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Dietary spermidine improves cognitive function.

Sabrina Schroeder1, Sebastian J Hofer2, Andreas Zimmermann3

  • 1Institute of Molecular Biosciences, NAWI Graz, University of Graz, 8010 Graz, Austria; BioTechMed-Graz, 8010 Graz, Austria.

Cell Reports
|April 14, 2021
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Summary
This summary is machine-generated.

Dietary spermidine crosses the blood-brain barrier, enhancing brain mitochondrial function and cognition in aged mice. Higher spermidine intake in humans is linked to reduced cognitive impairment risk.

Keywords:
Pink1agingautophagycognitive functiondietary spermidinememorymitochondriamitophagy

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Area of Science:

  • Neuroscience
  • Gerontology
  • Molecular Biology

Background:

  • Cognitive decline is a major aspect of brain aging.
  • Dietary spermidine, a polyamine, shows health-protective and lifespan-extending properties by promoting autophagy.
  • Mechanisms linking spermidine to cognitive function and brain aging are not fully understood.

Purpose of the Study:

  • To investigate the effects of dietary spermidine on brain function and cognitive performance.
  • To explore the role of autophagy and mitochondrial function in spermidine-mediated cognitive enhancement.
  • To examine the association between dietary spermidine intake and cognitive impairment in humans.

Main Methods:

  • Administered dietary spermidine to aged mice and a Drosophila aging model.
  • Assessed cognitive performance using behavioral tasks (homecage, spatial learning, olfactory associative learning).
  • Analyzed hippocampal mitochondrial function, eIF5A hypusination, and autophagy-related gene expression (Atg7, Parkin, Pink1).
  • Utilized large-scale prospective human data to correlate dietary spermidine intake with cognitive impairment risk.

Main Results:

  • Dietary spermidine crossed the blood-brain barrier in mice, increasing hippocampal eIF5A hypusination and mitochondrial function.
  • Spermidine feeding improved spatial learning and homecage behaviors in aged mice.
  • In Drosophila, spermidine enhanced mitochondrial respiratory capacity, dependent on Atg7, Parkin, and Pink1.
  • Neuron-specific Pink1 knockdown negated spermidine's cognitive benefits in flies.
  • Human data revealed a link between higher dietary spermidine intake and reduced risk of cognitive impairment.

Conclusions:

  • Dietary spermidine can enhance cognitive function by improving mitochondrial and autophagic pathways in the brain.
  • The autophagy regulator Atg7 and mitophagy mediators Parkin and Pink1 are crucial for spermidine's beneficial effects on cognition.
  • Spermidine represents a potential dietary intervention for mitigating age-related cognitive decline.