Alzheimer's disease (AD) is a neurodegenerative disease associated with senile plaques (SP) and neurofibrillary tangles (NFTs) in the brain. With aging of the population, AD has become the most common form of dementia. However, the mechanisms leading to AD are still under investigation, and there are currently no specific drugs for its treatment. Therefore, further study on the pathogenesis of AD to develop new drugs for AD treatment remains a top priority. Several studies have suggested that intracellular calcium homeostasis is dysregulated in AD, and this has been implicated in the deposition of amyloid β (Aβ), hyperphosphorylation of tau protein, abnormal synaptic plasticity, and apoptosis, all of which are involved in the occurrence and development of AD. In addition, some based on pathways linking calcium homeostasis and AD have achieved results in AD treatment. This review comprehensively explores the relationship between calcium homeostasis and the pathogenesis of AD to provide a theoretical basis for the future exploration of AD and the development of novel therapeutic drugs.
Keywords: Aβ; apoptosis; calcium homeostasis; synaptic plasticity; tau; therapy.
© 2022 Ge et al.