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35 results about "Chronic traumatic encephalopathy" patented technology

Brain degeneration due to repeated head traumas.

Mobile phone for treating a patient with dementia

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.
Owner:ELECTROCORE

Micro-RNA, autoantibody and protein markers for diagnosis of neuronal injury

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, Pakinson 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.
Owner:BANYAN BIOMARKERS INC

Methods and kits for diagnosing, assessing or quantitating drug use, drug abuse and narcosis, internuclear ophthalmoplegia, attention deficit hyperactivity disorder (ADHD), chronic traumatic encephalopathy, schizophrenia spectrum disorders and alcohol consumption

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.
Owner:NEW YORK UNIV

Chronic Traumatic Encephalopathy in Blast-Exposed Individuals

The invention is based on the surprising discovery that as few as one episode of blast exposure increases the risk of CTE. Blast exposure is associated with chronic traumatic encephalopathy, impaired neuronal function, and persistent cognitive deficits in blast-exposed military veterans and experimental animals. Early diagnosis and assessment of risk permits physicians to prescribe treatment to reduce or slow progression of impairment before the onset of overt symptoms that become apparent decades after an initial insult or trauma to brain tissue. The invention provides methods and compositions for diagnosis and prognosis of individuals at risk of long term complications related to blast injury or concussive injury.
Owner:TRUSTEES OF BOSTON UNIV +1

Detection of Brain Injury

ActiveUS20150344954A1Improve long-term prognosisGood and poor survivalBiocideNervous disorderInjury brainCerebral injury
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.
Owner:UNIVERSITY OF MONTANA

Protein biomarkers for acute, subacute and chronic traumatic injuries of the central nervous system

ActiveUS20170146555A1Disease diagnosisBiological testingTraumatic spinal cord injuryBrain traumas
Proteins that are differentially expressed or elevated in tissue and biofluids after central nervous system injuries are described. Elevated or reduced levels of the proteins, alone or in various combinations or ratios, can be used to assess severity of central nervous system injury (CNS injury) including traumatic brain injury (TBI), traumatic spinal cord injury (SCI) and chronic traumatic encephalopathy (CTE). Time course measurements post CNS-injury of these proteins can be used to monitor progress or recovery over periods up to several months. Differentiation of acute, subacute and chronic injury can be diagnosed by comparing the protein levels in CNS-injury patients at days 1-3, day 4-10 with levels at day 30-180 in comparison with normal controls.
Owner:THE RES FOUND OF STATE UNIV OF NEW YORK +1

Compounds and methods for reducing tau expression

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.
Owner:BIOGEN MA INC

Compounds and methods for reducing tau expression

InactiveUS20190211332A1Maintaining and improving motor functionReduce maintenanceNervous disorderDNA/RNA fragmentationBiologyS syndrome
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.
Owner:BIOGEN IDEC MA INC

Isoquinoline derivatives as perk inhibitors

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.
Owner:GLAXOSMITHKLINE INTPROP DEV LTD

Isoquinoline derivatives as perk inhibitors

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: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-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, 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 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.
Owner:GLAXOSMITHKLINE INTPROP DEV LTD

Oral formulations and uses thereof

Disclosed are therapeutic oral formulations comprising particular substituted pyridine based compounds, their manufacture, and methods and uses of said formulations in treating substance P mediated pathways in the brain such as elevated intracranial pressure or the modification of expression of (hyper)-phosphorylated tau protein (tau) in the brain for indications such as, but not limited to concussion, post-concussive (or post-concussion) syndrome (PCS), chronic traumatic encephalopathy (CTE), traumatic brain injury (TBI) and stroke.
Owner:EUSTRALIS PHARMA LIMITED TRADING AS PRESSURA NEURO

Chronic Traumatic Encephalopathy Limiting Sports Helmet

A smart hard shell helmet for protection of head injury having a plurality of air filled inflatable bladders inside the shell, a valve on at least one bladder that responds to a controller, at least one flexible extendible strap extended from the bladder to a one point on the inside of the helmet, accelerometers operably connected to the helmet and wearer's head for sensing g force changes, pressure sensors in the bladders, an electrically actuated valve responsive to pressure and force measurement determined by the controller thresholds being met, and the valve exhausts a portion of the air in the bladder to the atmosphere extending the strap to the second state followed by the strap returning to the first state by drawing atmospheric air through the valve and re-inflating the bladder.
Owner:SHAKESPEARE W JEFFREY

