Inhibition of high-fat diet-induced miRNA ameliorates tau toxicity in Drosophila.

Autor: Singh MK; Metabolism and Neurophysiology Research Group, Disease Target Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea., Ryu TH; Metabolism and Neurophysiology Research Group, Disease Target Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea., Nguyen MN; Metabolism and Neurophysiology Research Group, Disease Target Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea; Department of Bioscience, University of Science and Technology (UST), Daejeon, 34113, Republic of Korea., Yu K; Metabolism and Neurophysiology Research Group, Disease Target Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea; Department of Bioscience, University of Science and Technology (UST), Daejeon, 34113, Republic of Korea. Electronic address: kweonyu@kribb.re.kr.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Nov 12; Vol. 733, pp. 150446. Date of Electronic Publication: 2024 Jul 25.
DOI: 10.1016/j.bbrc.2024.150446
Abstrakt: Alzheimer's disease (AD), caused by amyloid beta (Aβ) plaques and Tau tangles, is a neurodegenerative disease characterized by progressive memory impairment and cognitive dysfunction. High-fat diet (HFD), which induces type 2 diabetes, exacerbates Aβ plaque deposition in the brain. To investigate the function of HFD in Tau-mediated AD, we fed an HFD to the Drosophila Tau model and found that HFD aggravates Tau-induced neurological phenotypes. Since microRNAs (miRNAs) are biomarkers for diabetes and AD, we evaluated the expression levels of common miRNAs of HFD and AD in HFD-fed Tau model fly brains. Among the common miRNAs, the expression levels of Let-7 and miR-34 were increased. We found that the inhibition of these miRNAs alleviates Tau-mediated AD phenotypes. Our research provides valuable insights into how HFD accelerates tau toxicity. Additionally, our work highlights the therapeutic potential of targeting Let-7 and miR-34 to develop innovative treatment approaches for AD.
Competing Interests: Declaration of competing interest The authors have no financial interests in this manuscript.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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