11 results about "Frontotemporal Lobe Dementia" patented technology

The present invention pertains to the anti-inflammatory therapeutic effect of xantohumol in spinal cord injury (SCI). The continuous administration of xanthohumol for 1-8 weeks to SCI rats resulted in improved results in 4 clinical tests used and in lowering and faster elimination of macrophages from the SCI lesion. Since the infiltration of the SCI lesion by numerous phagocytic macrophages indicates a severe destructive inflammation of extraordinary longevity, administration of xanthohumol is neuroprotective and resulted in a better and faster recovery of the locomotor function and the strength and sensory function in the hind limbs, in a shorter period of paralysis of the urinary bladder and in the recovery of the body weight lost due to the SCI surgery. Since the traumatic brain injury (TBI) involving the white matter, and stroke involving the white matter initiate the severe destructive inflammation as in the SCI, the administration of xanthohumol is expected to be anti-inflammatory and neuroprotective in both brain diseases. Since neurodegenerative diseases including Alzheimer's disease, frontotemporal dementia and Parkinson's disease, immune mediated neuroinflammation including multiple sclerosis and neuromyelitis optica and cerebrospinal infections have inflammatory pathogenesis involving microgliosis and infiltration by macrophages, the administration of xanthohumol is expected to result in therapeutic inhibition of progression of all above diseases as well as of related neurodegenerative, immune mediated and infectious diseases of the brain and of the spinal cord.

The present invention provides a method of treating frontotemporal dementia, or a childhood genetic neurodegenerative disease such as Ataxia Telangiectasia (A-T), or neurodegenerative diseases such as Parkinson's disease or neuropsychiatric diseases comprising administering to a subject in need thereof an effective amount of chlorite composition, such as sodium chlorite. The present invention thereby provides a method of modulating the immune system in a subject in need thereof. Described herein are methods of administration and treatment.

An EEG-based dementia diagnosis assistance device according to the present embodiment comprises: an EEG data preprocessing unit for preprocessing a collected EEG data set of a test subject, the collected EEG data set being divided into time intervals by setting a window length and a shift length; an Hjorth parameter extraction unit for extracting, for each time interval, Hjorth parameters including an activity index, a mobility index, and a complexity index; and a dementia classification unit for classifying the test subject into one from among a Alzheimer's disease (AD) group, a frontotemporal dementia (FTD) group, and a cognitive normal (CN) group on the basis of the extracted Hjorth parameters. Therefore, AD, FTD, and CN subjects can be classified using Hjorth parameters composed of three major indicators of activity, mobility, and complexity through time domain analysis on EEG datasets.

Aspects of the disclosure relate to methods and compositions (e.g., kits) for detecting anti-repeat-associated non-ATG (RAN) protein antibodies in a subject (e.g., a subject that has been administered a therapeutic anti-RAN protein antibody or a vaccine against a disease or disorder associated with RAN protein expression, translation, and / or accumulation, for example amyotrophic lateral sclerosis (ALS) and / or frontotemporal dementia (FTD)). In some embodiments, methods described by the disclosure comprise detecting one or more anti-RAN protein antibodies in a biological sample obtained from a subject by an electrochemiluminescence-based immunoassay using one or more target di-amino acid repeat peptides. In some embodiments, the disclosure relates to kits comprising one or more di-amino acid repeat peptides and an electrochemiluminescence-based immunoassay plate and / or reagents.

Among other things, the present disclosure provides oligonucleotide compositions and methods thereof. In some embodiments, oligonucleotides comprise various chemical modifications of sugars, nucleobases, and / or internucleotidic linkages and patterns thereof and are usefill for exon skipping. In some embodiments, the present disclosure provides technologies useful for skipping cryptic exons of stathmin-2(STMN2) transcripts. In some embodiments, the present disclosure provides technologies useful for modulating STMN2 transcript splicing. In some embodiments, the present disclosure provides methods for preventing or treating conditions, disorders or diseases including neurodegenerative diseases, e.g,, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

