Fine Tuning of Intracellular Ca2+ Content by Pharmacological Agents – A Strategy to Prevent Synapse Loss in Alzheimer Disease Hippocampal Neurons

Author(s): Elena Popugaeva*

Journal Name: Current Alzheimer Research

Volume 17 , Issue 12 , 2020

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Alzheimer disease is the dominant form of elderly dementia. Today all clinical trials that target β-amyloid have failed to indicate that β-amyloid may not be a causative agent in AD pathogenesis. Thus there is a need to search for alternative ways to treat AD patients.

Neuronal store-operated calcium entry is a fine-tuning mechanism that regulates intracellular Ca2+ content. Recent evidence suggests that store-operated calcium channels may be targeted with pharmacological agents in order to prevent synapse loss, recover long-term potentiation and change behavior.

Current mini-review discusses basic chemical structures that modulate intracellular calcium dysbalance via targeting store-operated calcium channels and their applicability as anti-AD pharmacological agents.

Keywords: Alzheimer's disease, calcium hypothesis, nSOCE, pharmacological agents, β-amyloid, pharmacological.

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Article Details

Year: 2020
Published on: 22 February, 2021
Page: [1065 - 1071]
Pages: 7
DOI: 10.2174/1567205018666210119145735
Price: $65

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