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Modulating the Microbiota-gut-brain Axis: A Promising Strategy for Alzheimer's Disease Prevention and Management.
Ritu Kainth1,2, Ajay Singh Kushwah2
1IK Gujral Punjab Technical University, Kapurthala, Jalandhar, Punjab, 144601, India.
CNS & Neurological Disorders Drug Targets
|June 17, 2026
Summary
Gut microbiota changes (dysbiosis) are linked to Alzheimer's disease (AD) progression. Modulating the gut microbiome through diet or probiotics may help manage AD by reducing neuroinflammation and improving cognitive function.
Area of Science:
- Neuroscience
- Microbiology
- Gastroenterology
Background:
- Alzheimer's disease (AD) is characterized by cognitive decline and neuropathology.
- Gut microbiota dysbiosis is increasingly implicated in AD pathogenesis via the microbiota-gut-brain axis (MGBA).
Purpose of the Study:
- To investigate the mechanistic links between gut microbiota alterations and AD development.
- To evaluate the therapeutic potential of modulating the gut microbiome for AD management.
Main Methods:
- Analysis of preclinical animal models and clinical studies.
- Examination of bacterial metabolites, microbial components (LPS, amyloids), and interventions (probiotics, diet).
- Assessment of neuroinflammation, amyloid-beta (Aβ) deposition, blood-brain barrier (BBB) integrity, and cognitive behavior.
Main Results:
- Gut dysbiosis correlates with heightened neuroinflammation, microglial activation, reduced short-chain fatty acids (SCFAs), and impaired BBB function.
- Bacterial products like LPS and amyloids may exacerbate Aβ aggregation and tau hyperphosphorylation.
- Probiotics and diets rich in fiber/polyphenols restored microbial balance, increased SCFAs, reduced Aβ, and improved cognition in models.
Conclusions:
- Gut microbiota modulation is a promising complementary strategy for AD management.
- Restoring microbial balance can mitigate neurodegeneration by targeting inflammation and metabolic pathways.
- Further human trials are needed to confirm the clinical efficacy of MGBA-targeted therapies for AD.
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