Jangampalli Adi Pradeepkiran, Javaria Baig, Ashley Seman, P Hemachandra Reddy
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引用次数: 0
Abstract
Alzheimer's disease (AD) is characterized by the accumulation of amyloid β and phosphorylated τ protein aggregates in the brain, which leads to the loss of neurons. Under the microscope, the function of mitochondria is uniquely primed to play a pivotal role in neuronal cell survival, energy metabolism, and cell death. Research studies indicate that mitochondrial dysfunction, excessive oxidative damage, and defective mitophagy in neurons are early indicators of AD. This review article summarizes the latest development of mitochondria in AD: 1) disease mechanism pathways, 2) the importance of mitochondria in neuronal functions, 3) metabolic pathways and functions, 4) the link between mitochondrial dysfunction and mitophagy mechanisms in AD, and 5) the development of potential mitochondrial-targeted therapeutics and interventions to treat patients with AD.
阿尔茨海默病（AD）的特征是淀粉样蛋白β和磷酸化τ蛋白聚集在大脑中，导致神经元丧失。在显微镜下，线粒体的功能是独一无二的，在神经元细胞存活、能量代谢和细胞死亡中发挥着举足轻重的作用。研究表明，神经元线粒体功能障碍、过度氧化损伤和有丝分裂缺陷是老年痴呆症的早期指标。这篇综述文章总结了线粒体在 AD 中的最新进展：1）疾病机制途径；2）线粒体在神经元功能中的重要性；3）代谢途径和功能；4）AD 中线粒体功能障碍和有丝分裂机制之间的联系；5）开发潜在的线粒体靶向疗法和干预措施以治疗 AD 患者。
期刊介绍：
Edited by Stephen G. Waxman, The Neuroscientist (NRO) reviews and evaluates the noteworthy advances and key trends in molecular, cellular, developmental, behavioral systems, and cognitive neuroscience in a unique disease-relevant format. Aimed at basic neuroscientists, neurologists, neurosurgeons, and psychiatrists in research, academic, and clinical settings, The Neuroscientist reviews and updates the most important new and emerging basic and clinical neuroscience research.
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