Alzheimer’s Disease-associated peptide Aβ42 mobilises ER Ca2+ via InsP3R-dependent and -independent mechanisms

Alzheimer’s Disease-associated peptide Aβ42 mobilises ER Ca2+ via InsP3R-dependent and -independent mechanisms

Dysregulation of Ca2+ homeostasis is considered to contribute to the toxic action of the Alzheimer’s Disease (AD) associated Amyloid-β-peptide (Aβ). Ca2+ fluxes across the plasma membrane and release from intracellular stores have both been reported to underlie the Ca2+ fluxes induced by Aβ42. Here,...

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Bibliographic Details
Main Authors: Laura E Allan, Geert eBultynck, Tomas eLuyten, Hozeefa eAmijee, Martin D Bootman, H Llewelyn eRoderick
Format: Article
Language:English
Published: Frontiers Media S.A. 2013-11-01
Series:Frontiers in Molecular Neuroscience
Subjects:
Endoplasmic Reticulum
signalling
Alzheimer’s disease
Aβ oligomers
calcium/Ca2+
InsP3/IP3
Online Access:http://journal.frontiersin.org/Journal/10.3389/fnmol.2013.00036/full

Internet

http://journal.frontiersin.org/Journal/10.3389/fnmol.2013.00036/full

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