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Microglia-Derived Interleukin 23: A Crucial Cytokine in Alzheimer's Disease?
Louisa Nitsch1, Linda Schneider2, Julian Zimmermann1
1Department of Neurology, University Hospital Bonn, Bonn, Germany.
Abstract:
Neuronal cell death, amyloid β plaque formation and development of neurofibrillary tangles are among the characteristics of Alzheimer's disease (AD). In addition to neurodegeneration, inflammatory processes such as activation of microglia and astrocytes are crucial in the pathogenesis and progression of AD. Cytokines are essential immune mediators of the immune response in AD. Recent data suggest a role of interleukin 23 (IL-23) and its p40 subunit in the pathogenesis of AD and corresponding animal models, in particular concerning microglia activation and amyloid β plaque formation. Moreover, in animal models, the injection of anti-p40 antibodies resulted in reduced amyloid β plaque formation and improved cognitive performance. Here, we discuss the pathomechanism of IL-23 mediated inflammation and its role in AD.
Insights
Interleukin 23 (IL-23) plays a key role in Alzheimer's disease (AD) pathogenesis by promoting inflammation and plaque formation. Targeting IL-23 with antibodies reduced amyloid plaques and improved cognition in animal models.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer's disease (AD) is characterized by neuronal death, amyloid plaques, and neurofibrillary tangles.
- Inflammatory processes, including microglia and astrocyte activation, are critical in AD pathogenesis.
- Cytokines are key immune mediators in the AD inflammatory response.
Purpose of the Study:
- To investigate the role of interleukin 23 (IL-23) and its p40 subunit in Alzheimer's disease (AD) pathogenesis.
- To explore the potential of targeting IL-23 as a therapeutic strategy for AD.
Main Methods:
- Review of current literature on IL-23 and its involvement in AD.
- Discussion of pathomechanisms of IL-23 mediated inflammation in AD.
- Analysis of data from animal models investigating the effects of anti-p40 antibodies.
Main Results:
- IL-23 and its p40 subunit are implicated in AD pathogenesis, particularly in microglia activation and amyloid β plaque formation.
- In animal models, anti-p40 antibody injection reduced amyloid β plaque load.
- Treatment with anti-p40 antibodies led to improved cognitive performance in AD animal models.
Conclusions:
- IL-23 is a significant mediator of inflammation in Alzheimer's disease.
- Targeting the IL-23/p40 pathway presents a promising therapeutic avenue for AD treatment.
- Further research into IL-23's role could lead to novel AD interventions.
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