Journal of Alzheimer's disease reports · 2026
Spermidine protects mitochondria against amyloid-β oligomers.
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Mosca Drake, Parfenova Ekaterina, Bie Yuan, Mutsaers Anthony, Spagnuolo Paul A
Аннотация
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 in vitro model and assess the therapeutic effect of spermidine (SPD) against extracellular Aβ oligomers.
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 in vitro.
OBJECTIVE: Establish a robust AD pathological in vitro model and assess the therapeutic effect of spermidine (SPD) against extracellular Aβ oligomers.
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 in vitro.