Neuroinflammation and Anti-Inflammatory Strategies in Alzheimer's Disease

Chronic inflammation of the brain, or neuroinflammation, contributes to the progression of Alzheimer’s disease by promoting neuronal injury and cognitive decline. In Alzheimer’s, overactive microglia and astrocytes release excess cytokines and shift lipid mediators from pro-resolving to pro-inflammatory profiles, exacerbating amyloid-β deposition and tau pathology. Recent work has elucidated how these immune processes evolve across early and late disease stages, and has identified multiple anti-inflammatory strategies: from selective cyclooxygenase inhibitors to novel biologics targeting microglial receptors, and natural compounds that both scavenge free radicals and suppress inflammatory cascades. Integrating biomarker-guided approaches with an improved understanding of glial biology now underpins efforts to fine-tune therapeutic timing, aiming to rebalance immune dynamics and slow neurodegenerative changes in patients worldwide.

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Neuroinflammation and Anti-Inflammatory Strategies in Alzheimer's Disease publication trend

The graph below shows the total number of articles in neuroinflammation and anti-inflammatory strategies in alzheimer's disease across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroinflammation: Sustained activation of the immune response in the central nervous system involving glial cells and soluble mediators.

Microglia: Resident immune cells of the brain that mediate surveillance, phagocytosis and release of inflammatory factors.

Amyloid-β: Peptide fragments that aggregate into extracellular plaques and trigger immune activation in Alzheimer’s disease.

Tau protein: Microtubule-associated protein that forms neurofibrillary tangles when abnormally phosphorylated.

Cytokine: Small signalling protein released by immune cells to regulate inflammation and cell recruitment.

Pro-resolving lipid mediators: Bioactive lipids, such as resolvins, that promote termination of inflammatory responses and tissue repair.

Cyclooxygenase-2: Enzyme that converts arachidonic acid into prostaglandins, key drivers of inflammatory signalling.

References

1. Differential effect of an evolving amyloid and tau pathology on brain phospholipids and bioactive lipid mediators in rat models of Alzheimer-like pathology. Journal of Neuroinflammation (2024).
2. The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets. CNS Neuroscience & Therapeutics (2024).
3. Licochalcone A Inhibits Prostaglandin E2 by Targeting the MAPK Pathway in LPS Activated Primary Microglia. Molecules (2023).
4. A Path Toward Precision Medicine for Neuroinflammatory Mechanisms in Alzheimer's Disease. Frontiers in Immunology (2020).