17 results about "Neuropathology" patented technology

The invention relates to the technical field of medical treatment, and particularly discloses a training method for delaying development of Alzheimer's disease, which comprises the following steps: (a) a neural pathway activation stage: generating a dynamic three-dimensional space navigation task through a virtual reality system and displaying a color coding path to a patient; the method comprises the following steps: (c) a lymphatic driving stage: starting a 40Hz multi-mode stimulation combination after metabolic regulation reaches the standard, and (d) a closed-loop optimization stage: detecting saliva exosome A beta 42 concentration or EEG gamma wave power every two weeks, each time is 40 minutes every day, and the steps (a)-(b)-(c) are executed in sequence; neuropathology is improved, compared with the prior art, the hippocampus atrophy rate is remarkably reduced, the A beta 42 pathological deposition removal efficiency is high, and the white matter fiber integrity is improved; the cognitive function of the patient is enhanced, the space navigation capability is optimized, and the attention and work memory are improved.

The invention relates to methods and compositions for preventing or treating a neuropathology in a subject associated with or induced or caused by a P. gingivalis infection, preventing the deposition of or reducing the level of P. gingivalis gingipain in neuronal tissue, delaying the onset of a P. gingivalis-induced or associated neuropathology, for preventing or slowing the rate of abnormal protein deposition in the neuronal tissue, and / or reducing neuroinflammation, the methods comprising administering an RNA polynucleotide encoding a protein comprising or consisting of: - one or more amino acid sequences of an active site of an Arg- or Lys-gingipain of P. gingivalis, or a sequence that is at least 80% identical thereto; and / or - the amino acid sequence of one or more adhesin binding motifs (ABMs) of an adhesin domain of an Arg- or Lys-gingipain of P. gingivalis, or a sequence that is at least 80% identical thereto, wherein the polynucleotide is capable of being translated in a mammalian cell.

Methods of differentiating and quantifying modifications in the tau protein in bio-fluids to detect, classify, and treat a plurality of tauopathies are disclosed. The disclosed methods include liquid chromatographic mass spectrometric analyses on isolated tau protein fragments to identify and quantify deamidated or isomerized asparagines or aspartic acids indicative of a neuropathology associated with a tauopathy.

Methods of differentiating and quantifying modifications in the tau protein in bio-fluids to detect, classify, and treat a plurality of tauopathies are disclosed. The disclosed methods include liquid chromatographic mass spectrometric analyses on isolated tau protein fragments to identify and quantify deamidated or isomerized asparagines or aspartic acids indicative of a neuropathology associated with a tauopathy.

The present invention relates to the biomedical and biopharmaceutical sectors. Specifically, it relates to a chimeric antigen comprising the combination of the amino- and carboxy-terminal regions of the amyloid-beta peptide (Aβ), the amino- and carboxy-terminal regions of the tau protein, and a T-cell epitope. The pharmaceutical composition comprising this chimeric antigen and at least one pharmaceutically acceptable vaccine adjuvant increases the efficacy of immunotherapy for the prevention and treatment of Alzheimer's disease (AD). The chimeric antigen exerts its action by stimulating a multi-target humoral response with high titers of anti-Aβ and anti-tau antibodies simultaneously. This promotes the combined elimination of toxic Aβ and tau species from the brain, thereby preventing or significantly improving the clinical symptoms and neuropathology of AD.

The present invention relates to a method of treating or preventing neuropathology induced or associated with Porphyromonas gingivalis using a chimeric or fusion protein comprising a first polypeptide linked to a second polypeptide, wherein: A) the first polypeptide comprises or consists of the following: an amino acid sequence of an active site of Arg gingival protease or Lys gingival protease of Porphyromonas gingivalis, or a sequence at least 80% identical thereto; and B) the second polypeptide comprises or consists of the amino acid sequence of the adhesin domain of the Arg gingival protease or Lys gingival protease of Porphyromonas gingivalis; wherein the second polypeptide comprises one or more sequences of an adhesin binding motif (ABM), and wherein the second polypeptide: a) does not comprise: a sequence of a cleaved adhesin domain (CAD) or a portion thereof; and / or b) comprising an amino acid sequence substantially corresponding to the full length of the DUF2436 domain of the Arg gingival protease or Lys gingival protease; and / or c) comprises one or more cysteine amino acid substitutions in the adhesin domain as compared to the naturally occurring Arg gingival protease or Lys gingival protease sequence in the corresponding region, and / or d) comprises one or more additional amino acid motif substitutions as defined herein.

