is used for identifying key nodes related to cognitive defects; the stimulation target screening module is used for determining an individualized stimulation target of the target object according to the nerve regulation potential target and the key node of the target object; the time domain interference electrical stimulation simulation and implementation module is used for performing electrical stimulation on the individualized stimulation target spot; and the dynamic feedback adjustment module is used for dynamically adjusting the stimulation parameters and enhancing the personalized regulation and control effect. By adopting the method and the device, the specific brain region directly related to the cognitive impairment can be determined, so that the targeting and the accuracy of treatment are enhanced.

The invention discloses bifidobacterium longum capable of regulating circadian rhythm and remarkably improving cognitive memory ability and application of the bifidobacterium longum, and belongs to the technical field of microorganisms. The bifidobacterium longum GDMCC No: 65850 provided by the invention can effectively relieve rhythm gene expression disorder caused by sleep deprivation, thereby relieving cognitive defects of mice with circadian rhythm disorder. Besides, the intervention of the bifidobacterium longum GDMCC No: 65850 can regulate the intestinal flora health and the change of the intestinal metabolite level, promote the generation of neuroprotective metabolite and reduce the cognitive ability decline caused by circadian rhythm disorder. According to the bifidobacterium longum, the application range of the bifidobacterium longum as probiotics is expanded, and the bifidobacterium longum has a huge application prospect in products for relieving cognitive memory ability decline induced by circadian rhythm disorder.

The invention discloses a self-adaptive education system based on knowledge gene evolution, and belongs to the technical field of knowledge gene evolution. The system comprises a dynamic knowledge graph engine, a defect response type training sequence generator, a multi-modal memory intensifier and a hypercycle coordination module, wherein the dynamic knowledge graph engine decomposes subject knowledge into heritable units and constructs a dynamic association network of which the weight is updated in real time along with a learning data flow; a defect response type training sequence generator generates a target variable type training sequence according to the cognitive defect node coordinates; the multi-modal memory intensifier generates multi-sensory nerve coding pulses according to training feedback; and the hypercycle coordination module is connected in series with the modules to form a self-adaptive closed loop of knowledge modeling, defect clearing, memory curing and knowledge iteration. The system can generate a cognitive defect thermodynamic diagram, realizes accurate positioning of cognitive vulnerabilities, provides clear targets for teaching intervention, and improves the pertinence and effectiveness of adaptive education.

Alkoxy-substituted N-benzyl-2-phenylacetamide compounds and derivatives are G-protein coupled receptor (GPR) 88 modulators for use in the treatment of a disease mediated by GPR88. Indications include Tourette's Syndrome, Huntington's Disease (HD), Addiction, Parkinson's Disease (PD), Schizophrenia, and Attention Deficit Hyperactivity Disorder (ADHD), choreiform movements, speech delay, learning disabilities, depression, hyperkinetic movement disorders characterised by chorea and / or dystonia, psychosis, cognitive deficits in schizophrenia, affective disorders, bipolar disorder, Alzheimer's disease and basal ganglia disorders.

The present application relates to the technical field of cognitive impairment rehabilitation, in particular to a brain cognitive recovery training scheme analysis system and method for cognitive impairment, comprising five units of basic information acquisition, cognitive test execution, test report generation, norm updating and training scheme analysis, wherein the norm database is modeled in multiple dimensions according to age, educational background and medical history, a regional correction factor is introduced, data freshness is verified by means of blockchain storage, an adaptive sequence is generated for cognitive test, multi-modal data such as correct answer rate, touch screen trajectory and eye movement data are collected, time domain signal separation and denoising are performed, the training scheme analysis unit locates cognitive defects, matches the training module, monitors the brain electrical theta wave and P300 latency through biological feedback, dynamically adjusts the training intensity and frequency, promotes neural circuit reorganization and improves rehabilitation accuracy.

Disclosed are compounds of formula (I) wherein G1 is as antagonists of the muscarinic acetylcholine receptor M4 (mAChR M4) for use in the treatment of e.g. a neurodegenerative disorder, a movement disorder, or a brain disorder, such as e.g. Parkinson's disease, drug-induced Parkinsonism, dystonia, Tourette's syndrome, dyskinesias, schizophrenia, cognitive deficits associated with schizophrenia, excessive daytime sleepiness, attention deficit hyperactivity disorder (ADHD), Huntington's disease, chorea, cerebral palsy, and progressive supranuclear palsy. An exemplary compound is e.g. (2,5-difluoro-4-(6-(((3aR,5s,6aS)-2-((tetrahydro-2H-pyran-4-yl)methyl)octahydrocyclopenta[c]pyrrol-5-yl)amino)pyridazin-3-yl)phenyl)(imino)(methyl)-λ6-sulfanone (e.g. example 12; compound no. 7) Pharmacological data on the activity of the compounds in an mAChR M4 cell-based assay are provided (e.g. table 2).TABLE 2Human M4Cpd. No.IC50 (nM)Emin (%)*113.44239.62318.5345846575.4361883746.0385607918.43101.821186.231243.42138.63*% ACh maximum at 30 μM.

