Electroacupuncture's Impact on the Hippocampal RAGE/LRP1 Receptor System in SAMP8 Mice

Zhitao Hou1,2,3,4,5, Jindi Ma1, Xian Zhang1

  • 1College of Basic Medical and Sciences, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, 150040, China.

Advanced Biology
|April 8, 2025
PubMed

Insights

Electroacupuncture (EA) improves age-related cognitive impairment by reducing amyloid-beta plaques and enhancing brain repair mechanisms. This non-pharmacological approach shows promise for treating cognitive decline.

Area of Science:

  • Neuroscience
  • Gerontology
  • Integrative Medicine

Background:

  • Age-related cognitive impairment (ARCI) is associated with beta-amyloid (Aβ) accumulation.
  • Disrupted blood-brain barrier (BBB) transport, involving RAGE and LRP1, contributes to ARCI.
  • Senescence-accelerated mouse prone 8 (SAMP8) mice model ARCI.

Purpose of the Study:

  • To investigate the effects of electroacupuncture (EA) on cognitive function in SAMP8 mice.
  • To analyze EA's impact on hippocampal pathology and neurotransmitter levels.
  • To examine EA's influence on the RAGE/LRP1 system and Aβ clearance.

Main Methods:

  • EA was applied at Zusanli (ST36) and Baihui (GV20) acupoints in SAMP8 mice.
  • Cognitive performance was assessed.
  • Hippocampal pathology, neurotransmitter levels (dopamine, norepinephrine, serotonin, 5-HIAA), Aβ42, RAGE, LRP1, VCAM-1, ICAM-1, ApoE, and NF-κB expression were measured.

Main Results:

  • EA significantly improved cognitive performance in SAMP8 mice.
  • EA reduced hippocampal neuronal degeneration and decreased Aβ42 levels.
  • EA modulated neurotransmitters, downregulated RAGE, VCAM-1, ICAM-1, and upregulated LRP1 and ApoE, facilitating Aβ clearance.

Conclusions:

  • Electroacupuncture demonstrates potential as a non-pharmacological treatment for age-related cognitive impairment.
  • EA promotes cognitive improvement through neuroprotection and enhanced Aβ clearance.
  • The findings suggest EA influences BBB integrity and Aβ metabolism via the RAGE/LRP1 pathway.

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