Alzheimer’s disease (AD) is the most common human neurodegenerative ailment, the most prevalent (>95%) late-onset type of which has a still uncertain etiology. The progressive decline of cognitive functions, dementia, and physical disabilities of AD are caused by synaptic losses that progressively disconnect key neuronal networks in crucial brain areas, like the hippocampus and temporoparietal cortex,and critically impair language, sensory processing, memory, and conscious thought. AD’s two main hallmarks are fibrillar amyloid-beta(fAbeta) plaques in extracellular spaces and intracellular accumulation of fAbeta peptides and neurofibrillary tangles (NFTs). It is still undecided whether either or both these AD hallmarks cause or result from the disease. Recently, the dysregulation of calcium homeostasis has been advanced as a novel cause of AD. In this case,a suitable candidate of AD driver would be the Abeta peptides–binding/activated calcium-sensing receptor (CaSR),whose intracellular signalling is triggered by Abeta peptides. In this review, we briefly discuss CaSR’s roles in normal adult human astrocytes (NAHAs) and their possible impacts on AD.
File in questo prodotto:
Non ci sono file associati a questo prodotto.