Alzheimer’s disease (AD) is a neurodegenerative disease associated with senile plaques (SP) and neurofibrillary tangles (NFTs) in the brain. Abnormal accumulation of a specific protein, β-amyloid (Aβ), in brain neurons plays a central role in the pathogenesis of this neurodegenerative disease.
Changes in intracellular calcium signalling are related to Alzheimer’s disease. Studies have demonstrated that Aβ upregulates calcium in neurons, causing intracellular calcium overload, which causes abnormal neuronal metabolism, neuronal apoptosis, and memory decline
The mechanism by which calcium influences AD progression is, large amounts of calcium influx cause calcium homeostasis disorder, which causes neuronal structure damage, cell necrosis, and dysfunction, increased intracellular calcium concentrations lead to the deposition of Aβ; intracellular calcium overload causes abnormal phosphorylation of tau and inhibits its binding to microtubules, eventually resulting in neurofibrillary tangles, and calcium homeostasis disorder leads to abnormal synaptic plasticity in the brain, which is associated with cognitive impairment in patients with AD.
