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Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway.

Yu Liu1, Ye Liu2, Liping Shi3

  • 1Department of Epidemiology and Health Statistics, School of Public Health, Ningxia Medical University, Yinchuan 750004, China; Department of Medical Administration, Baotou Central Hospital, Baotou, Inner Mongolia 014040, China.

Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)
|January 21, 2025
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Summary

Selenium supplementation improved memory and learning in Alzheimer

Keywords:
APP/PS1/tau 3 × Tg-AD miceAlzheimer’s diseaseBDNFCREBSeleniumTrkB

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Area of Science:

  • Neuroscience
  • Nutritional Biochemistry

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder impacting cognition, particularly in older adults.
  • Selenium is an essential micronutrient vital for physiological processes; its deficiency is linked to disease and accelerated aging.
  • Cognitive impairment in AD may be influenced by nutritional factors like selenium.

Purpose of the Study:

  • To investigate the therapeutic potential of selenium in ameliorating cognitive deficits in a mouse model of Alzheimer's disease (3× Tg-AD mice).
  • To elucidate the molecular mechanisms underlying selenium's effects, specifically its relationship with the Brain-Derived Neurotrophic Factor (BDNF)/Tropomyosin receptor kinase B (TrkB) pathway.

Main Methods:

  • Utilized the 3× Tg-AD mouse model for dietary selenium intervention.
  • Assessed learning and memory through behavioral experiments.
  • Quantified selenium, glutathione peroxidase (GSH-Px), amyloid-beta (Aβ), phosphorylated tau (P-tau), BDNF, TrkB, and CREB levels using biochemical assays, RT-qPCR, and Western blotting; examined neuronal apoptosis via transmission electron microscopy.

Main Results:

  • Selenium supplementation significantly improved spatial learning and memory in 3× Tg-AD mice.
  • Elevated selenium and GSH-Px levels were observed in the brain tissue of supplemented mice, alongside enhanced neuronal integrity.
  • Expression of BDNF, TrkB, and phosphorylated CREB (p-CREB) significantly increased, indicating activation of the BDNF/TrkB pathway.

Conclusions:

  • Dietary selenium effectively ameliorates cognitive impairment in a mouse model of Alzheimer's disease.
  • The beneficial effects of selenium are mediated through the activation of the BDNF/TrkB signaling pathway.
  • Selenium shows promise as a potential therapeutic agent for managing cognitive decline in Alzheimer's disease.