Dietary marine hydrolysate alleviates D-galactose-induced brain aging by attenuating cognitive alterations, oxidative stress and inflammation through the AGE-RAGE axis

PLoS One. 2024 Oct 24;19(10):e0309542. doi: 10.1371/journal.pone.0309542. eCollection 2024.

Abstract

Aging represents a natural and unavoidable phenomenon in organisms. With the acceleration of population aging, investigations into aging have garnered widespread global interest. One of the most striking aspects of human aging is the decline in brain function, a phenomenon intricately tied to the onset of neurodegenerative conditions. This study aimed to assess the impact of a fish hydrolysate, rich in low-molecular-weight peptides and n-3 LC-PUFAs, on cognitive function, inflammatory response, and oxidative stress via the AGE-RAGE axis in a mouse model of accelerated aging. This model induces cognitive decline and biochemical alterations akin to those observed during natural aging. The findings revealed that fish hydrolysate exhibited a protective effect against cognitive impairment induced by D-galactose. This effect was associated with increased protein expression of SOD1 and decreased genetic expression of IL-6 and advanced glycation end products (AGE). Consequently, within the realm of preventive and personalized nutrition, fish hydrolysate emerges as a promising avenue for mitigating age-related declines in memory function.

MeSH terms

  • Aging* / drug effects
  • Animals
  • Brain* / drug effects
  • Brain* / metabolism
  • Cognition / drug effects
  • Cognitive Dysfunction / chemically induced
  • Cognitive Dysfunction / metabolism
  • Cognitive Dysfunction / prevention & control
  • Galactose*
  • Glycation End Products, Advanced* / metabolism
  • Inflammation* / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress* / drug effects
  • Receptor for Advanced Glycation End Products* / metabolism
  • Superoxide Dismutase-1 / genetics
  • Superoxide Dismutase-1 / metabolism

Substances

  • Galactose
  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Interleukin-6
  • Superoxide Dismutase-1