LAUSR

It is well known that dysregulation of Ca2+ homeostasis is involved in Alzheimeŕs disease (AD), a neurodegenerative disorder characterized by the presence of toxic aggregates of amyloid β-peptide (Aβ) and neurofibrillary tangles of tau. Alteration of calcium signaling has been linked to Aβ and tau pathologies, although the understanding of underlying molecular and cellular mechanisms is far from clear. This review summarizes the functional inhibition of plasma membrane Ca2+-ATPase (PMCA) by Aβ and tau, and its modulation by calmodulin and the ionic nature of phospholipids. The data obtained until now in our laboratory suggest that PMCA injury linked to Aβ and tau can be significantly involved in the cascade of events leading to intracellular calcium overload associated to AD.