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作 者:Robert Vink Frances Corrigan
机构地区:[1]Clinical and Health Sciences,University of South Australia,Adelaide,SA,Australia [2]Adelaide Medical School,University of Adelaide,Adelaide,SA,Australia
出 处:《Neural Regeneration Research》2022年第9期1963-1964,共2页中国神经再生研究(英文版)
基 金:supported,in part,by a grant from the National Health and Medical Research Council of Australia。
摘 要:The association between traumatic brain injury(TBI)and an increased risk of neurodegeneration has been recognized for some decades now(Faden and Loane,2015),with recent evidence suggesting that a history of TBI,either as repeated concussive/mild TBI insults typically experienced by some athletes or less commonly as a single moderate/severe injury,may be linked with an increased risk of developing a specific form of neurodegeneration known as chronic traumatic encephalopathy(CTE)(McKee et al.,2016).The pathognomonic lesions of CTE are hyperphosphorylated tau aggregates,initially in neurons and astrocytes close to blood vessels at the base of the sulci,but later spreading throughout the brain(McKee et al.,2016).Recent work has focused on developing diagnostic criteria for traumatic encephalopathy syndrome,the clinical disorder associated with CTE,which is thought to encompass cognitive impairment and/or neurobehavioral impairment characterized by explosiveness,impulsivity and emotional lability(Katz et al.,2021).
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