The Role of Gut Microbiota Alterations in Modulating Neuroinflammation and Disease Progression in Alzheimer’s and Parkinson’s Disease

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Background: Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two leading neurodegenerative disorders worldwide. Growing evidence highlights gut microbiota dysbiosis as a critical factor influencing neuroinflammation, pathological protein aggregation, and clinical progression.
Objective: To synthesise current evidence on the role of gut microbiota alterations in modulating neuroinflammation and disease progression in AD and PD.
Methods: A narrative review was conducted, integrating data from human observational studies, meta-analyses, animal models, and interventional trials. Microbial taxa shifts, metabolite changes, and mechanistic pathways were systematically examined.
Results: Both AD and PD are characterised by reduced microbial diversity, depletion of short-chain fatty acid–producing bacteria, and enrichment of pro-inflammatory taxa. In PD, dysbiosis strongly correlates with α-synuclein aggregation, gastrointestinal prodromes, and motor dysfunction. In AD, altered tryptophan metabolism, amyloid deposition, and tau pathology have been linked to microbial and metabolic disturbances. Animal models provide causal evidence, while human studies remain largely associative. Early interventions such as dietary modulation, probiotics, and fecal microbiota transplantation show promise, but long-term neurological benefits are unproven.
Conclusion: Gut microbiota dysbiosis emerges as both a potential biomarker and therapeutic target in AD and PD. Although mechanistic insights are compelling, robust longitudinal studies and well-powered clinical trials are needed to establish causality and evaluate the translational potential of microbiome-targeted therapies.