44 results about "Traumatic encephalopathy" patented technology

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 present invention provides minimally invasive methods of detecting, diagnosing, and assessing neuronal damage associated with traumatic brain injury (TBI) or chronic traumatic encephalopathy (CTE). Specific species of microRNAs (miRNA), small, noncoding RNA molecules that play gene regulatory functions, are correlated with cellular damage and oxidative stress following TBI or CTE, allowing for rapid, minimally-invasive diagnosis and assessment of brain injury. The early identification and longitudinal assessment of neuronal damage in subjects suffering from or at risk of suffering from a TBI (e.g., football players, boxers, military personnel, fall victims) will improve clinical outcomes by guiding critical medical and behavioral decision making.

Processes and materials are provided for the detection, diagnosis, or determination of the severity of a neurological injury or condition, including traumatic brain injury, multiple-organ injury, stroke, Alzeimer's disease, Parkinson disease and Chronic Traumatic Encephalopathy (CTE). The processes and materials include biomarkers detected or measured in a biological sample such as whole blood, serum, plasma, or CSF. Such biomarkers include Tau and GFAP proteins, their proteolytic breakdown products, brain specific or enriched micro-RNA, and brain specific or enriched protein directed autoantibodies. The processes and materials are operable to detect the presence of absence of acute, subacute or chronic brain injuries and predict outcome for the brain injury.

The invention provides methods for diagnosing, assessing or quantitating drug use, drug abuse or narcosis or for differentiating drug use, drug abuse or narcosis from brain injury in a subject by tracking eye movement of at least one eye of the subject, analyzing eye movement of at least one eye of the subject, comparing eye movement of at least one eye of the subject the normal or mean eye movement; and, optionally calculating a standard deviation or p value for eye movement of at least one eye of the subject as compared to the normal or mean eye movement.

The invention is directed to substituted isoquinoline derivatives and uses thereof. Specifically, the invention is directed to compounds according to Formula I and the use of compounds of Formula (I)in treating disease states: (I) wherein R1, R2, R3, R4, R5, R6, R7 and X are as defined herein. The compounds of the invention are inhibitors of PERK and can be useful in the treatment of cancer, pre-cancerous syndromes and diseases associated with activated unfolded protein response pathways, such as Alzheimer's disease, spinal cord injury, traumatic brain injury, ischemic stroke, stroke, Parkinson disease, diabetes, metabolic syndrome, metabolic disorders, Huntington's disease, Creutzfeldt-Jakob Disease, fatal familial insomnia, Gerstmann-Str ussler-Scheinker syndrome, and related prion diseases, amyotrophic lateral sclerosis, progressive supranuclear palsy, myocardial infarction, cardiovascular disease, inflammation, organ fibrosis, chronic and acute diseases of the liver, fatty liver disease, liver steatosis, liver fibrosis, chronic and acute diseases of the lung, lung fibrosis, chronic and acute diseases of the kidney, kidney fibrosis, chronic traumatic encephalopathy (CTE), neurodegeneration, dementias, frontotemporal dementias, tauopathies, Pick's disease, Neimann-Pick's disease, amyloidosis, cognitive impairment, ather osclerosis, ocular diseases, arrhythmias, in organ transplantation and in the transportation of organs for transplantation. Accordingly, the invention is further directed to pharmaceutical compositions comprising a compound of the invention. The inventionis still further directed to methods of inhibiting PERK activity and treatment of disorders associated therewith using a compound of the invention or a pharmaceutical composition comprising a compound of the invention.

Peptide 6 and in particular, Peptide 021, may be used to treat tauopathies, such as frontotemporal dementia with Parkinsonism linked to chromosome-17 (FTDP-17) tau, corticobasal degeneration, Pick disease, progressive supranuclear palsy, Guam Parkinsonism dementia complex, dementia pugilistica also known as traumatic encephalopathy or traumatic brain injury, ceroid neuronal lipofusinosis, Hallerworden Sptaz disease, Alzheimer's disease, and adults with Down syndrome.

