Publication Date: 2010 Mar 10 PMID: 20216546
Authors: Johnson, V. E. - Stewart, W. - Smith, D. H.
Journal: Nat Rev Neurosci
Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-beta (Abeta) plaques - one of the hallmarks of AD - may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Abeta plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Abeta genesis and catabolism following TBI.
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