Arabinoxylan ameliorates memory deficits and amyloid pathology in male 5 × FAD mice via modulation of gut microbiota structure

Nov 10, 2025Neuroscience

Arabinoxylan improves memory and reduces amyloid buildup in male Alzheimer's model mice by changing gut bacteria

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Abstract

AD mice exhibited depletion of short chain fatty acids (SCFAs) and transcriptomic dysregulation in the hippocampus.

AD is associated with an altered gut microbiota composition linked to brain molecular dysregulation.
A dietary intervention with arabinoxylan increased SCFAs-producing bacteria in the AD mice.
Butyric acid levels were elevated following arabinoxylan treatment, which reversed changes in aging and synaptic plasticity-related gene expression.
Arabinoxylan may alleviate AD-like symptoms by enhancing the microbiota-gut-brain axis through the enrichment of beneficial bacteria.

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Alzheimer's disease (AD), a prevalent neurodegenerative disorder, is primarily characterized by β-amyloid (Aβ) deposition. Current therapies alleviate symptoms but lack agents capable of modifying disease progression. Meanwhile, cross-regional studies indicate that AD patients exhibit disrupted gut microbiota composition, which is closely associated with cerebral molecular dysregulation. Building on this gut-brain connection, this study aimed to attenuate AD progression by targeting gut microbiota through microbially metabolized carbohydrates. Specifically, using 5 × FAD mice modeling AD pathology, we conducted 16S rRNA sequencing, targeted metabolomics of microbiota-derived metabolites, and bulk RNA sequencing experiments to investigate gut-brain axis alterations. Our results show that AD mice exhibited gut dysbiosis, depletion of short chain fatty acids (SCFAs), and transcriptomic dysregulation in the hippocampus, particularly affecting aging and synaptic plasticity-related genes. Dietary intervention with arabinoxylan significantly increased SCFAs-producing bacteria (Oscillospiraceae and Eubacterium_coprostanoligenes_group), elevated butyric acid, and thereby reversed expression levels of these aging and synaptic plasticity-related genes. Mechanistically, arabinoxylan alleviated AD-like symptoms by modulating the microbiota-gut-brain (MGB) axis; this beneficial effect occurred through enrichment of probiotic bacteria that produce SCFAs to regulate hippocampal synaptic plasticity genes. Collectively, this work proposes arabinoxylan as a novel prebiotic strategy and identifies candidate therapeutic targets for AD treatment.

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Arabinoxylan ameliorates memory deficits and amyloid pathology in male 5 × FAD mice via modulation of gut microbiota structure

Abstract

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