Abstract
Cytomegalovirus (CMV) has been suggested as a contributing force behind the impaired immune responsiveness in the elderly, with decreased numbers of naïve T-cells and an increased proportion of effector T-cells. Immunological impairment is also implicated as a part of the pathogenesis in Alzheimer’s disease (AD). The aim of this study was to investigate whether AD patients present with a different CMV-specific CD8 immune profile compared to non-demented controls. Blood samples from 50 AD patients and 50 age-matched controls were analysed for HLA-type, CMV serostatus and systemic inflammatory biomarkers. Using multi-colour flow cytometry, lymphocytes from peripheral blood mononuclear cells were analysed for CMV-specific CD8 immunity with MHC-I tetramers A01, A02, A24, B07, B08 and B35 and further classified using CD27, CD28, CD45RA and CCR7 antibodies. Among CMV seropositive subjects, patients with AD had significantly lower proportions of CMV-specific CD8 T-cells compared to controls, 1.16 % vs. 4.13 % (p=0.0057). Regardless of dementia status, CMV seropositive subjects presented with a lower proportion of naïve CD8 cells and a higher proportion of effector CD8 cells compared to seronegative subjects. Interestingly, patients with AD showed a decreased proportion of CMV-specific CD8 cells but no difference in general CD8 differentiation.
Highlights
Alzheimer’s disease (AD) is the most common form of dementing disorder and is characterised by a deterioration of cognitive and functional capacity
CMV serostatus and HLA allele distribution were comparable between groups, but the AD group contained a larger proportion of APOE ε4 allele carriers
Studying an age-related disease, we had expected AD patients to present with a phenotype of premature immunosenescence and expanded clones of CMVspecific CD8 cells
Summary
Alzheimer’s disease (AD) is the most common form of dementing disorder and is characterised by a deterioration of cognitive and functional capacity. In addition to the main pathological changes, other features of the affected brain often include vascular alterations with deposition of Aβ in the vessel walls, especially in carriers of the Apolipoprotein (APOE ) ε4 allele [4], as well as various inflammatory reactions [5]. It is not completely understood how amyloid plaques, neurofibrillary degeneration, vascular alterations, inflammation and immune responses are related to each other and whether any infectious agents can influence the disease process
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