Distinct temporal and anatomical distributions of amyloid-β and tau abnormalities following controlled cortical impact in transgenic mice

Traumatic brain injury (TBI) is a major environmental risk factor for Alzheimer's disease. Intracellular accumulations of amyloid-β and tau proteins have been observed within hours following severe TBI in humans. Similar abnormalities have been recapitulated in young 3xTg-AD mice subjected to t...

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Veröffentlicht in:	PloS one 2011-09, Vol.6 (9), p.e25475-e25475
Hauptverfasser:	Tran, Hien T, Sanchez, Laura, Esparza, Thomas J, Brody, David L
Format:	Artikel
Sprache:	eng
Schlagworte:	Abnormalities Accumulation Alzheimer Disease - etiology Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amygdala Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Animals Axons - metabolism Axons - pathology Biology Brain Brain Injuries - complications Brain Injuries - metabolism Brain Injuries - pathology Cortex Cytotoxicity Disease control Disease Models, Animal Environmental risk Fornix Head injuries Health risks Humans Hypotheses Immunoglobulins Immunoreactivity Medicine Metabolism Mice Mice, Transgenic Mutation Neurodegenerative diseases Neurology Pathology Phosphatase Presenilin 1 Presenilin-1 - genetics Presenilin-1 - metabolism Proteins Risk Factors Rodents Task forces Tau protein tau Proteins - genetics tau Proteins - metabolism Time Factors Transgenic animals Transgenic mice Traumatic brain injury
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