The invention discloses a construction method and application of a fetal-derived autism rodent model, according to the method, a fatty acid methyl ester sulfonate solution (such as C16MES or C18MES) with the concentration of 6 mg / L is continuously given to a pregnant rodent from the 8.5 th day of pregnancy to the 21 days after offspring birth, and the influence of environmental exposure in the pregnancy period on fetal neurodevelopment is simulated. The offspring animals are subjected to multi-dimensional behavioral tests such as an open field experiment, a bead burying experiment, a self-hair combing experiment, a three-room social experiment and a new object recognition experiment, and the typical autism-like behaviors including social obstacles, inscribed plate repetition behaviors, anxiety and cognitive defects are shown. Compared with an existing gene editing or post-birth intervention model, the method targets a neural development key early-stage window period, is simple and convenient to operate and comprehensive in phenotype, and can more truly simulate an environment and gene interaction mechanism. The model can be used for screening intrauterine environment interferents and developing early diagnosis markers and therapeutic drugs.

The present disclosure provides methods of treating Alzheimer's Disease (AD) and rescuing cognitive deficits associated with AD in a subject having an apoE4 / 4 genotype, by administering a therapeutically effective amount of the loop-diuretic bumetanide to the subject. Also disclosed are kits for performing the method, including one or more doses of a bumetanide formulation; and which may also include instructions for treating a patient having an apoE4 / 4 genotype by administering bumetanide, and / or instructions and reagents for testing / identifying a subject having an apoE4 / 4 genotype.

Cycloalkylmethoxy- and cycloalkyloxy-substituted N-benzyl-2-phenylacetamide compounds and derivatives are G-protein coupled receptor (GPR) 88 modulators for use in the treatment of a disease mediated by GPR88. Indications include Tourette's Syndrome, Huntington's Disease (HD), Addiction, Parkinson's Disease (PD), Schizophrenia, and Attention Deficit Hyperactivity Disorder (ADHD), choreiform movements, speech delay, learning disabilities, depression, hyperkinetic movement disorders characterised by chorea and / or dystonia, psychosis, cognitive deficits in schizophrenia, affective disorders, bipolar disorder, Alzheimer's disease and basal ganglia disorders.

The embodiment of the invention provides a reading and related cognitive ability defect recognition device and method. The device comprises a test content generation module which is used for generating test content for testing the reading capability of a user according to basic information of the user under the condition that the reading capability defect risk of the user is determined, and displaying the test content to the user through an operation interface; the cognitive defect identification module is used for acquiring a response result of the user for the test content, and identifying whether the user has reading and related cognitive ability defects based on the response result; and the defect factor matching module is used for matching the users according to different reading-related cognitive ability defect factors under the condition of determining that the users have reading and related cognitive ability defects, and determining the reading-related cognitive ability defect factors matched with the users. By adopting the mode, whether the user has the reading ability defect or not can be identified, and the essential factors which really cause the reading ability defect of the user can also be identified.

The invention relates to the technical field of cognitive impairment rehabilitation, in particular to a human brain cognitive recovery training scheme analysis system and method for cognitive impairment, and the system comprises a basic information acquisition unit, a cognitive test execution unit, a test report generation unit, a norm updating unit and a training scheme analysis unit, a norm database performs multi-dimensional layered modeling according to age, education background and medical history, introduces a regionalized correction factor, stores an evidence through a block chain and verifies data freshness, generates an adaptive sequence through cognitive testing, collects answer accuracy, a touch screen track and eye movement data in a multi-modal manner, performs time domain signal separation and denoising, and trains a scheme analysis unit to position cognitive defects. The training module is matched, the incubation period of electroencephalogram theta waves and P300 is monitored through biological feedback, the training intensity and frequency are dynamically adjusted, neural circuit recombination is promoted, and rehabilitation accuracy is improved.

The present invention relates to a compound of formula (I) wherein R1 represents a (C1-C6)alkyl group, a spiro(C5-C11)bicyclic ring, a fused phenyl group, a substituted phenyl group, a R′-L- group, wherein L is either a single bond or a (C1-C3)alkanediyl group, and R′ represents a (C3-C8)cycloalkyl group, abridged (C6-C10)cycloalkyl group, a (C3-C8)heterocycloalkyl group, or a (C3-C8)heteroaryl group, or a R′-L- group wherein L is a (C1-C3)alkanediyl group, and R′ is an optionally substituted phenyl group, and wherein R2 represents a hydrogen atom or a (C1-C3)alkyl group or any of its pharmaceutically acceptable salt. The present invention further relates to a composition comprising a compound of formula (I) and a process for manufacturing said compound as well as its synthesis intermediates. It also relates to said compound for use as a medicament, in particular in the treatment and / or prevention of cognitive deficits associated with Down syndrome; Alzheimer's disease; dementia; tauopathies; Parkinson's disease; CDKL5 Deficiency Disorder; Phelan-McDermid syndrome; autism; type 1 and type 2 diabetes; abnormal folate and methionine metabolism; osteoarthritis; Duchenne muscular dystrophy; several cancers; neuroinflammation, anemia and viral and unicellular infections and for regulating body temperature.

