iScienceOct 27, 2026

How specific cell types in memory and hormone control areas respond to nutrition and metabolism in Alzheimer's disease

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 28, 2026

Abstract

High fructose consumption increased the expression of C3 in ependymal cells and inflammatory genes in microglia in a mouse model of Alzheimer's disease.

Fructose consumption may exacerbate inflammatory responses in the brain associated with Alzheimer's disease.
Docosahexaenoic acid (DHA) and nicotinamide riboside (NR) could normalize the elevated expression of inflammatory genes caused by fructose.
Both DHA and NR may reverse the detrimental transcriptional changes linked to amyloid-beta in various brain cell types.
DHA and NR treatments are associated with a restoration of hippocampal oligodendrocyte levels that are decreased in Alzheimer's disease.
DHA treatment may reduce the number of inflammatory microglia, while NR could increase the proportion of neurons in the hippocampus.

Simplified

To understand the potential of modulating metabolism for therapeutic development for Alzheimer's disease (AD), we investigated the effects of high fructose consumption as a potential risk, and docosahexaenoic acid (DHA) and nicotinamide riboside (NR) as potentially beneficial, on cell type-specific transcriptomic responses in the hippocampus and hypothalamus of the 5xFAD mouse model. Fructose increased the expression of C3, encoding complement component 3, in ependymal cells and inflammatory genes in microglia, which were normalized by DHA and NR. NR and DHA reversed Aβ-associated transcriptional signatures across cell types, but the effects were modified by fructose. DHA and NR treatments reversed the AD-associated decrease in hippocampal oligodendrocytes, with DHA further reducing hippocampal microglia and increasing hypothalamic astrocytes, and NR further increasing hippocampal neuronal proportions. Our study supports the impact of metabolic regulation of AD-associated cell types and pathways and provides molecular support for utilizing nutritional modulators for AD intervention.

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How specific cell types in memory and hormone control areas respond to nutrition and metabolism in Alzheimer's disease

Abstract

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