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Eur J Pharmacol. 2014 Sep 15;739:83-95. doi: 10.1016/j.ejphar.2013.11.012. Epub 2013 Dec 6.

Calcium channelopathies and Alzheimer's disease: insight into therapeutic success and failures.

Author information

1
Department of Neuroscience, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA.
2
Department of Neuroscience, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA. Electronic address: grace.stutzmann@rosalindfranklin.edu.

Abstract

Calcium ions are versatile and universal biological signaling factors that regulate numerous cellular processes ranging from cell fertilization, to neuronal plasticity that underlies learning and memory, to cell death. For these functions to be properly executed, calcium signaling requires precise regulation, and failure of this regulation may tip the scales from a signal for life to a signal for death. Disruptions in calcium channel function can generate complex multi-system disorders collectively referred to as "calciumopathies" that can target essentially any cell type or organ. In this review, we focus on the multifaceted involvement of calcium signaling in the pathophysiology of Alzheimer's disease (AD), and summarize the various therapeutic options currently available to combat this disease. Detailing the series of disappointing AD clinical trial results on cognitive outcomes, we emphasize the urgency to design alternative therapeutic strategies if synaptic and memory functions are to be preserved. One such approach is to target early calcium channelopathies centrally linked to AD pathogenesis.

KEYWORDS:

Alzheimer's disease; Amyloid; Brain; Calcium; Clinical trials; ER; IP3R; Neurodegeneration; Neuron; Ryanodine receptor; Synaptic plasticity

PMID:
24316360
DOI:
10.1016/j.ejphar.2013.11.012
[Indexed for MEDLINE]

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