Neuroinflammation in Aging and Neurodegenerative Disorders

Summary

Neuroinflammation is a hallmark of ageing and disorders such as Alzheimer’s disease, Parkinson’s disease and other dementias. In the ageing brain, microglia and astrocytes become primed, exhibiting heightened responsiveness to peripheral immune signals and release of pro-inflammatory cytokines. This chronic low-grade inflammation contributes to synaptic dysfunction, neuronal loss and impairment of cognitive and motor function. Age-related changes in the blood–brain barrier exacerbate the infiltration of peripheral immune cells and soluble factors, further amplifying neurodegenerative cascades. Recent advances have elucidated molecular pathways governing microglial activation, innate immune memory and resolution mechanisms, pointing towards therapeutic targets. Strategies that attenuate excessive glial activation or promote anti-inflammatory signalling show promise for slowing disease progression. Understanding the interplay between systemic health, lifestyle factors and central immune responses is critical for developing interventions to maintain brain resilience across the lifespan.

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Neuroinflammation in Aging and Neurodegenerative Disorders publication trend

The graph below shows the total number of articles in neuroinflammation in aging and neurodegenerative disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroinflammation: Activation of the brain’s immune cells, leading to the release of inflammatory mediators and potential neural damage.

Microglia: Resident immune cells of the central nervous system that regulate homeostasis, clear debris and mediate inflammatory responses.

Blood–brain barrier (BBB): A selective endothelial barrier that regulates the passage of cells and molecules between the bloodstream and the brain.

Innate immune memory: Long-lasting changes in innate immune cells that alter their response to subsequent stimuli, also known as training or tolerance.

Cytokine: A soluble protein secreted by immune cells that mediates communication, such as interleukins and tumour necrosis factors.

References

  1. The role of peripheral inflammatory insults in Alzheimer’s disease: a review and research roadmap. Molecular Neurodegeneration (2023).
  2. Hypoxia inducible factor-1α regulates microglial innate immune memory and the pathology of Parkinson’s disease. Journal of Neuroinflammation (2024).
  3. Exercise rejuvenates microglia and reverses T cell accumulation in the aged female mouse brain. Aging Cell (2024).
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