15 results about "Neurogenia" patented technology

The present invention relates to a novel fluorescent marker that selectively binds to tau protein, its use, a method for imaging neurofibrillary tangles of tau protein in the retina of a subject, as well as an apparatus allowing said method to be carried out.

The present invention concerns the use of peptidyl-prolyl isomerase cyclophilin 40 (CyP40) for reduction of neurotoxic fibrils and treatment and prevention of neurodegenerative diseases associated with amyloid fibril aggregation. Aspects of the invention include compositions, methods, dosage forms, and kits for treating or preventing a neurodegenerative disease or condition associated with amyloid fibril aggregation in a human or animal subject, and for disaggregating neurofibrillary aggregates in vitro or in vivo, using CyP40, or a biologically active fragment thereof.

Novel and useful compounds, such as 2,4-dihydropyrazolo[3',4':4,5]pyrano[2,3-b]pyridines, are disclosed herein. Such compounds may be employed in various treatments, alleviation, or prevention of a group of disorders, such as disorders associated with Tau (tubulin associated unit) protein aggregates, such as neurofibrillary tangles (NFTs), such as Alzheimer's disease (AD).

To provide technology that can be used to inhibit aggregation of β-amyloid protein (Aβ) and microtubule-binding protein Tau, which bring about senile plaque (senile plaque: AP) and neurofibrillary tangle (Neurofibrillary Tangle: NFT).SOLUTION: The present invention provides a protein aggregation inhibitor containing mesostructured particles of calcium hydrogen carbonate as an active ingredient.SELECTED DRAWING: Figure 2

The invention relates to generation, optimization and characterisation of VHH targeted against Tau MTBD (microtubule-binding domain) with high affinity, obtained by screening from a naïve synthetic library. The inventors optimized version of a lead VHH which is able to inhibit Tau aggregation in vitro and in HEK 293 aggregation-reporting cellular model, providing a new tool in Tau immunotherapies. Accordingly the invention relates to new VHH antibody that specifically binds with high affinity Tau species, especially the epitope region involved in Tau aggregation. Moreover, the inventors found that immunization with the optimized version of this lead VHH prevented the formation of neurofibrillary tangles induced by injection of extracellular h-AD in mouse model. Thus, these specific antibodies can be used for the therapy of tauopathy disorders such as Progressive supranuclear palsy (PSP).

Disclosed is a use of artemether in preventing and treating Alzheimer's disease. Artemether is a safe and effective compound for treatment against malaria. Artemether activates an AMPK signaling pathway in the brain of a transgenic mouse model of Alzheimer's disease, improves learning and memory abilities in the mouse model, reduces neuron apoptosis in the brain, improves function of choline acetyltransferase, inhibits activity of glial cells, and reduces amyloid plaque deposition, neurofibrillary tangle, and neuron loss, thereby providing an experimental basis for clinical research on the treatment of Alzheimer's disease.

The present disclosure provides novel approaches to the treatment of Alzheimer's disease, and other neurodegenerative disorders such as chronic traumatic encephalopathy (CTE) using novel therapeutics comprising agents that reduce the interaction of a tau seed interactor with intracellular tau proteins and thus reduce or inhibit the production of tau-associated neurofibrillary tangles.

Disclosed are substituted heterocyclic compounds of formula (I) and pharmaceutically acceptable salts thereof, which may be suitable for imaging tau aggregates, b-sheet aggregates, beta-amyloid aggregates or alpha-synuclein aggregates, and hence are useful in binding and imaging tau aggregates in Alzheimer's patients. More specifically, this invention relates to a method of using the compounds of formula (I) as tracers in positron emission tomography (PET) imaging to study tau deposits in brain in vivo to allow diagnosis of Alzheimer's disease and other neurodegenerative diseases characterized by tau pathology. The disclosure further relates to a method of measuring clinical efficacy of therapeutic agents for Alzheimer's disease and other neurodegenerative diseases characterized by tau pathology.

