Tier 3 — preclinical

Exploring the Role of Apigenin in Neuroinflammation: Insights and Implications

Karine Charrière, Vincent Schneider, Manon Perrignon-Sommet, Gérard Lizard, Alexandre Benani, Agnès Jacquin-Piques, Anne Vejux
International Journal of Molecular Sciences 2024 25(9):5041

Bibliography

PubMed
PMID 38732259
PubMed Central
PMC11084463
Funding
The review reports academic/institutional support; no apigenin product intervention was sponsored or tested.
Competing interests
The authors declared no conflict of interest.

Study snapshot

DesignNarrative review of apigenin and neuroinflammation
ModelPublished cell, animal and mechanistic literature across neurological and inflammatory conditions
SampleNot applicable; review article.
InterventionApigenin across published neuroinflammation models.
DurationNot applicable.
EndpointsMicroglial activation; Inflammatory cytokines; NF-kB and Nrf2 signaling; Oxidative stress; Neuronal injury; Cognitive and motor outcomes in animal models

What the study showed, in plain terms

This review evaluates apigenin as a possible modulator of neuroinflammation across conditions such as Alzheimer's disease, Parkinson's disease and multiple sclerosis. It describes anti-inflammatory and antioxidant mechanisms from experimental studies, but it does not establish that apigenin treats neurodegenerative disease in humans.

Key findings

Across preclinical studies, apigenin is associated with reduced inflammatory signaling, altered microglial responses, lower oxidative stress and improved neurological outcomes in several disease models. The review identifies NF-kB, Nrf2 and cytokine pathways as recurring mechanistic themes.

What this study can and cannot tell us

The evidence base is heterogeneous and predominantly cell and animal research. Doses, routes and disease models differ substantially, and clinical efficacy, optimal dose, brain exposure and long-term safety in humans remain unresolved.

Editorial review

Reviewed by the Biohack Blueprint research team

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