Alzheimer's Disease: From Immune Homeostasis to Neuroinflammatory Condition
Overview
Chemistry
Molecular Biology
Affiliations
Alzheimer's Disease is the most common cause in the world of progressive cognitive decline. Although many modifiable and non-modifiable risk factors have been proposed, in recent years, neuroinflammation has been hypothesized to be an important contributing factor of Alzheimer's Disease pathogenesis. Neuroinflammation can occur through the combined action of the Central Nervous System resident immune cells and adaptive peripheral immune system. In the past years, immunotherapies for neurodegenerative diseases have focused wrongly on targeting protein aggregates Aβ plaques and NFT treatment. The role of both innate and adaptive immune cells has not been fully clarified, but several data suggest that immune system dysregulation plays a key role in neuroinflammation. Recent studies have focused especially on the role of the adaptive immune system and have shown that inflammatory markers are characterized by increased CD4+ Teff cells' activities and reduced circulating CD4+ Treg cells. In this review, we discuss the key role of both innate and adaptive immune systems in the degeneration and regeneration mechanisms in the pathogenesis of Alzheimer's Disease, with a focus on how the crosstalk between these two systems is able to sustain brain homeostasis or shift it to a neurodegenerative condition.
The study on cuproptosis in Alzheimer's disease based on the cuproptosis key gene .
Chen G, Xi E, Gu X, Wang H, Tang Q Front Aging Neurosci. 2025; 16:1480332.
PMID: 39759399 PMC: 11696982. DOI: 10.3389/fnagi.2024.1480332.
Slotos R, Nguyen T, Fiska L, Friedland K, Endres K Commun Biol. 2025; 8(1):3.
PMID: 39753747 PMC: 11699115. DOI: 10.1038/s42003-024-07405-w.
Risk Factors and Diagnostic Model Construction of Chronic Pain with Cognitive Impairment.
Zhang C, Su Y, Zeng X, Zhu X, Gao R, Liu W J Pain Res. 2024; 17:4331-4342.
PMID: 39712461 PMC: 11662672. DOI: 10.2147/JPR.S485000.
Bifurcations in coupled amyloid-β aggregation-inflammation systems.
Chakrabarti K, Bakhtiari D, Rezaei-Ghaleh N NPJ Syst Biol Appl. 2024; 10(1):80.
PMID: 39080352 PMC: 11289389. DOI: 10.1038/s41540-024-00408-7.
Hofstra B, Kas M, Verbeek D Transl Psychiatry. 2024; 14(1):253.
PMID: 38862462 PMC: 11166962. DOI: 10.1038/s41398-024-02968-y.