Provided herein is a method of identifying a pre-stage neurofibrillary tangle (NFT) in a patient sample, including obtaining a sample from a patient suspected of having or at risk of developing a tauopathy, incubating the sample with a composition comprising a first binding reagent, wherein the first binding reagent is specific to Ser262 and / or Ser356 of a tau protein, and detecting binding between the first binding reagent and the tau protein, wherein detecting binding between the first binding reagent and the tau protein indicates the presence of a pre-stage NFT in the patient sample.

Provided are oligomeric agents, pharmaceutical compositions, and methods for reducing the amount or activity of APOE RNA in a cell or subject, and in certain instances reducing the amount of ApoE protein in a cell or subject. Such oligomeric agents, pharmaceutical compositions, and methods are useful to ameliorate at least one symptom of a neurodegenerative disease. Such symptoms include cognitive impairment, progressive memory loss, a decline in language skills, behavioral abnormality, dementia, difficulty performing daily activities, aphasia, agnosia, apraxia, loss of motor function, amyloid plaque, neurofibrillary tangle, and / or neuroinflammation.

Provided is a protein aggregation inhibitor containing meso-structured particles of calcium hydrogencarbonate as an active ingredient, as a technology that can be used in order to inhibit the aggregation of β-amyloid protein (Aβ) or microtubule-associated protein Tau which causes a senile plaque (AP) and a neurofibrillary tangle (NFT).

Described herein are methods of making and using a transgenic mouse model of Alzheimer's disease. Transgenic animal models and cell lines are disclosed for the study of Alzheimer's disease or Alzheimer's disease-type pathology. Methods of screening and identifying active agents for the treatment of Alzheimer's disease or Alzheimer's disease-type pathology are also provided.

Provided are oligomeric agents, pharmaceutical compositions, and methods for reducing the amount or activity of APOE RNA in a cell or subject, and in certain instances reducing the amount of ApoE protein in a cell or subject. Such oligomeric agents, pharmaceutical compositions, and methods are useful to ameliorate at least one symptom of a neurodegenerative disease. Such symptoms include cognitive impairment, progressive memory loss, a decline in language skills, behavioral abnormality, dementia, difficulty performing daily activities, aphasia, agnosia, apraxia, loss of motor function, amyloid plaque, neurofibrillary tangle, and / or neuroinflammation.

Provided herein are methods of administering ISIS 814907 for ameliorating Alzheimer's disease, reducing Tau RNA, or reducing Tau protein in a human subject in need thereof. In certain embodiments, the Alzheimer's disease is mild Alzheimer's disease, Mild Cognitive Impairment (MCI) Due to Alzheimer's Disease, and / or Alzheimer's Disease Dementia (e.g., Mild Alzheimer's Disease Dementia). In certain instances, methods are useful for ameliorating at least one symptom or hallmark of a disease or disorder associated with Tau protein. In certain instances, the disease or disorder associated with Tau protein is a neurodegenerative disease or disorder. In certain instances, the disease or disorder associated with Tau protein is Alzheimer's disease or Fronto-temporal Dementia (FTD). In certain embodiments, the Alzheimer's disease is mild Alzheimer's disease, Mild Cognitive Impairment (MCI) Due to Alzheimer's Disease, and / or Alzheimer's Disease Dementia (e.g., Mild Alzheimer's Disease Dementia). In certain instances, the disease or disorder associated with Tau protein is a tauopathy. In certain instances, the disease or disorder associated with Tau protein is Frontotemporal Dementia with Parkinsonism-17 (FTDP-17), Progressive Supranuclear Palsy (PSP), Chronic Traumatic Encephalopathy (CTE), Corticobasal Ganglionic Degeneration (CBD), Pick Disease, Argyrophilic Grain Disease (AGD), Globular Glial Tauopathies, Epilepsy, and / or Dravet's Syndrome. Such symptoms or hallmarks include loss of memory, cognitive decline, loss of ability to understand or express speech, abnormal behavior, loss of and impaired motor function, or increase in the number and / or volume of neurofibrillary inclusions.

Compounds comprising a triazole scaffold, compositions comprising same, and the use of such compounds and compositions to inhibit tubulin-associated unit (tau) protein and alpha-synuclein (α-syn) protein aggregation, including neurofibrillary tangles (NFTs) and Lewy bodies.