Hepatocyte-derived exosomal miR-122 mediates liver-to-brain crosstalk and neuroinflammation in alcohol-exposed Alzheimer's disease mice.

Repeated binge drinking in APP/PS1 Alzheimer’s disease mice increases hepatocyte-derived sEV release enriched in mature miR-122-5p, which is detected in brain and linked to neuroinflammation.

• Why it matters: Alcohol and AD both feature neuroinflammation, but how alcohol-driven liver injury communicates with the brain during AD progression is unclear.
• What they did: The study measured alanine aminotransferase, cytokine expression, sEV biogenesis/release, and miR-122-5p transfer; it also tested BV-2 microglia sensitization by hepatocyte sEVs and miR-122-5p mimic or inhibitor delivery.
• The result: Alcohol-exposed hepatocyte sEVs enhanced LPS-stimulated CCL2, CXCL2, CCL3, and TNF-α in microglia, and miR-122-5p mimic partially reproduced this effect while inhibitor delivery reversed it; ADAM10 was reduced in wild-type and AD brains after alcohol exposure.

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