The application discloses an interactive eyeball movement and neuropathology simulation teaching system, and relates to the technical field of medical education tools, and comprises a physical eyeball model module, a movement execution control module, a wireless communication module, a mobile terminal interaction module, a digital twin display module and a neuropathology simulation module. The system drives the physical eyeball to move in multiple degrees of freedom through a servo motor, and realizes wireless control and three-dimensional digital twin synchronous display through a mobile terminal. The system can simulate normal eyeball movement, the innervation relationship of the extraocular muscles, and the pathological state after the oculomotor nerve, the trochlear nerve and the abducens nerve are damaged, and can reproduce typical clinical signs through algorithms such as movement range limitation, resting position bias and dynamic gain adjustment, and can also control eyeball movement in real time according to user gestures and analyze movement abnormalities. The application has the functions of entity interaction, digital visualization and pathology simulation, and is suitable for medical teaching, neural rehabilitation training and clinical auxiliary teaching scenes.

The present invention relates to a quantitative electroencephalogram (QEEG) monitor and system capable of monitoring and displaying simultaneously neuropathological characteristic and activity of both sides of a subject's brain. The methods include various indices and examination of differences in these indices by which neurophysiological conditions or problems can be identified and treated. These methods, and the systems and devices using these methods preferably can be used for identifying these neurophysiological conditions or brain dysfunction with monitors and methods for seizure detection, for sedation monitoring, for anesthesia monitoring, and the like. These bilateral brain monitoring methods and systems, and the devices using these methods can be used by individuals or clinicians with little or no training in signal analysis or processing. These bilateral monitoring methods can also be used in a range of applications.

The invention relates to systems, methods, and computer-readable media for automated assessment of volumetric changes in brain regions of interest in preclinical animal models. Digital images of brain tissue cross-sections are processed using a convolutional neural network (CNN) to isolate regions of interest, followed by a transformer-based artificial intelligence model utilizing axial and patched attention for pixel classification. Segmentation accuracy is enhanced through a topological data analysis (TDA) algorithm, which refines results by constructing and evaluating simplicial complexes to ensure anatomical continuity. The refined segmentation data is used to calculate three-dimensional volumes based on the Cavalieri principle, and the results are displayed or stored for further analysis. The system offers improved accuracy, efficiency, and consistency over manual methods, supporting preclinical evaluation of therapies targeting neuropathology. Applications include tracking volumetric changes over time and facilitating high-throughput analyses in neurodegenerative disease research.

The invention discloses related application of a target compound in treatment of Alzheimer's disease, and relates to the field of biological medicine. In order to solve the problem that an existing autophagy inducer depending on an mTOR signal channel may cause side effects such as immunosuppression or metabolic disorder, the invention provides application of at least one small molecule compound of phytolaccin, 2-hydroxycinnamic acid, clevidipine butyrate or 3 ', 4', 7-trimethoxy quercetin as the autophagy inducer. The compound does not depend on an mTOR signal channel, has the blood-brain barrier penetrating capacity and can effectively induce autophagy. In caenorhabditis elegans and mouse Alzheimer's disease models, the compound shows a remarkable neuroprotective effect, accumulation of toxic protein aggregates such as beta-amyloid protein and over-phosphorylated tau in the brain can be reduced, cognitive impairment and related neuropathological characteristics are improved, and the compound can be used for preventing and treating neurological diseases. A new strategy is provided for treatment and / or prevention of Alzheimer's disease.

The invention relates to novel application of betulin, in particular to application of betulin in prevention and treatment of cognitive impairment after stroke, and belongs to the field of biological pharmacy. The betulin can obviously improve cognitive impairment and neuronal impairment of post-stroke cognitive impairment, obviously improve cognitive impairment and neuropathological change of post-stroke cognitive impairment, and can play a role in improving post-stroke cognitive impairment. According to the invention, betulinol ester is creatively used for preventing and treating cognitive impairment after stroke; the betulin disclosed by the invention can be used as a medicine for preventing and treating cognitive impairment after stroke, and also can be used as an adjuvant therapy for preventing and treating cognitive impairment after stroke clinically. The traditional Chinese medicine composition has good social benefits and is worthy of clinical popularization and application.

Techniques for treating acute ischemic stroke, and other neurological pathologies, are described herein. An example method includes identifying a portion of a brain including overactive neurons and outputting an electrical signal to at least one stimulation electrode disposed away from the portion of the brain by a distance in a range of about 0.5 mm to 1 cm. The electrical signal includes a low-frequency component including bursts having a frequency in a range of about 2 Hz to about 10 Hz. The electrical signal includes a high-frequency component comprising pulses having a frequency in a range of about 200 Hz to about 2 kHz.

