发病机制
钙信号传导
疾病
线粒体
钙
神经科学
阿尔茨海默病
信号转导
生物
细胞生物学
医学
病理
内科学
免疫学
作者
Darpan Raghav,Shatakshi Shukla,Pooja Jadiya
标识
DOI:10.1016/j.bbadis.2024.167169
摘要
Mitochondrial dysregulation is pivotal in Alzheimer's disease (AD) pathogenesis. Calcium governs vital mitochondrial processes impacting energy conversion, oxidative stress, and cell death signaling. Disruptions in mitochondrial calcium (mCa2+) handling induce calcium overload and trigger the opening of mitochondrial permeability transition pore, ensuing energy deprivation and resulting in AD-related neuronal cell death. However, the role of mCa2+ in non-neuronal cells (microglia, astrocytes, oligodendrocytes, endothelial cells, and pericytes) remains elusive. This review provides a comprehensive exploration of mitochondrial heterogeneity and calcium signaling, offering insights into specific differences among various brain cell types in AD.
科研通智能强力驱动
Strongly Powered by AbleSci AI