Ren Jiale, Xiang Beibei, Xueling Lin, Han Xiaolu, Yang Zhen, Zhang Mixia, Zhang Yanjun
School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Medical Experiment Center, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Heliyon. 2024 Aug 17;10(17):e36470. doi: 10.1016/j.heliyon.2024.e36470. eCollection 2024 Sep 15.
Alzheimer's disease (AD) is a neurological disease with memory loss and cognitive decline, which affects a large proportion of the aging population. Regrettably, there are no drug to reverse or cure AD and drug development for the primary theory of amyloid beta deposition has mostly failed. Therefore, there is an urgent need to investigate novel strategies for preventing AD. Recent studies demonstrate that imbalance of mitochondrial homeostasis is a driver in Aβ accumulation, which can lead to the occurrence and deterioration of cognitive impairment in AD patients. This suggests that regulating neuronal mitochondrial homeostasis may be a new strategy for AD. We summarize the importance of mitochondrial homeostasis in AD neuron and its regulatory mechanisms in this review. In addition, we summarize the results of studies indicating mitochondrial dysfunction in AD subjects, including impaired mitochondrial energy production, oxidative stress, imbalance of mitochondrial protein homeostasis, imbalance of fusion and fission, imbalance of neuronal mitochondrial biogenesis and autophagy, and altered mitochondrial motility, in hope of providing possible therapeutic approaches for AD.
阿尔茨海默病（AD）是一种伴有记忆丧失和认知衰退的神经疾病，影响着很大一部分老年人群。遗憾的是，目前尚无药物能够逆转或治愈AD，而且针对淀粉样β蛋白沉积这一主要理论的药物研发大多以失败告终。因此，迫切需要研究预防AD的新策略。最近的研究表明，线粒体稳态失衡是Aβ积累的一个驱动因素，这可能导致AD患者认知障碍的发生和恶化。这表明调节神经元线粒体稳态可能是治疗AD的一种新策略。在本综述中，我们总结了线粒体稳态在AD神经元中的重要性及其调节机制。此外，我们总结了有关AD患者线粒体功能障碍的研究结果，包括线粒体能量产生受损、氧化应激、线粒体蛋白质稳态失衡、融合与裂变失衡、神经元线粒体生物发生和自噬失衡以及线粒体运动改变，希望能为AD提供可能的治疗方法。
