112 results about "Frontotemporal Lobe Dementia" patented technology

The disclosure relates to oligomers capable of targeting RNA expressed from the human C9ORF72 gene containing a pathogenic hexanucleotide repeat expansion. Such oligomers are useful for, among other things, reducing or eliminating C9ORF72 RNA and / or proteins translated therefrom, and treating or preventing diseases or disorders caused by, or associated with, hexanucleotide repeat expansion, including familial frontotemporal dementia (FTD) and familial amyotrophic lateral sclerosis (ALS).

The invention is generally directed to methods and compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind a TREM2 protein, e.g., a mammalian TREM2 and / or human TREM2. The methods provided herein find use in preventing, reducing risk, or treating an individual having dementia, frontotemporal dementia, Alzheimer's disease, Nasu-Hakola disease, or multiple sclerosis.

The invention is generally directed to methods and compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind a TREM2 protein, e.g., a mammalian TREM2 and / or human TREM2. The methods provided herein find use in preventing, reducing risk, or treating an individual having dementia, frontotemporal dementia, Alzheimer's disease, Nasu-Hakola disease, or multiple sclerosis.

A method of treating tau pathologies, such as Alzheimer's disease, involving the administration of antibodies specific to the amino terminal region of human tau (amino acid residues 6-18 or 184-195) to provide passive immunization. The administration of such antibodies can reduce total tau levels, decrease tau hyperphosphorylation, and improve reference memory. Passive immunization with antibodies targeting the N-terminal projection domain of tau reduces both total and hyperphosphorylated tau was found effective in aged 3×Tg-AD mice, a generally accepted mouse model of Alzheimer's disease and frontotemporal dementia in humans.

The present invention relates to monoclonal anti-Sortilin antibodies which have been found useful in correcting a deficient level of progranulin (PGRN). In particular, these antibodies can be used in the treatment of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).

This invention relates to bis- and tris-dihydroxyaryl compounds and their methylenedioxy analogs and pharmaceutically acceptable salts and their use in the modulation of Sirtuin 1 (Sirt1) and there use in neuroprotection for subject suffering from neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, Amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease, including Parkinson's plus diseases such as multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration and dementia with Lewy bodies, and in the manufacture of medicaments for such Sirt1 modulation and neuroprotection.

The present invention relates to monoclonal anti-Sortilin antibodies which have been found useful in correcting a deficient level of progranulin (PGRN). In particular, these antibodies can be used in the treatment of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders such as Alzheimers disease (AD).

The invention relates to novel assays for the in vivo analysis of neurodegenerative diseases and the use of such assays to discover therapies capable of modulating such diseases.

Provided are compounds, methods, and pharmaceutical compositions for reducing the amount or activity of Tau mRNA in a cell or animal, and in certain instances reducing the amount of Tau protein in a cell or animal. Such compounds, methods, and pharmaceutical compositions are useful to ameliorate at least one symptom of a neurodegenerative disease. Such symptoms include loss of memory, loss of motor function, and increase in the number and / or volume of neurofibrillary inclusions. Such neurodegenerative diseases include tauopathies, Alzheimer's Disease, Fronto-temporal Dementia (FTD), FTDP-17, Progressive Supranuclear Palsy (PSP), Chronic Traumatic Encephalopathy (CTE), Corticobasal Ganglionic Degeneration (CBD), Epilepsy, and Dravet's Syndrome.

The invention relates to the technical field of biology, and particularly provides a screening method of an infective gene capture probe related to dementia, a capture genome, a product and an application. The method provides a screening condition of the capture probe. The screening condition is optimized, and the method specifically comprises restriction on the related condition of selection of atarget section, the length of the capture probe, requirements on specificity, GC content, the number of probes and the like. The infective gene capture probe related to dementia comprises coding regions of 11 genes, infective genes for detecting five kinds of diseases of Alzheimer's disease, frontotemporal dementia, dementia related to Parkinson's diseases, dementia related to amyotrophic lateralsclerosis and lewy body dementia can be realized, and reference can be provided for molecular genetics diagnosis of ill individuals, screening of familial Alzheimer's diseases, frontotemporal dementia, the dementia related to Parkinson's diseases, the dementia related to amyotrophic lateral sclerosis and the lewy body dementia, and corresponding heredity consultation.

