%0 Journal Article
%T Mild traumatic brain injury: a risk factor for neurodegeneration
%A Brandon E Gavett
%A Robert A Stern
%A Robert C Cantu
%A Christopher J Nowinski
%A Ann C McKee
%J Alzheimer's Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/alzrt42
%X A complex interaction between genetic and environmental risk factors has often been a suspected trigger for the development of neurodegenerative disease. Yet of all the possible environmental risk factors put forth, trauma to the central nervous system is one of the most consistent candidates for initiating the molecular cascades that result in Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis [1-3]. Recent evidence also suggests that mild traumatic brain injury (TBI), including repetitive concussive and subconcussive trauma, can provoke another distinctive neurodegeneration: chronic traumatic encephalopathy (CTE) [4].CTE has to date only been described neuropathologically in individuals with a history of repetitive closed head injury, most often occurring in the context of contact sports. It remains to be determined whether there is a genetic susceptibility to the development of CTE and whether a single severe traumatic head injury may also be causative.CTE is a progressive tauopathy with a distinct clinical and neuropathological profile that becomes symptomatic many years after an individual experiences repeated concussive or subconcussive blows to the head. The characteristic features of CTE include: extensive tau immunoreactive neurofibrillary tangles and astrocytic tangles throughout the frontal and temporal cortices in a patchy, superficial distribution, with focal epicenters at the depths of sulci and around small vessels; extensive tau neurofibrillary tangles in the limbic and paralimbic regions, diencephalon, basal ganglia and brainstem; and a relative paucity of ¦Â-amyloid (A¦Â) deposits, although diffuse plaques are present in roughly one-half of the cases. In advanced disease, there are also macroscopic abnormalities: generalized cerebral atrophy and enlarged ventricles; atrophy of the medial temporal lobe structures and mammillary bodies; cavum septi pellucidi, often with fenestrations; and pallor of the substantia nigr
%U http://alzres.com/content/2/3/18