Open AccessIntracellular calcium signalling in Alzheimer’s disease
Author(s) -
Hermes Marina,
Eichhoff Gerhard,
Garaschuk Olga
Publication year - 2010
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2009.00976.x
Subject(s) - intracellular , neuroscience , context (archaeology) , microbiology and biotechnology , in vivo , alzheimer's disease , biology , calcium signaling , calcium in biology , disease , in vitro , amyloid (mycology) , homeostasis , signalling , medicine , pathology , biochemistry , genetics , paleontology , botany
• Introduction• Dysregulation of Ca 2+ homeostasis in AD‐ Aβ accumulation causes Ca 2+ dyshomeostasis‐ Ca 2+ dyshomeostasis increases Aβ production• Presenilins and Ca 2+ homeostasis• Dysregulation of Ca 2+ homeostasis in vivo• AD‐mediated hyperactivity and synaptic network dysfunction• Neuronal hyperactivity: implications for humans• Plaque vicinity• ConclusionsMore than two decades ago, dysregulation of the intracellular Ca 2+ homeostasis was suggested to underlie the development of Alzheimer’s disease (AD). This hypothesis was tested in numerous in vitro studies, which revealed multiple Ca 2+ signalling pathways able to contribute to AD pathology. It remained, however, unclear whether these pathways are also activated in vivo , in cells involved in signal processing in the living brain. Here we review recent data analysing intracellular Ca 2+ signalling in vivo in the context of previous in vitro findings. We particularly focus on the processes taking place in the immediate vicinity of amyloid plaques and on their possible role for AD‐mediated brain dysfunction.