Peptide 6 and in particular, Peptide 021, may be used to treat tauopathies, such as frontotemporal dementia with Parkinsonism linked to chromosome-17 (FTDP-17) tau, corticobasal degeneration, Pick disease, progressive supranuclear palsy, Guam Parkinsonism dementia complex, dementia pugilistica also known as traumatic encephalopathy or traumatic brain injury, ceroid neuronal lipofusinosis, Hallerworden Sptaz disease, Alzheimer's disease, and adults with Down syndrome.

The present invention relates to a method for the prevention and / or treatment of chronic traumatic encephalopathy comprising administration of an effective amount of aprepitant (otherwise known as emend, fosaprepitant, ivemend, L754030, and ONO-7436). The invention further relates to the inhibition of progression of a disease, condition or state associated with tau hyperphosphorylation, and the treatment of a subject with a concussive injury.

The present invention relates to a method of preventing and / or treating chronic traumatic encephalopathy.

Devices, systems and methods are disclosed that allow a patient to self-treat neurodegenerative diseases, such as dementia, Alzheimer's disease, ischemic stroke, post-concussion syndrome, chronic traumatic encephalopathy and the like by electrical noninvasive stimulation of a vagus nerve. The system comprises a handheld stimulator that is applied to the surface of the patient's neck, wherein the stimulator comprises or is joined to a smartphone. A camera of the smartphone may be used to position and reposition the stimulator to a particular location on the patient's neck. The system may also comprise a base station that is used to meter the charging of a rechargeable battery within the stimulator. The base station and stimulator transmit data to one another regarding the status of a stimulation session.

The invention relates to compounds, compositions and methods to effectively treat traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE). As a result of administering a therapeutically effective amount of 3-phenyl-N-[2,2,2-trichloro-1-[[(8-quinolinylamino) thioxomethyl] amino] ethyl]-2-propenamide and / or guanabenz, the effects of traumatic brain injury are mitigated and / or the development of chronic traumatic encephalopathy is reduced or precluded.

The invention discloses means of utilizing Noble Gases for inhibition of pathogenic processes associated with Alzheimer's Disease progression, as well as reversal of Alzheimer's Disease. In one embodiment compositions containing xenon gas are administered alone or together with therapeutic interventions for treatment of Alzheimer's Disease. In another embodiment, taupathies such as chronic traumatic encephalopathy are treated by administration of xenon or Noble Gas containing mixtures.

The invention is directed to substituted pyrrolidinone and imidazolidinone derivatives. Specifically, the invention is directed to compounds according to Formula I:wherein R1, R2, R3, R4, R5, R6, R7, X and Y are as defined herein.The compounds of the invention are inhibitors of PERK and can be useful in the treatment of cancer, pre-cancerous syndromes and diseases / injuries associated with activated unfolded protein response pathways, such as Alzheimer's disease, spinal cord injury, traumatic brain injury, ischemic stroke, stroke, Parkinson's disease, diabetes, metabolic syndrome, metabolic disorders, Huntington's disease, Creutzfeldt-Jakob Disease, fatal familial insomnia, Gerstmann-Sträussler-Scheinker syndrome, and related prion diseases, amyotrophic lateral sclerosis, progressive supranuclear palsy, myocardial infarction, cardiovascular disease, inflammation, organ fibrosis, chronic and acute diseases of the liver, fatty liver disease, liver steatosis, liver fibrosis, chronic and acute diseases of the lung, lung fibrosis, chronic and acute diseases of the kidney, kidney fibrosis, chronic traumatic encephalopathy (CTE), neurodegeneration, dementias, frontotemporal dementias, tauopathies, Pick's disease, Neimann-Pick's disease, amyloidosis, cognitive impairment, atherosclerosis, ocular diseases, arrhythmias, in organ transplantation and in the transportation of organs for transplantation. Accordingly, the invention is further directed to pharmaceutical compositions comprising a compound of the invention. The invention is still further directed to methods of inhibiting PERK activity and treatment of disorders associated therewith using a compound of the invention or a pharmaceutical composition comprising a compound of the invention.