作者: Victoria E. Johnson , William Stewart , Douglas H. Smith
DOI: 10.1038/NRN2808
关键词:
摘要: Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI the development of Alzheimer's disease (AD) later life been demonstrated, it shown that amyloid-β (Aβ) plaques — one hallmarks AD may be found patients within hours following TBI. Here, we explore mechanistic underpinnings link AD, focusing on hypothesis rapid Aβ plaque formation result from accumulation amyloid precursor protein damaged axons a disturbed balance genesis catabolism