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The effects of astaxanthin treatment on a rat model of Alzheimer's disease.

Abstract
Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory loss and dementia, could be a consequence of the abnormalities of cortical milieu, such as oxidative stress, inflammation, and/or accompanied with the aggregation of β-amyloid. The majority of AD patients are sporadic, late-onset AD, which predominantly occurs over 65 years of age. Our results revealed that the ferrous amyloid buthionine (FAB)-infused sporadic AD-like model showed deficits in spatial learning and memory and with apparent loss of choline acetyltransferase (ChAT) expression in medial septal (MS) nucleus. In hippocampal CA1 region, the loss of pyramidal neurons was accompanied with cholinergic fiber loss and neuroinflammatory responses including glial reaction and enhanced expression of inducible nitric oxide synthase (iNOS). Surviving hippocampal CA1 pyramidal neurons showed the reduction of dendritic spines as well. Astaxanthin (ATX), a potent antioxidant, reported to improve the outcome of oxidative-stress-related diseases. The ATX treatment in FAB-infused rats decreased neuroinflammation and restored the ChAT + fibers in hippocampal CA1 region and the ChAT expression in MS nucleus. It also partly recovered the spine loss on hippocampal CA1 pyramidal neurons and ameliorated the behavioral deficits in AD-like rats. From these data, we believed that the ATX can be a potential option for slowing the progression of Alzheimer's disease.
AuthorsMu-Hsuan Chen, Tsyr-Jiuan Wang, Li-Jin Chen, Ming-Ying Jiang, Yueh-Jan Wang, Guo-Fang Tseng, Jeng-Rung Chen
JournalBrain research bulletin (Brain Res Bull) Vol. 172 Pg. 151-163 (07 2021) ISSN: 1873-2747 [Electronic] United States
PMID33932491 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
Chemical References
  • Xanthophylls
  • astaxanthine
  • Nitric Oxide Synthase Type II
Topics
  • Alzheimer Disease (drug therapy)
  • Animals
  • CA1 Region, Hippocampal (drug effects, metabolism)
  • Cholinergic Neurons (drug effects, metabolism)
  • Dendritic Spines (drug effects, metabolism)
  • Disease Models, Animal
  • Male
  • Maze Learning (drug effects)
  • Nitric Oxide Synthase Type II (metabolism)
  • Rats
  • Treatment Outcome
  • Xanthophylls (pharmacology, therapeutic use)

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