9 results about "Neuropathology" patented technology

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.

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 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 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.

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.