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Ca2+ dysfunction in neurodegenerative disorders: Alzheimer's disease
Article first published online: 22 JUN 2011
Copyright © 2011 International Union of Biochemistry and Molecular Biology, Inc.
Volume 37, Issue 3, pages 189–196, May/June 2011
How to Cite
Fedrizzi, L. and Carafoli, E. (2011), Ca2+ dysfunction in neurodegenerative disorders: Alzheimer's disease. BioFactors, 37: 189–196. doi: 10.1002/biof.157
- Issue published online: 21 JUN 2011
- Article first published online: 22 JUN 2011
- Manuscript Accepted: 11 MAR 2011
- Manuscript Received: 10 MAR 2011
- Alzheimer's disease;
More than one century ago “a peculiar disorder of the cerebral cortex” was noticed in a middle-aged patient who had been affected by dementia in the last years of his life. The postmortem hallmarks of his brain were protein plaques, neurofibrillary tangles, and atherosclerotic changes: the neuropathologist who found these alterations and gave his name to the disease that underlied them was Alois Alzheimer (Alzheimer et al., Clin Anat 1995;8:429–431). Following its discovery, the disease has been studied with a vigor that went parallel to the increase of its social importance. The amount of information amassed in the literature is impressive, but knowledge on the mechanism underlying its onset and its progression is still very limited. Numerous hypotheses on the molecular pathogenesis of the Alzheimer's disease (AD) have been proposed and two have gradually gained wide consensus: (i) the amyloid cascade hypothesis, first proposed on the basis of the toxicity evoked by the deposition of amyloid β (Aβ) aggregates; (ii) the Ca2+ hypothesis, which focuses on the correlation between the dysfunction of Ca2+ homeostasis and the neurodegeneration process. This succinct review will discuss the essential aspects of the role of Ca2+ homeostasis dysregulation in the onset and development of AD.