Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Neuroinflammation in Alzheimer's Disease: The Role of Obesity, Gut Microbiota, and Therapeutic Potential of Omega-3 Fatty Acids and Neural Stem Cells.

Morovati A., Moussa Y., Kalupahana NS., Zu Y., Jun H., Fokar M.

Narrative Review on Neuroinflammation, Chronic Inflammation, Immune Modulation, published in J Nutr (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
J Nutr (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
41687786
DOI
10.1016/j.tjnut.2026.101407

Abstract (original English)

Alzheimer's disease (AD) is a multifaceted neurodegenerative disorder characterized by progressive cognitive decline. According to the amyloid cascade hypothesis, amyloid-β (Aβ) accumulation plays a central role in initiating and driving AD progression. However, therapeutic strategies targeting Aβ have yielded limited and inconsistent clinical benefits, highlighting the need for broader, multitargeted approaches. Growing evidence identifies neuroinflammation as a central, disease-modifying mechanism in AD pathogenesis, supported by elevated inflammatory markers and immune-related genetic risk variants in patients. Multiple factors converge to sustain maladaptive neuroinflammation, including aging, genetic susceptibility, obesity, and the gut microbiota. Obesity, marked by white adipose tissue expansion and chronic low-grade systemic inflammation, promotes blood-brain barrier dysfunction and primes microglia toward proinflammatory phenotypes. In parallel, gut microbiota dysbiosis alters microbial metabolite production, increasing gut permeability, systemic endotoxemia, and neuroinflammatory signaling. Obesity is also associated with alterations in gut microbiota composition and metabolite profiles. Together, these metabolic and microbial cues mechanistically link peripheral dysfunction to central immune activation, accelerate amyloid and tau pathology, and are further amplified

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansAlzheimer DiseaseObesityFatty Acids, Omega-3Gastrointestinal MicrobiomeAnimalsNeural Stem CellsNeuroinflammatory DiseasesInflammation

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