Among the neurodegenerative diseases, Alzheimer's disease (AD) is a predominant public health issue, affecting 16 million people around the world. It is clinically manifested by the presence of amyloid plaques (Aβ) and neurofibrillary tangles (NFT) within the brain. Due to intraneuronal processing, Aβ interacts with cellular targets such as mitochondria, ER, and Golgi apparatus and hampers their normal functions. Alteration in the mitochondrial function, closely related to the production of reactive oxygen species (ROS), Ca⁺² overload, and apoptosis in the brain, is one of the key pathological events studied in AD pathogenesis. It is also an important pivot for the intracellular interaction with ER and Golgi through signal transduction and membrane contact to regulate cell survival and death mechanism. Alteration in mitochondrial function is intimately connected with abnormal ER or Golgi function. Stimuli that enhance perturbation in the normal ER or Golgi organelles function can involve mitochondria mediated apoptotic cell death. In this review, we address the importance of the mitochondria and their cross talk with ER and Golgi in AD pathogenesis and animal models with a therapeutic strategy to improve the mitochondrial functions.

中文翻译：

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线粒体与阿尔茨海默氏病其他目标之间的相声对话。

在神经退行性疾病中，阿尔茨海默氏病（AD）是主要的公共卫生问题，影响了全世界1600万人。它的临床表现是脑内存在淀粉样斑块（Aβ）和神经原纤维缠结（NFT）。由于神经内处理，Aβ与细胞靶标如线粒体，ER和高尔基体相互作用，并妨碍其正常功能。线粒体功能的改变与活性氧（ROS），Ca ^+2的产生密切相关超负荷和脑中的细胞凋亡是AD发病机理中研究的关键病理事件之一。它也是通过信号转导和膜接触来调节细胞存活和死亡机制的细胞与ER和高尔基体相互作用的重要枢纽。线粒体功能的改变与ER或高尔基体功能异常密切相关。增强正常ER或高尔基细胞器功能扰动的刺激可能涉及线粒体介导的凋亡细胞死亡。在这篇综述中，我们通过改善线粒体功能的治疗策略，探讨了线粒体的重要性及其与ER和高尔基体的相互影响在AD发病机理和动物模型中的作用。