title: Intracellular calcium signalling in Alzheimer's disease.
abstract: More 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.
authors.affiliation: University of Tübingen, Institute of Physiology II, Tübingen, Germany.
authors.forename: Marina
authors.initials: M
authors.lastname: Hermes
authors.forename: Gerhard
authors.initials: G
authors.lastname: Eichhoff
authors.forename: Olga
authors.initials: O
authors.lastname: Garaschuk
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D016874:Neurofibrillary Tangles / Q000473:pathology; D053763:Presenilins / Q000235:genetics / Q000378:metabolism; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D013569:Synapses / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D053763:Presenilins; D020033:Protein Isoforms; D002118:Calcium