ReviewJournal of neural transmission (Vienna, Austria : 1996)2026
The pathogenic role of gut microbiota dysbiosis in Alzheimer's disease: a narrative review of neuroimaging evidence.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Dementia is a progressive and ultimately life-limiting condition that represents a major cause of disability worldwide. Alzheimer’s disease (AD) is the most prevalent form of dementia that constitutes approximately 60–70% of cases and is marked by progressive cognitive and functional decline. Neuropathologically, AD is defined by extracellular amyloid-β (Aβ) plaque accumulation and intracellular deposition of hyperphosphorylated tau. Despite extensive research, the mechanisms underlying AD pathogenesis remain incompletely understood. Increasing evidence implicates gut microbiota dysbiosis as a contributing factor via the MGBA, a bidirectional communication system linking gastrointestinal and central nervous system function. To elucidate this relationship, we conducted a narrative review of neuroimaging studies—primarily positron emission tomography (PET) and magnetic resonance imaging—investigating the pathogenic role of gut microbiota alterations in AD. More specifically, we summarized findings of structural changes of gut microbiota dysbiosis–related AD in brain regions such as hippocampal, white matter integrity loss, and disrupted connectivity, whereas we summarized the PET imaging findings such as neuroinflammation and increased Aβ or tau pathology linked to microbiota-driven immune and metabolic signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.