A Specialized Nutritional Formulation Prevents Hippocampal Glial Activation and Memory Impairment Induced by Amyloid-β Oligomers in Mice

J Alzheimers Dis. 2021;83(3):1113-1124. doi: 10.3233/JAD-210139.

Abstract

Background: Alzheimer's disease (AD) is the most common cause of dementia in the elderly and is characterized by progressive cognitive decline. Considerable evidence supports an important role of amyloid-β oligomers (AβOs) in the pathogenesis of AD, including the induction of aberrant glial activation and memory impairment.

Objective: We have investigated the protective actions of a nutritional formulation, denoted AZ formulation, on glial activation and memory deficits induced by intracerebroventricular (i.c.v.) infusion of AβOs in mice.

Methods: Two-month-old male mice were treated orally with AZ formulation or isocaloric placebo for 30 consecutive days. Microglial and astrocytic activation were analyzed by immunohistochemistry in the hippocampus 10 days after i.c.v. infusion of AβOs (n = 5 mice per experimental condition). Memory loss was assessed by the novel object recognition (NOR) test (n = 6-10 mice per experimental condition).

Results: Oral treatment with the AZ formulation prevented hippocampal microglial and astrocytic activation induced by i.c.v. infusion of AβOs. The AZ formulation further protected mice from AβO-induced memory impairment.

Conclusion: Results suggest that administration of the AZ formulation may comprise a promising preventative and non-pharmacological strategy to reduce brain inflammation and attenuate memory impairment in AD.

Keywords: Alzheimer’s disease; amyloid-β; astrocytes; memory; microglia; non-pharmacological approaches.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / prevention & control
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Diet Therapy*
  • Disease Models, Animal
  • Encephalitis / prevention & control*
  • Hippocampus / physiology*
  • Male
  • Mice
  • Neuroglia / metabolism*
  • Neurons / metabolism

Substances

  • Amyloid beta-Peptides