ArticleJournal of Alzheimer's disease reports
Spermidine protects mitochondria against amyloid-β oligomers.
Article in Journal of Alzheimer's disease reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
5 authors.
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Abstract
Background: Alzheimer's disease (AD) is a neurodegenerative condition characterized by amyloid-β (Aβ) plaques in the brain. In early pathological conditions, Aβ oligomers localize in mitochondria to promote disease progression by causing mitochondrial dysfunction. Objective: Establish a robust AD pathological Methods: In this study, high-resolution respirometry, flow cytometry, and immunoblotting techniques were used to characterize the negative effects of Aβ oligomer localization in mitochondria and assess the potential neuroprotective effects of SPD. Results: Oligomeric Aβ accumulates in and causes mitochondrial dysfunction, as evidenced by increased mitochondrial superoxide production, decreased mitochondrial mass, and decreased maximal mitochondrial respiration and spare reserve capacity. SPD, an endogenously produced polyamine that can also be provided through exogenous supplementation, improved these markers and protected mitochondria of oligomer-treated cells. Conclusions: SPD ameliorated mitochondrial dysfunction caused by Aβ oligomers
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