In the context of Alzheimer’s disease, increased levels of beta-amyloid (Aβ) induce calcium (Ca2+) influx through NMDA receptors (NR1 and NR2) in hippocampal neurons. This Ca2+ influx and a decrease in calpastatin levels result in the dysregulation of calpain activity leading to the cleavage of a series of proteins involved in the formation of senile plaques and neurofibrillary tangles as well as in synaptic dysfunction.
