线粒体
神经科学
神经保护
疾病
机制(生物学)
生物能学
生物
阿尔茨海默病
氧化应激
淀粉样蛋白(真菌学)
医学
生物信息学
细胞生物学
病理
内科学
认识论
哲学
作者
Eugenia Trushina,Thi Kim Oanh Nguyen,Sergey Trushin
出处
期刊:JPAD
[SERDI]
日期:2023-01-01
标识
DOI:10.14283/jpad.2023.108
摘要
Despite recent FDA approval of anti-amyloid antibodies for Alzheimer’s Disease, strategies that target early molecular mechanisms and could delay or change the disease trajectory are still needed. Mitochondria emerge as a signaling organelle that could modulate multiple molecular mechanisms to enhance cellular bioenergetics and promote neuronal survival. Approaches to enhance mitochondrial function could promote healthy aging delaying the onset of age-related diseases such as Alzheimer’s Disease. Some of these strategies have been recently tested in clinical trials. Emerging evidence demonstrates that in response to mild energetic stress, mitochondria could orchestrate a robust adaptive stress response activating multiple neuroprotective mechanism. The objective of this review is to highlight recent development of mitochondria-targeting therapeutics for neurodegenerative diseases, mitochondria complex I inhibitors in particular.
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