The present disclosure provides the use of compounds of Formulae (I), (II), (III), (III-A), and (III-B) (e.g., metformin) in treating a neurological disease associated with repeat expansions and / or RAN protein accumulation, reducing the level of one or more repeat associated non-ATG (RAN) proteins, and reducing the accumulation of RAN proteins in a subject and / or biological sample. Also provided is the use of compounds of Formulae (I), (II), (III), (III-A), and (III-B) (e.g., metformin) in inhibiting RAN protein translation in a subject and in a biological sample (e.g., cells, tissue). Also provided in the present disclosure are pharmaceutical compositions, kits, and uses of compounds of Formulae (I), (II), (III), (III-A), and (III-B) (e.g., metformin) for treating diseases associated with repeat expansions. Exemplary diseases associated with repeat expansions include, but are not limited to, C9ORFf72 amyotrophic lateral sclerosis (ALS), or C9ORFf72 frontotemporal dementia; myotonic dystrophy type 1 (DM1) and myotonic dystrophy type 2 (DM2); spinocerebellar ataxia; Huntington's disease; Fragile X Tremor Ataxia Syndrome (FXTAS); and Fragile XE syndrome (FRAXE).

The present invention provides oligonucleotides, compositions, and methods for preventing and / or treating various pathological conditions, disorders, or diseases. [Solution] In some embodiments, the provided technology comprises nucleic acid base modification, sugar modification, internucleotide linkage modification and / or patterns thereof, and has improved properties, activity and / or selectivity. In some embodiments, the provided technology targets MAPT. In some embodiments, the disclosure provides MAPT oligonucleotides, compositions and methods for preventing and / or treating MAPT-related conditions, disorders or diseases, such as Alzheimer's disease (AD) or frontotemporal dementia (FTD).

This invention discloses a class of 3-substituted phthalide compounds (I) and their pharmaceutically acceptable salts, their preparation methods, pharmaceutical compositions, and their use in the preparation of drugs for the treatment and / or prevention of neurological diseases, including but not limited to vascular dementia, Alzheimer's disease, frontotemporal dementia, Prion's disease, Lewy body dementia, Parkinson's disease, Huntington's disease, HIV-related dementia, multiple sclerosis, amyotrophic lateral sclerosis, neuropathic pain, ischemic stroke, hemorrhagic stroke, and neurological damage caused by traumatic brain injury;

This invention discloses a class of piperidine alkyl dihydroxyphthalide compounds (I) and their pharmaceutically acceptable salts, their preparation methods, pharmaceutical compositions, and their use in the preparation of medicaments for treating and / or preventing diseases by means of anti-oxidative stress, inhibition of amyloid aggregation, metal ion complexation, or anti-neuroinflammatory effects, including but not limited to vascular dementia, Alzheimer's disease, frontotemporal dementia, Prion's disease, Lewy body dementia, Parkinson's disease, Huntington's disease, HIV-related dementia, multiple sclerosis, amyotrophic lateral sclerosis, neuropathic pain, ischemic stroke, hemorrhagic stroke, and neurological damage caused by traumatic brain injury;

Disclosed herein are compositions and methods for reducing expression of C9ORF72 mRNA and protein in an animal with C9ORF72 specific inhibitors. Such methods are useful to treat, prevent, or ameliorate neurodegenerative diseases in an individual in need thereof. Such C9ORF72 specific inhibitors include antisense compounds. Examples of neurodegenerative diseases that can be treated, prevented, and ameliorated with the administration C9ORF72 specific inhibitors include amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), corticalbasal degeneration syndrome (CBD), atypical Parkinsonian syndrome, and olivopontocerellar degeneration (OPCD).

The application discloses application of a gamma-aminobutyric acid derivative in treatment of TDP-43 proteinopathy, and discloses application of a gamma-aminobutyric acid derivative or an enantiomer thereof or a pharmaceutically acceptable salt thereof in preparation of a medicine for preventing and / or treating a TDP-43 abnormal aggregation related disease, wherein the TDP-43 abnormal aggregation related disease is amyotrophic lateral sclerosis, sporadic inclusion body myositis, Parkinson's disease, Alzheimer's disease, frontotemporal dementia and Huntington's disease.