Novel methods of treating a neurodegenerative disease in a mammal in need thereof

The present invention provides a method of treating or ameliorating a neurodegenerative disease in a mammal, the method comprising administering to the mammal a therapeutically effective amount of a neurodegenerative disease drug, wherein the drug is a substrate of an ABC transporter inhibitor, wherein the mammal is further administered a therapeutically effective amount of an ABC transporter inhibitor, whereby the neurodegenerative disease is treated in the mammal. In certain embodiments, the neurodegenerative disease comprises at least one selected from the group consisting of spinal cord injury, Alzheimer's disease, Parkinson's disease, Huntington's disease, prion disease, amyotrophic lateral sclerosis, a tauopathy, and chronic traumatic encephalopathy.
Owner:THOMAS JEFFERSON UNIV

Treatment of cerebral hypoxia including stroke, chronic traumatic encephalopathy, and traumatic brain injury

PendingUS20220023350A1Enhance regenerative activityNervous disorderAntibody ingredientsBrain HypoxiaInjury brain
Disclosed are methods, compositions of matter, and means of treatment or prophylaxis using fibroblasts possessing regenerative properties for the treatment of brain injuries including stroke, transient ischemic injuries, chronic traumatic encephalopathy, traumatic brain injury, and tauopathies. Embodiments of the disclosure administer fibroblasts with regenerative properties either systemically, locally, or a combination of the two prior to, concurrent with, or subsequent to a brain injury. In some embodiments of the disclosure fibroblasts or products thereof, are administered intranasally, intrathecally, and / or intravenously.
Owner:FIGENE

Method for Preventing and/or Treating Chronic Traumatic Encephalopathy - III

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.
Owner:EUSTRALIS PHARMA LIMITED TRADING AS PRESSURA NEURO

Noble gas treatment of alzheimer's disease and taupathies

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.
Owner:NOBILIS THERAPEUTICS INC

Mobile phone for treating a patient with dementia

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.
Owner:ELECTROCORE

Chemical Compounds

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.
Owner:GLAXOSMITHKLINE INTELLECTUAL PROPERTY (NO 2) LTD

Glial fibrillary acidic protein targeting immuno- and aptamer-based-therapy for neuroinjury, neurodegeneration, neuro-disease, and neuro-repair

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Active immunization with GFAP protein or GFAP peptide or passive immunization with anti-GFAP antibodies or treatment with a GFAP-binding aptamer can be used to reduce the post-TBI induced expression of GFAP, Tau and p-Tau in brain cortex tissues to attenuate the increased serum levels of GFAP after brain injury, and reduce the serum levels of pNF-H, Tau and p-Tau TBI. In addition, GFAP immunization can alleviate anxiety behavior and improve cognitive performance post-injury. Thus, active or passive GFAP immunization or administration of GFAP-binding aptamer(s) provides a treatment with therapeutic value in suppressing astroglial activation / astrogliosis, and in treating neural injuries such as traumatic brain injury, stroke, spinal cord injury, cerebral hemorrhage, or neurodegenerative diseases such as chronic traumatic encephalopathy, Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, amyotrophic lateral sclerosis, frontotemporal dementia, and other dementias.
Owner:UNIV OF FLORIDA RES FOUNDATION INC

Inhibition of Tau Propagation

Provided are novel methods of inhibiting the propagation of pathological forms of tau between cells of the central nervous system by administration of an inhibitor of LRP1. LRP1 was discovered to facilitate the endocytosis of pathological forms of tau which enables the propagation of tau aggregates and resulting neurodegeneration. These methods enable the prevention and treatment of various tauopathies, such as Alzheimer's, chronic traumatic encephalopathy, corticobasal degeneration, and others.
Owner:RGT UNIV OF CALIFORNIA
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