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Expression of HLA-DR, CD80, and CD86 in Healthy Aging and Alzheimer's Disease
Stefan Busse1, Johann Steiner1,2, Juliane Alter1
1Department of Psychiatry, University of Magdeburg, Magdeburg, Germany.
Insights
Monocyte immune responses in Alzheimer's disease (AD) are linked to aging, not AD itself. Immune markers like HLA-DR, CD80, and CD86 increase with age, but not due to AD pathology or rivastigmine treatment.
Area of Science:
- Immunology
- Neuroscience
- Gerontology
Background:
- Monocytes and macrophages are potential therapeutic targets for Alzheimer's disease (AD) and aging.
- The role of these immune cells in neurodegenerative disorders like AD is not well understood.
Purpose of the Study:
- To investigate the number and immune marker expression (HLA-DR, CD80, CD86) of CD14+ monocytes in healthy aging and in AD patients.
- To assess the impact of rivastigmine treatment on these monocyte markers in AD patients.
Main Methods:
- Quantified CD14+ monocytes and measured HLA-DR, CD80, and CD86 expression in peripheral blood.
- Studied healthy volunteers across a wide age range (20-79 years).
- Analyzed AD patients at diagnosis and during 52 weeks of rivastigmine treatment.
Main Results:
- Monocyte count remained stable with age and in AD patients.
- Expression of HLA-DR, CD80, and CD86 on monocytes increased significantly with age.
- No significant differences in monocyte markers were observed between AD patients and age-matched controls, nor after rivastigmine treatment.
Conclusions:
- Increased expression of HLA-DR, CD80, and CD86 on monocytes is attributed to immunosenescence (aging of the immune system), not AD pathology.
- Rivastigmine treatment did not alter these age-related changes in monocyte immune markers in AD patients.
Abstract:
Although monocytes and macrophages could serve as new therapeutic targets for treatment of Alzheimer's disease (AD) and aging of the human innate immune system, its role in the pathogenesis of neurodegenerative disorders such as AD are only poorly understood. We have addressed this here by determining the number of CD14+ monocytes and the frequency of HLA-DR-, CD80-, and CD86-expression in peripheral blood from healthy volunteers aged 20-79 years, and in AD patients at diagnosis and after 12, 30, and 52 weeks of rivastigmine treatment. While the number of CD14+ monocytes remained constant, the expression of HLA-DR, CD80, and CD86 by monocytes increased with age. However, no differences were identified by comparing AD patients with age-matched healthy controls or following treatment of AD patients with rivastigmine. These results indicate that changes in the expression of HLA-DR, CD80, and CD86 are caused by immunosenescence rather than by AD pathology or treatment of AD patients with rivastigmine.
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