The present invention is concerned with deuterium-enriched isobutyl and cyclohexylmethyl sulfonamides of formula I and II, and pharmaceutically acceptable salts and methods of use thereof for the treatment of general anxiety disorders, major depressive disorders, attention deficit disorders, attention deficit hyperactivity disorder, Alzheimer's disease, frontotemporal dementia, cognitive impairment associated with age-related dementia, schizophrenia, migraine, sleep disorders, neurodegenerative diseases and obesity.

The invention relates to methods and kits for the differential diagnosis of Alzheimer's disease (AD) versus frontotemporal dementia (FTD), using biomarkers TNF-α, FAS-L and CK18, taken from a biological sample. Differences in biomarker levels can be used to distinguish between AD and FTD The invention is based on a discovered correlation between FTD and markers FAS-L and CK18. Therefore the invention also relates to the diagnosis of FTD using FAS-L and CK18. The serum concentrations of these biomarkers can further be used as an index of the severity of disease, and may occur in conjunction with clinical-based diagnostic testing and neuro-imaging assessment.

Non-invasive method for diagnosing or prognosing Alzheimer's disease, frontotemporal dementia, or other dementia involving isolating astrocyte-derived exosomes (ADEs) and neuron-derived exosomes (NDEs) from a human biological sample (i.e., plasma, serum, urine or cerebrospinal fluid), analyzing cargo extracts of the ADEs and NDEs to detect at least one specified protein or microRNA biomarker, comparing the levels and activities of detected biomarker(s) to those in control samples to identify a statistically significant difference between the detected biomarker(s) and corresponding biomarker(s) in the control sample to determine presence of Alzheimer's disease, frontotemporal dementia, or other dementia; and testing effects of drugs on levels and activities of each biomarker, as well as effects of drugs administered to test subjects on levels and activities of each biomarker in ADEs and NDEs from subsequently obtained biological samples.

Provided are methods for reducing the amount or activity of C90RF72 RNA, and in certain instances of reducing the amount of C90RF72 protein, in an animal. Such methods are useful to prevent or ameliorate at least one symptom of a neurodegenerative disease. Such symptoms include anxiety, reduced spatial learning, and memory loss. Such neurodegenerative diseases include amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), corticalbasal degeneration syndrome (CBD), atypical Parkinsonian syndrome, and olivopontocerellar degeneration (OPCD).

Non-invasive method for diagnosing or prognosing Alzheimer's disease, frontotemporal dementia, or other dementia involving isolating astrocyte-derived exosomes (ADEs) and neuron-derived exosomes (NDEs) from a human biological sample (i.e., plasma, serum, urine or cerebrospinal fluid), analyzing cargo extracts of the ADEs and NDEs to detect at least one specified protein or microRNA biomarker, comparing the levels and activities of detected biomarker(s) to those in control samples to identify a statistically significant difference between the detected biomarker(s) and corresponding biomarker(s) in the control sample to determine presence of Alzheimer's disease, frontotemporal dementia, or other dementia; and testing effects of drugs on levels and activities of each biomarker, as well as effects of drugs administered to test subjects on levels and activities of each biomarker in ADEs and NDEs from subsequently obtained biological samples.

The present invention discloses a method to recover and restore dendritic and synaptic neuron connections that have been degraded or destroyed by neurodegenerative diseases. In the present invention tryptamines are used to induce neuro plasticity and restore both dendritic density and synaptic connections of neurons in the brain. In the preferred embodiment LSD given in micro doses can induce dendritic and synaptic genesis in neuronal networks and improve the quality of life of people with neurodegenerative diseases such as Alzheimer's, Huntington's, Multiple Sclerosis, Parkinson's and Frontotemporal dementia.

The invention provides recombinant protein as well as a preparation method and application thereof. The recombinant protein comprises Tau protein and hepatitis B virus core protein. The recombinant protein adopts Tau294-305 and the hepatitis B virus core protein to perform recombination, T294-HBc for fusion expression is self-assembled into HBc chimeric virus-like particles, with surface displaying Tau294-305, and vaccine is good in homogeneity, simple to prepare, high in immunogenicity and small in side effect, and has a good application prospect in terms of the treatment of dementia, such asalzheimer disease, frontotemporal dementia, corticobasal degeneration, Pick disease and progressive supranuclear palsy, caused by Tau lesion.

