Abstract
Alzheimer disease (AD), depicted by the formation of amyloid β-protein plaque(Aβ), has been recognized for dementia and epilepsy. The pathological mechanism of AD is complicated and it remains unclear. Currently, most therapies are focusing on elimination of Aβ plaque and preventing the breakdown of acetylcholine to prevent neuron cell death, however, most of these drugs fail to improve cognitive functions in AD patients. Therefore, the development of novel therapies for AD is in urgent need. Emerging evidences show that cellular sodium (Na+) signals play a significant role in neurol physiology. Aβ oligomer upregulates the expression of Nav1.6, leading to cognition loss, epilepsy, and malfunction of neuron development (shorter neurite length is observed during Aβ-interfered neuron development), indicating that sodium channel may be a target for treating AD. This review summarizes current development of molecular mechanisms linking sodium dysregulation with AD pathologies and discusses potential therapies for AD by correcting Na+ disruption.
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