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Upregulation of AMPK ameliorates Alzheimer disease-like tau pathology and memory impairment

Pain & Central Nervous System Daily News

2020 JUL 06 (NewsRx) -- By a News Reporter-Staff News Editor at Pain & Central Nervous System Daily News -- Investigators discuss new findings in Neurodegenerative Diseases and Conditions - Alzheimer Disease. According to news reporting originating in Wuhan, People’s Republic of China, by NewsRx journalists, research stated, “The studies have shown that 5 ‘-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is involved in Alzheimer’s disease (AD) pathology, but the effects of AMPK on AD-like Tau abnormal phosphorylation and its underlying mechanism remains unclear. Herein, we found that the mRNA expression and activity of AMPK are significantly decreased in the brains of the aging C57 mice and 3 x Tg AD mice when compared with their respective control.”

Funders for this research include National Nature Scientific Foundation of China, Natural Science Foundation of Anhui province.

The news reporters obtained a quote from the research from the Huazhong University of Science and Technology, “Moreover, when downregulation of AMPK with AAV-siAMPK-eGFP in the hippocampus CA3 of 3-month-old C57 mice, the mice display AD-like Tau hyperphosphorylation, fear memory impairment, and glycogen synthase kinase-3 beta (GSK3 beta) activity increased. On the other hand, there are also AD-like Tau hyperphosphorylation, impairment of fear memory, and AMPK activity decreased in streptozotocin (STZ) mice. Interestingly, AMPK overexpression could efficiently rescue AD-like Tau phosphorylation and brain impairment in STZ mice. Moreover, the activity of GSK3 beta and the level of Tau phosphorylation (Ser396 and Thr231 sites) were significantly decreased in HEK293 Tau cells transfected by AMPK plasmid or treated with agonists salicylate (SS), but GSK3 beta agonists Wortmannin (Wort) could ablate AMPK-mediated Tau dephosphorylation. Taken together, the study indicated that AMPK reduces Tau phosphorylation and improves brain function and inhibits GSK3 beta in AD-like model.”

According to the news reporters, the research concluded: “These findings proved that AMPK might be a new target for AD in the future.”

For more information on this research see: Upregulation of Ampk Ameliorates Alzheimer’s Disease-like Tau Pathology and Memory Impairment. Molecular Neurobiology, 2020;():. Molecular Neurobiology can be contacted at: Springer, One New York Plaza, Suite 4600, New York, Ny, United States. (Springer - www.springer.com; Molecular Neurobiology - http://www.springerlink.com/content/0893-7648/)

Our news correspondents report that additional information may be obtained by contacting X.W. Zhou, Huazhong University of Science and Technology, School of Basic Medicine, Dept. of Pathophysiology, Wuhan 430030, People’s Republic of China. Additional authors for this research include L. Wang, N. Li, F.X. Shi, W.Q. Xu, Y. Cao, Y. Lei, J.Z. Wang and Q. Tian.

The direct object identifier (DOI) for that additional information is: https://doi.org/10.1007/s12035-020-01955-w. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

(Our reports deliver fact-based news of research and discoveries from around the world.)