Researchers from Shenzhen University Report Findings in Alzheimer Disease (Selenomethionine Mitigates Cognitive Decline by Targeting Both Tau Hyperphosphorylation and Autophagic Clearance in an Alzheimer's Disease Mouse Model)
By a News Reporter-Staff News Editor at Genomics & Genetics Weekly -- Fresh data on Neurodegenerative Diseases and Conditions - Alzheimer Disease are presented in a new report. According to news reporting out of Shenzhen, People's Republic of China, by NewsRx editors, research stated, "Tau pathology was recently identified as a key driver of disease progression and an attractive therapeutic target in Alzheimer's disease (AD). Selenomethionine (Se-Met), a major bioactive form of selenium (Se) in organisms with significant antioxidant capacity, reduced the levels of total tau and hyperphosphorylated tau and ameliorated cognitive deficits in younger triple transgenic AD (3xTg-AD) mice."
Our news journalists obtained a quote from the research from Shenzhen University, "Whether Se-Met has a similar effect on tau pathology and the specific mechanism of action in older 3xTg-AD mice remains unknown. Autophagy is a major self-degradative process to maintain cellular homeostasis and function. Autophagic dysfunction has been implicated in the pathogenesis of multiple age-dependent diseases, including AD. Modulation of autophagy has been shown to retard the accumulation of misfolded and aggregated proteins and to delay the progression of AD. Here, we found that 3xTg-AD mice showed significant improvement in cognitive ability after a 3-month treatment with Se-Met beginning at 8 months of age. In addition to attenuating the hyperphosphorylation of tau by modulating the activity of Akt/glycogen synthase kinase-3 beta and protein phosphatase 2A, Se-Met-induced reduction of tau was also mediated by an autophagy-based pathway. Specifically, Se-Met improved the initiation of autophagy via the AMP-activated protein kinase-mTOR (mammalian target of rapamycin) signaling pathway and enhanced autophagic flux to promote the clearance of tau in 3xTg-AD mice and primary 3xTg neurons. Thus, our results demonstrate for the first time that Se-Met mitigates cognitive decline by targeting both the hyperphosphorylation of tau and the autophagic clearance of tau in AD mice."
According to the news editors, the research concluded: "These data strongly support Se-Met as a potent nutraceutical for AD therapy."
For more information on this research see: Selenomethionine Mitigates Cognitive Decline by Targeting Both Tau Hyperphosphorylation and Autophagic Clearance in an Alzheimer's Disease Mouse Model. Journal of Neuroscience, 2017;37(9):2449-2462. Journal of Neuroscience can be contacted at: Soc Neuroscience, 11 Dupont Circle, NW, Ste 500, Washington, DC 20036, USA. (Society for Neuroscience - www.sfn.org/; Journal of Neuroscience - www.sfn.org/index.aspx?pagename=JournalOfNeuroscience)
Our news journalists report that additional information may be obtained by contacting G.L. Song, Shenzhen Univ, Coll Life Sci & Oceanog, Shenzhen Key Lab Marine Bioresources & Ecol, Shenzhen 518060, People's Republic of China. Additional authors for this research include Q.Y. Wu, R. Zheng, C. Chen, Y. Chen, Q. Liu, P.R. Hoffmann, J.Z. Ni and G.L. Song (see also Neurodegenerative Diseases and Conditions - Alzheimer Disease).
Keywords for this news article include: Shenzhen, People's Republic of China, Asia, Central Nervous System Diseases and Conditions, Neurodegenerative Diseases and Conditions, Brain Diseases and Conditions, Organoselenium Compounds, Enzymes and Coenzymes, Alzheimer Disease, Selenomethionine, Tauopathies, Pathology, Dementia, Genetics, Kinase, Shenzhen University.
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