The application discloses a target strategy and a drug intervention method for improving Primrose syndrome, and belongs to the technical field of biological medicine. The experiment proves that Momordin Ic can significantly improve the SUMO level of ZBTB20 in vitro cells or Primrose syndrome (PS) mice, can effectively improve the defects of reduced neuron dendritic branching in the hippocampal CA1 region of the PS mice in pathology, can enhance the complexity, and can improve the cognitive and emotional disorders such as memory impairment and anxiety-like behavior of the PS mice to different degrees in behavior. The application discloses that Momordin Ic can improve the PS-related neuropathological changes and behavioral cognitive defects by targeting the SENP1-ZBTB20-SUMO pathway, and provides a new candidate molecule and a clear action target for developing potential therapeutic drugs for Primrose syndrome.

The application discloses a VR training system based on the cognitive function defect characteristics of children's attention deficit hyperactivity disorder, relates to the technical field of digital medical treatment, and comprises a data acquisition module, a data evaluation module, a VR training module, a dynamic adjustment module, a result output module and a collaborative work module; the application constructs an objective quantitative model by fusing multi-modal data, accurately identifies three ADHD subtypes and the degree of cognitive defect of each dimension, solves the problem that traditional evaluation is highly subjective, and divides cold / hot executive function double-path training based on the CAPS theory, dynamically customizes task matching according to the subtypes, realizes accurate matching of defects and training, additionally, through real-time monitoring of eye movement and physiological indexes, automatically adjusts task difficulty and feedback strategies, maintains the best challenge level, can effectively improve the participation and training continuity of children, and finally achieves the goal of high-efficiency, high-interest and side-effect-free personalized digital therapy.

The present application relates to the technical field of cognitive deficit assessment, and in particular to a method, device and equipment for detecting brain connection patterns based on cognitive function defects. First, the present application constructs a prediction model, which uses the individual's whole-brain structural and functional connection group data to obtain the brain weight network of the cognitive process through a machine learning algorithm, and then uses a large-scale multivariate edge-by-edge analysis method to compare the abnormal brain connection group patterns between different diagnostic groups. By comparing the abnormal connection group characteristics of each diagnostic group obtained by the large-scale multivariate edge-by-edge analysis method with the cognition-related connection group characteristics, it can be identified whether these abnormalities involve cognition-related core brain areas, thereby determining whether the abnormalities are related to cognitive defects. By comparing the degree of sharing and differences in abnormal connection group patterns between different diagnostic groups, it can be determined whether the cross-diagnostic cognitive defects are derived from shared macroscopic brain network abnormalities or from the neuropathological basis specific to each diagnosis.

The present invention generally relates to a specific pregnenolone derivative for its use for the treatment of a cognitive disorders. More particularly, the invention relates to a compound of Formula (I)for its use in the treatment of cognitive disorders. Indeed, the compound of the invention is in vivo very potent in correcting the cognitive impairments observed in cognitive disorders.

The invention relates to application of polyphyllin II in preparation of a medicine for relieving learning and memory impairment induced by diethyl hexyl phthalate (DEHP). Aiming at neurotoxicity and cognitive defects caused by DEHP exposure, the invention reveals that the polyphyllin II plays roles through dual mechanisms: inhibiting release of inflammatory factors such as TNF-alpha, IL-6 and the like, down-regulating expression of TNFAIP1, activating a CREB signal channel and recovering protein levels of BDNF and Bcl-2; miR-93 expression is up-regulated, TNFAIP1 is inhibited in a targeted manner, and DEHP-induced synaptic plasticity injury is blocked. According to the technical scheme, polyphyllin II and DEHP are combined for use, and behavioristics and histology verify that the learning and memory ability of mice is remarkably improved (the incubation period is shortened, and the target quadrant residence time is recovered by 40% or above), neuron loss is reversed, and synaptic protein down-regulation is performed (the synaptic protein is recovered to a healthy group by 85% or above, plt, 0.01).

The application discloses a kind of full-discipline problem solving cognitive precision diagnosis method, system and equipment based on standard thinking map, belong to artificial intelligence, educational big data mining and natural language processing technical field, method includes: loading standard thinking map with six-dimensional cognitive node as benchmark;Student original answer is parsed into cognitive action sequence by pre-training model;Based on semantic similarity, construct bipartite graph, use dynamic programming algorithm to align student action sequence with atlas optimum;In the alignment process, encounter skip step, then trigger large language model reasoning and insert implicit cognitive action to complete logical breakpoint;After alignment, traverse mapping pair, calculate weighted Euclidean distance to lock the first cognitive defect breakpoint deviating from threshold and stop subsequent tracing;Finally, retrieve and generate structured diagnostic report from six-dimensional error label library. Through implicit logic completion and first failure node locking, the deep cognitive precision attribution of non-standardized answer is realized, and the diagnostic reliability and granularity are greatly improved.