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