Apolipoprotein E knockout may affect cognitive function in D-galactose-induced aging mice through the gut...

Area of Science:

• Neuroscience
• Microbiology
• Aging Research

Background:

• The gut microbiota significantly impacts central nervous system (CNS) disorders.
• Apolipoprotein E (ApoE) influences gut microbiota composition and is linked to CNS health.
• The precise mechanism of ApoE's effect on cognitive dysfunction via the gut microbiota-brain axis remains unclear.

Purpose of the Study:

• To investigate the role of Apolipoprotein E (ApoE) in cognitive function and the gut microbiota-brain axis in aging mice.
• To examine how ApoE deletion affects cognitive performance, hippocampal structure, and synaptic protein expression.
• To explore the impact of ApoE deletion on gut microbiota, hippocampal metabolites, lipids, and oxidative stress in aging.

Main Methods:

• Utilized wild-type and ApoE knockout (ApoE-/-) mice to model aging.
• Assessed cognitive function, hippocampal ultrastructure, and expression of synaptophysin (SYP) and postsynaptic density 95 (PSD-95).
• Analyzed gut microbiota composition, hippocampal metabolite profiles, lipid levels, and oxidative stress markers.

Main Results:

• ApoE deletion exacerbated cognitive dysfunction and hippocampal synaptic damage in aging mice.
• ApoE deficiency led to reduced gut microbial diversity and altered hippocampal metabolic profiles.
• The absence of ApoE aggravated dyslipidemia and oxidative stress in the aging mouse model.

Conclusions:

• Loss of ApoE negatively impacts cognitive function in aging mice.
• ApoE deletion alters gut microbiota composition, potentially mediating cognitive decline through the gut microbiota-brain axis.
• These findings highlight ApoE's critical role in maintaining cognitive health and gut-brain axis integrity during aging.