Na+-K+-ATPase, a potent neuroprotective modulator against Alzheimer disease

Alzheimer disease (AD) is a neurodegenerative disorder clinically characterized by progressive cognitive and memory dysfunction, which is the most common form of dementia. Although the pathogenesis of neuronal injury in AD is not clear, recent evidences suggest that Na+-K+-ATPase plays an important role in AD, and may be a potent neuroprotective modulator against AD. This review aims to provide readers with an in-depth understanding of Na+-K+-ATPase in AD through these modulations of some factors that are as follows, which leads to the change of learning and memory in the process of AD. The deficiency in Na+, K+-ATPase a1, a2 and a3 isoform genes induced learning and memory deficits, and a isoform was evidently changed in AD, revealing that Na+, K+-ATPase a isoform genes may play an important role in AD. Some factors, such as beta-amyloid, cholinergic and oxidative stress, can modulate learning and memory in AD through the mondulation of Na+-K+-ATPase activity. Some substances, such as Zn, s-Ethyl cysteine, s-propyl cysteine, citicoline, rivastigmine, Vit E, memantine, tea polyphenol, curcumin, caffeine, Alpinia galanga (L.) fractions, and Bacopa monnieri could play a role in improving memory performance and exert protective effects against AD by increasing expression or activity of Na+, K+-ATPase.