A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury - Wikidata - wikimedia - TriplyDB

A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury

A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury

http://www.wikidata.org/entity/Q34458328

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Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma The cysteine protease cathepsin B is a key drug target and cysteine protease inhibitors are potential therapeutics for traumatic brain injury The Neuroprotective Properties of the Amyloid Precursor Protein Following Traumatic Brain Injury Cathepsin B is a New Drug Target for Traumatic Brain Injury Therapeutics: Evidence for E64d as a Promising Lead Drug Candidate Aging, neurodegenerative disease, and traumatic brain injury: the role of neuroimaging Traumatic brain injury, neuroinflammation, and post-traumatic headaches Neurobiological consequences of traumatic brain injury Animal models of traumatic brain injury Chronic neuropathologies of single and repetitive TBI: substrates of dementia?Neurochemical profile of dementia pugilistica Molecular mechanisms of cognitive dysfunction following traumatic brain injury Self-reported head injury and risk of late-life impairment and AD pathology in an AD center cohort Examining the relationship between head trauma and neurodegenerative disease: A review of epidemiology, pathology and neuroimaging techniques Depletion of GGA1 and GGA3 mediates postinjury elevation of BACE1 Alzheimer Disease and Its Growing Epidemic: Risk Factors, Biomarkers, and the Urgent Need for Therapeutics.Amyloid precursor protein-induced axonopathies are independent of amyloid-beta peptides.The evolution of cost-efficiency in neural networks during recovery from traumatic brain injury A neprilysin polymorphism and amyloid-beta plaques after traumatic brain injury.Amyloid imaging with carbon 11-labeled Pittsburgh compound B for traumatic brain injury.Distinct temporal and anatomical distributions of amyloid-β and tau abnormalities following controlled cortical impact in transgenic mice Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis.Acute reduction of microglia does not alter axonal injury in a mouse model of repetitive concussive traumatic brain injury.Calcineurin and glial signaling: neuroinflammation and beyond Axonal pathology in traumatic brain injury.Brain temperature and its fundamental properties: a review for clinical neuroscientists.Inflammation and white matter degeneration persist for years after a single traumatic brain injury.Lipolysaccharide-Induced Neuroinflammation Is Associated with Alzheimer-Like Amyloidogenic Axonal Pathology and Dendritic Degeneration in Rats.The problem of axonal injury in the brains of veterans with histories of blast exposure Chronic neurodegeneration after traumatic brain injury: Alzheimer disease, chronic traumatic encephalopathy, or persistent neuroinflammation?Runx1t1 (Runt-related transcription factor 1; translocated to, 1) epigenetically regulates the proliferation and nitric oxide production of microglia Mild traumatic brain injury and diffuse axonal injury in swine.Effects of traumatic brain injury and posttraumatic stress disorder on Alzheimer's disease in veterans, using the Alzheimer's Disease Neuroimaging Initiative.Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain.Chronic traumatic encephalopathy and athletes.From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy?Therapy development for diffuse axonal injury.Traumatic axonal injury in the mouse is accompanied by a dynamic inflammatory response, astroglial reactivity and complex behavioral changes Dura mater is a potential source of Aβ seeds.

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A lack of amyloid beta plaques despite persistent accumulation of amyloid beta in axons of long-term survivors of traumatic brain injury

http://www.wikidata.org/entity/Q34458328

description

2008 nî lūn-bûn

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2008 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2008 թվականի մայիսին հրատարակված գիտական հոդված

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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prefLabel

A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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J.1750-3639.2008.00176.X

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Brain Pathology

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A lack of amyloid beta plaques ...... vors of traumatic brain injury

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Douglas H Smith

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Kunihiro Uryu

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Victoria E Johnson

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Xiao-Han Chen

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P2860

Axonal transport of amyloid precursor protein is mediated by direct binding to the kinesin light chain subunit of kinesin-I

Identification of the major Abeta1-42-degrading catabolic pathway in brain parenchyma: suppression leads to biochemical and pathological deposition

Axonal transport defects: a common theme in neurodegenerative diseases

Axonal transport, amyloid precursor protein, kinesin-1, and the processing apparatus: revisited

Presenilin-dependent transcriptional control of the Abeta-degrading enzyme neprilysin by intracellular domains of betaAPP and APLP

Kinesin-mediated axonal transport of a membrane compartment containing beta-secretase and presenilin-1 requires APP

Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury.

Metabolism of amyloid beta peptide and pathogenesis of Alzheimer's disease. Towards presymptomatic diagnosis, prevention and therapy.

The neprilysin (NEP) family of zinc metalloendopeptidases: genomics and function.

Ischaemic brain damage is still common in fatal non-missile head injury.

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scholarly article

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2

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John Q. Trojanowski

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5358519

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18492093

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traumatic brain injury

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3014260

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