Calcium Deregulation in Alzheimer’s Disease
Pp. 202-215 (14)
Vitor S. Alves, Fernanda L. Ribeiro, Daniela R. de Oliveira and Fernando A. Oliveira
The first ideas proposed by Zaven Khachaturian about the calcium (Ca2+)
hypothesis of brain aging foster researchers into cellular and molecular mechanisms
trying to explain Ca2+ alterations of brain function and cognitive deficits. Alzheimer’s
disease (AD) is dementia causally linked to aging, therefore Ca2+ cellular processes
underlying aging-related impairments in the brain may share similarities to severe
dementia, as in AD. The effective control of cytosolic Ca2+ is essential for the
modulation of various processes and pathways of neuronal signaling, and its
inefficiency or deregulation can lead to austere pathological conditions. This chapter
shows pieces of evidence of Ca2+ deregulation in AD and its consequences, focusing on
intrinsic properties of the neurons.
Afterhyperpolarization, Aging, Alzheimer’s Disease Diagnosis,
Dementia, Learning and Memory, Neurodegeneration, Neuronal Susceptibility.
Laboratory of Cellular and Molecular Neurobiology (LaNeC); Center for Mathematics, Computation and Cognition, Federal University of ABC (UFABC), Sao Bernardo do Campo, Sao Paulo, Brazil.