InflammopharmacologyJul 6, 2026

Brain inflammation in Alzheimer's and Parkinson's diseases: harmful processes and new drug targets

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 7, 2026

Abstract

Neuroinflammation is recognized as a key contributor to neurodegenerative diseases, notably Alzheimer's disease and Parkinson's disease.

Chronic activation of brain immune cells in response to misfolded proteins may lead to maladaptive immune signaling and cytokine release.
This chronic inflammation is associated with synaptic dysfunction and neuronal loss, contributing to clinical deterioration.
Specific factors, such as gut-brain axis inflammation in Parkinson's disease and genetic factors like APOE4 and TREM2, influence these processes.
Advancements in fluid biomarkers and neuroimaging have enhanced early detection and monitoring of neuroinflammation.
Emerging therapeutic strategies focus on targeting immune cell activity, cytokine signaling, and genetic risk factors to potentially modify disease progression.

Simplified

Neuroinflammation is now widely recognized as a key contributor to the initiation and progression of neurodegenerative diseases, particularly Alzheimer's disease (AD) and Parkinson's disease (PD). Chronic activation of brain-resident immune cells, including microglia and astrocytes, in response to misfolded protein aggregates such as amyloid-β and tau in AD and α-synuclein in PD, promotes maladaptive immune signaling, sustained cytokine release, and disruption of the blood-brain barrier (BBB). This chronic brain inflammation leads to synaptic dysfunction, neuronal loss and ultimately clinical deterioration. These processes are accompanied by disease-specific factors, such as inflammation of the gut-brain axis in PD and genetic modulators including APOE4, TREM2, and LRRK2. Furthermore, the development of fluid biomarkers together with neuroimaging techniques has improved early detection and monitoring of neuroinflammation leading to personalized therapeutic approaches. Clinical trials targeting microglial phenotypes, cytokine signaling, inflammasome activity, and genetic risk factors are emerging therapeutic strategies. Model limitations and heterogeneity of patients present challenges, but insights into neuroimmune interactions could provide a path forward for disease-modifying strategies. The present review aims to summarize new knowledge about the protective and detrimental aspects of neuroinflammation in AD and PD, providing an analysis on these developing prospects for targeted interventions toward slowing or stopping neurodegeneration.

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Funding

Competing interests

Declarations. Competing interests: The authors declare no competing interests.

PubMed

Brain inflammation in Alzheimer's and Parkinson's diseases: harmful processes and new drug targets

Abstract

Full Text

Funding

Competing interests

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