The invention relates to an application of a pyrazine compound in preparation of drugs. The drugs can be used for treating neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, frontotemporal dementia (FTD), vascular dementia, HIV-related dementia, multiple sclerosis, progressive lateral sclerosis, Friedreich's ataxia, neuropathic pain or glaucoma, inflammation, oxidative damage, and mitochondrial-related diseases.

Disclosed are compounds of formula (1)-(V): where the substituents are as provided herein. Further disclosed are methods of inhibiting tau aggregation, treating or ameliorating a tauopathy or cancer by administration of such a compound. Tau is a microtubule-binding protein that accumulates in a number of neurodegenerative disorders, including frontotemporal dementia and Alzheimer's disease (AD). The presence of abnormal tau correlates with neuron loss and memory deficits in patients with AD and other neurodegenerative disorders that involve tau accumulation.

A method for treating a condition selected from Alzheimer's disease, mild cognitive impairment, age-associated dementia, and frontotemporal dementia, comprises administering to a patient in need of such treatment a safe and effective amount of a compound having the formula:wherein R is selected from hydrogen, alkyl, alkoxy, arylalkyl, aryloxyalkyl, cinnamyl and acyl; and R1 and R2 are independently selected from hydrogen, alkyl, alkoxy, hydroxy, halogen, cyano, amino and nitro; with the proviso that if R is methyl, R1 and R2 are not both hydrogen; and the compound comprises pharmaceutically acceptable salts thereof.

The present invention is concerned with deuterium-enriched sulfonamides of formula 1, their pharmaceutically acceptable salts and methods of use thereof for the treatment of anxiety disorders including, General Anxiety Disorder (GAD), Panic Disorder (PD), Post-Traumatic Stress Disorder (PTSD), Social Phobia (SP), Health Anxiety (Hypochondriasis), depression, major depressive disorders, unipolar depression, bipolar I depression disorder, bipolar II depression disorder, treatment-resistant depression, single episodic and recurrent major depressive disorders, depression in the medically ill, attention deficit hyperactivity disorder (ADHD), attention deficit disorder (ADD), Obsessive-Compulsive Disorder (OCD), Obsessive-Compulsive Personality Disorder (OCPD), Autism Spectrum Disorder (ASD), schizophrenia, psychosis, epilepsy, seizures, hot flashes due to menopause, age-related macular degeneration (AMD), premature ejaculation, male erectile dysfunction, sexual dysfunction, obesity, eating disorders, bulimia nervosa, anorexia nervosa, angina, migraine, pain, nociception, sleep disorders, insomnia, fibromyalgia, alcohol withdrawal, autism, Rett's syndrome, cyclothymic disorder, neural injury, neurodegenerative diseases, Parkinson's disease, Parkinson's disease psychosis, Huntington disease, Alzheimer's disease, frontotemporal dementia, cognitive impairment associated with age-related dementia, Alzheimer's disease, schizophrenia, psychosis, depression, pain or discomfort associated with surgery and pain or discomfort associated with medical illness.

The present invention relates to O-GlcNAc hydrolase (OGA) inhibitors. The invention is also directed to pharmaceutical compositions comprising such compounds, to processes for preparing such compounds and compositions, and to the use of such compounds and compositions for the prevention and treatment of disorders in which inhibition of OGA is beneficial, such as tauopathies, in particular Alzheimer's disease or progressive supranuclear palsy; and neurodegenerative diseases accompanied by a tau pathology, in particular amyotrophic lateral sclerosis or frontotemporal lobe dementia caused by C9ORF72 mutations.

The present invention provides tacrolimus for use in the treatment in a human subject of a TDP-43 proteinopathy, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementias (FTDs), wherein the tacrolimus is for administration at a therapeutically-effective dose which does not cause immunosuppression in the subject.

Provided herein are compositions and methods for reducing expression of C9orf72 transcripts in cells containing expanded intronic GGGGCC regions, including those in subjects having or at risk of developing amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Provided herein are a double-stranded oligonucleotides of 13 to 22 nucleobases in length targeting a GGGGCC expanded repeat region in an intron of C9orf72, comprises (a) 3-5 central mismatches (within bases 9-14) within a target sequence comprising the expanded repeat sequence, or (h) 3-5 mismatches outside of the seed sequence (bases 2-8 within the guide strand complementary to the expanded repeat sequence).