Journal
NATURE REVIEWS NEUROSCIENCE
Volume 11, Issue 5, Pages 361-370Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn2808
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Funding
- US National Institutes of Health [NS038104, NS056202]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038104, P01NS056202] Funding Source: NIH RePORTER
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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 (A beta) 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 A beta plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between A beta genesis and catabolism following TBI.
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