Nesfatin-1 ameliorates pathological abnormalities in Drosophila hTau model of Alzheimer's disease.

Autor: Yang JY; School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, South Korea., Baek SE; School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, South Korea., Yoon JW; School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, South Korea., Kim HS; School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, South Korea., Kwon Y; KNU-G LAMP Project Group, KNU-Institute of Basic Sciences, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea., Yeom E; School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea; School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, South Korea; KNU-G LAMP Project Group, KNU-Institute of Basic Sciences, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu, 41566, South Korea. Electronic address: yeb@knu.ac.kr.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Oct 01; Vol. 727, pp. 150311. Date of Electronic Publication: 2024 Jun 25.
DOI: 10.1016/j.bbrc.2024.150311
Abstrakt: In human Alzheimer's disease (AD), the aggregation of tau protein is considered a significant hallmark, along with amyloid-beta. The formation of neurofibrillary tangles due to aberrant phosphorylation of tau disrupts microtubule stability, leading to neuronal toxicity, dysfunction, and subsequent cell death. Nesfatin-1 is a neuropeptide primarily known for regulating appetite and energy homeostasis. However, the function of Nesfatin-1 in a neuroprotective role has not been investigated. In this study, we aimed to elucidate the effect of Nesfatin-1 on tau pathology using the Drosophila model system. Our findings demonstrate that Nesfatin-1 effectively mitigates the pathological phenotypes observed in Drosophila human Tau overexpression models. Nesfatin-1 overexpression rescued the neurodegenerative phenotypes in the adult fly's eye and bristle. Additionally, Nesfatin-1 improved locomotive behavior, neuromuscular junction formation, and lifespan in the hTau AD model. Moreover, Nesfatin-1 controls tauopathy by reducing the protein level of hTau. Overall, this research highlights the potential therapeutic applications of Nesfatin-1 in ameliorating the pathological features associated with Alzheimer's disease.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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