Department of Brain Sciences, The Weizmann Institute of Science, Rehovot 7630031, Israel.
Toxins (Basel). 2023 Mar 6;15(3):202. doi: 10.3390/toxins15030202.
Neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease, significantly reduce the quality of life of patients and eventually result in complete maladjustment. Disruption of the synapses leads to a deterioration in the communication of nerve cells and decreased plasticity, which is associated with a loss of cognitive functions and neurodegeneration. Maintaining proper synaptic activity depends on the qualitative composition of mitochondria, because synaptic processes require sufficient energy supply and fine calcium regulation. The maintenance of the qualitative composition of mitochondria occurs due to mitophagy. The regulation of mitophagy is usually based on several internal mechanisms, as well as on signals and substances coming from outside the cell. These substances may directly or indirectly enhance or weaken mitophagy. In this review, we have considered the role of some compounds in process of mitophagy and neurodegeneration. Some of them have a beneficial effect on the functions of mitochondria and enhance mitophagy, showing promise as novel drugs for the treatment of neurodegenerative pathologies, while others contribute to a decrease in mitophagy.
神经退行性疾病，如阿尔茨海默病或帕金森病，会显著降低患者的生活质量，并最终导致完全失调。突触的破坏导致神经细胞之间的通讯恶化和可塑性降低，这与认知功能的丧失和神经退行性变有关。维持适当的突触活动取决于线粒体的定性组成，因为突触过程需要足够的能量供应和精细的钙调节。线粒体定性组成的维持是通过自噬来实现的。自噬的调节通常基于几种内部机制，以及来自细胞外部的信号和物质。这些物质可能直接或间接增强或削弱自噬。在这篇综述中，我们考虑了一些化合物在自噬和神经退行性变过程中的作用。其中一些化合物对线粒体功能有有益的影响，并增强自噬，有望成为治疗神经退行性病变的新型药物，而另一些化合物则会导致自噬减少。
