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- Title
Neuroglobin attenuates Alzheimer-like tau hyperphosphorylation by activating Akt signaling.
- Authors
Chen, Li-Ming; Xiong, Yan-Si; Kong, Fan-Li; Qu, Min; Wang, Qun; Chen, Xiao-Qian; Wang, Jian-Zhi; Zhu, Ling-Qiang
- Abstract
J. Neurochem. (2012) 120, 157-164. Abstract Neuroglobin (Ngb) is a recently identified member of hemoglobin family, distributed mainly in central and peripheral nervous systems. Recent studies suggest that Ngb can protect neural cells from β-amyloid-induced toxicity in Alzheimer disease (AD). Hyperphosphorylation of tau is another characterized pathological hallmark in the AD brains; however, it is not reported whether Ngb also affects tau phosphorylation. In this study, we found that the level of Ngb was significantly reduced in Tg2576 mice (a recognized mouse model of AD) and TgMAPt mice, and the level of Ngb was negatively correlated with tau phosphorylation. Over-expression of Ngb attenuates tau hyperphosphorylation at multiple AD-related sites induced by up-regulation of glycogen synthase kinase-3β (GSK-3β), a crucial tau kinase. While Ngb activates Akt and thus inhibits GSK-3β, simultaneously inhibition of Akt abolishes the effects of Ngb on GSK-3β inhibition and tau hyperphosphorylation. Our data indicate that Ngb may attenuate tau hyperphosphorylation through activating Akt signaling pathway, implying a therapeutic target for AD.
- Subjects
HEMOGLOBINS; CENTRAL nervous system; AMYLOID beta-protein precursor; ALZHEIMER'S disease; PHOSPHORYLATION
- Publication
Journal of Neurochemistry, 2012, Vol 120, Issue 1, p157
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/j.1471-4159.2011.07275.x