神经退行性变
自噬
溶酶体
自噬体
创伤性脑损伤
细胞生物学
神经科学
化学
生物
医学
生物化学
疾病
内科学
细胞凋亡
精神科
酶
作者
Xulong Ding,Shuqiang Cao,Qing Wang,Bin Du,Kefeng Lu,Shiqian Qi,Ying Cen,Qing‐Zhang Tuo,Weibo Liang,Peng Lei
标识
DOI:10.1002/advs.202306399
摘要
Abstract Traumatic brain injury (TBI) leads to progressive neurodegeneration that may be caused by chronic traumatic encephalopathy (CTE). However, the precise mechanism remains unclear. Herein, the study identifies a crucial protein, axonemal dynein light intermediate polypeptide 1 (DNALI1), and elucidated its potential pathogenic role in post‐TBI neurodegeneration. The DNALI1 gene is systematically screened through analyses of Aging, Dementia, and TBI studies, confirming its elevated expression both in vitro and in vivo. Moreover, it is observed that altered DNALI1 expression under normal conditions has no discernible effect. However, upon overexpression, DNALI1 inhibits autophagosome‐lysosome fusion, reduces autophagic flux, and exacerbates cell death under pathological conditions. DNALI1 silencing significantly enhances autophagic flux and alleviates neurodegeneration in a CTE model. These findings highlight DNALI1 as a potential key target for preventing TBI‐related neurodegeneration.
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