认知功能衰退
疾病
小窝蛋白1
神经科学
痴呆
肌萎缩侧索硬化
神经发生
小窝
氧化应激
神经保护
自噬
炎症
医学
生物
生物信息学
心理学
信号转导
细胞生物学
免疫学
内科学
细胞凋亡
生物化学
作者
Wenxin Tang,Yansong Li,Yan Li,Qiang Wang
标识
DOI:10.1016/j.neubiorev.2021.06.044
摘要
Cognitive decline (CD), which related to vascular dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis and diabetes mellitus, is a growing health concern that has a great impact on the patients' quality of life. Although extensive efforts, the mechanisms of CD are still far from being clarified, not to mention the effective treatment and prevention strategies. Caveolin-1 (Cav-1), a trans-membrane protein, is a major component of the caveolae structure and scaffolding proteins. Recently, ample evidence depicts a strong correlation between Cav-1 and CD, however, the specific role of Cav-1 in CD has not been clearly examined and how they might be connected have yet to be identified. This review seeks to provide a comprehensive overview about how Cav-1 modulates pathogeneses of CD-associated diseases. In summary, Cav-1 can promote structural and functional plasticity of neurons, improve neurogenesis, relieve mitochondrial dysfunction, inhibit inflammation and suppress oxidative stress, which have shed light on the idea that Cav-1 may be an efficacious therapeutic target to treat CD.
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