title: Na⁺-K⁺-ATPase, a potent neuroprotective modulator against Alzheimer disease.
abstract: 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. 1. The deficiency in Na⁺, K⁺-ATPase α1, α2 and α3 isoform genes induced learning and memory deficits, and α isoform was evidently changed in AD, revealing that Na⁺, K⁺-ATPase α isoform genes may play an important role in AD. 2. Some factors, such as β-amyloid, cholinergic and oxidative stress, can modulate learning and memory in AD through the mondulation of Na⁺-K⁺-ATPase activity. 3. 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.
authors.affiliation: Pharmacy Department, College of Chemical and Pharmaceutical Engineering, Hebei University of Science and Technology, Shijiazhuang, Hebei, China.
authors.forename: Li-Nan
authors.initials: LN
authors.lastname: Zhang
authors.forename: Yong-Jun
authors.initials: YJ
authors.lastname: Sun
authors.forename: Shuo
authors.initials: S
authors.lastname: Pan
authors.forename: Jun-Xia
authors.initials: JX
authors.lastname: Li
authors.forename: Yin-E
authors.initials: YE
authors.lastname: Qu
authors.forename: Yao
authors.initials: Y
authors.lastname: Li
authors.forename: Yong-Li
authors.initials: YL
authors.lastname: Wang
authors.forename: Zi-Bin
authors.initials: ZB
authors.lastname: Gao
mesh_terms: D000544:Alzheimer Disease / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control / Q000628:therapy; D000818:Animals; D001921:Brain / Q000201:enzymology* / Q000378:metabolism; D019587:Dietary Supplements; D004789:Enzyme Activation / Q000187:drug effects; D004790:Enzyme Induction / Q000187:drug effects; D006801:Humans; D007527:Isoenzymes / Q000737:chemistry / Q000172:deficiency / Q000378:metabolism; D009474:Neurons / Q000201:enzymology* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use; D018697:Nootropic Agents / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D021122:Protein Subunits / Q000819:agonists / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000172:deficiency / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D018696:Neuroprotective Agents; D018697:Nootropic Agents; D021122:Protein Subunits; D000254:Sodium-Potassium-Exchanging ATPase