Pharmacological or genetic inactivation of MAGL reduces neuroinflammation and neuropathology in animal models of AD. However, global inactivation of MAGL induces functional tolerance of CB IR, which reduces the effectiveness of pharmacotherapies. Evidence has shown that selective inactivation of MAGL in astrocytes, but not in neurons, reduces neuropathology and synaptic and cognitive impairments in TBI. In particular, results showed that inactivation of astrocytic MAGL attenuates AD neuropathology and prevents deterioration in LTP, spatial learning and memory in AD animals. This shows that neuroprotective effects of global MAGL inactivation largely result from limiting 2-AG degradation in astrocytes, rather than in neurons. Therefore, selective inactivation of astrocytic MAGL provides a better therapeutic outcome for AD, as this greatly minimizes the potential adverse effects resulting from global inactivation-induced disruption of 2-AG degradation in neurons and in other peripheral tissues. To this end, an AAV-mediated gene silencing approach to knock MAGL selectively in astrocytes is presented.

Applicants sought to express human iduronate-2-sulfatase (hIDS) in the brain endothelium of a mouse model of Mucopolysaccharidosis type II (MPSII, Hunter's syndrome) to enable enzyme secretion into the brain parenchyma. In this disorder, IDS deficiency results in the pathophysiological accumulation of heparan and dermatan sulfate GAGs. To test the hypothesis, Applicants chose AAV-BI30, an AAV9-derived capsid that has an enhanced in vivo tropism specific to the endothelium in the rodent CNS and can transduce human brain vascular endothelial cells in vitro more efficiently than AAV9. Applicants show that systemic delivery of AAV-BI30: hIDS restored IDS enzyme activity in the brain, liver, and serum of IDS-KO mice (FIG. 1). Importantly, AAV-BI30-mediated gene transfer resulted in the correction of GAG accumulation in the brain (FIG. 2). This effect was not observed when using the AAV-BI30 vector packaging a non-secreting version of hIDS. These findings highlight that targeting endothelial cells throughout the CNS is a promising approach for delivering enzymes across the BBB and restoring lysosomal metabolism.

The application relates to the field of biomedical technology, and particularly relates to application of bone marrow-derived suppressor cells in preparation of drugs or reagents for treating Alzheimer's disease. The application supplements exogenous mMDSCs in an AD model transgenic mouse for the first time, improves the AD condition aggravated by Pg from two aspects of function and neuropathology, obtains certain curative effect, has clinical application potential, provides a new strategy and research and development direction for preparation of drugs or reagents for promoting Alzheimer's disease caused by Porphyromonas gingivalis, and has guiding significance.

The invention relates to an early screening system based on Alzheimer's disease, which belongs to the technical field of early screening of Alzheimer's disease and comprises an interactive sensing module, a behavior capture module, a gait analysis module, a feature extraction module, an intelligent analysis module and a feedback output module. The interactive perception module is used for presenting and dynamically adjusting a work memory backtracking task, a scene memory reconstruction task and a meta-memory task, and the behavior capture module is used for collecting eye movement data of a user in the testing process. According to the method, behavior indexes and AD core biomarkers are clearly associated, so that the screening result has a neuropathology basis, the scientificity and interpretation of evaluation are enhanced, the system has a self-optimization function, the model can be updated through continuous learning increment, and a visual three-dimensional cognitive map and personalized intervention suggestions are output, so that the system has a good application prospect. An efficient and quantifiable decision support tool is provided for clinical diagnosis and health management, and finally non-invasive, low-cost and efficient early risk prevention and control of the Alzheimer's disease are achieved.

The invention relates to the field of biomedicine and biopharmacy. Specifically, the present invention relates to a chimeric antigen comprising a combination of amino and carboxyl terminal regions of amyloid beta peptide (Abeta), amino and carboxylic acid terminal regions of tau protein, and T cell epitopes. A pharmaceutical composition comprising the chimeric antigen and at least one pharmaceutically acceptable vaccine adjuvant improves the efficacy of immunotherapy in the prevention and treatment of Alzheimer's disease (AD). The chimeric antigens function by simultaneously stimulating multi-target bodily fluid reactions with high titers of anti-A [beta] and anti-tau antibodies. The toxic forms of A beta and tau can be jointly eliminated from the brain, so that the clinical symptoms and neuropathology of AD are prevented or remarkably improved.