Alzheimer’s disease (AD) is the most common cause of dementia with a worldwide prevalence of about 25 million in 2010, and is expected to double by 2030 because of increased life expectancy. Cerebral amyloid-β aggregation is the earliest recognizable pathological event in AD. The driving force for the AD is disruption in the balance between production and clearance of aggregated amyloid. The ubiquitin proteasome system (UPS) and autophagy are complementary mechanisms that accomplish important cellular housekeeping functions: removal of protein aggregates, turnover of organelles as well as the elimination of intracellular pathogens.
Progressive decline of physiological function is the characteristic of aging and this is distinctly manifest in the immune system. It results in inadequate initiation and resolution of immune responses – immunosenescence – and a chronic low-grade inflammation –inflammaging. This chronic Condition linked to metabolic syndrome, atherosclerosis, and cancer and Alzheimer’s disease. Senescent and hyperactive microglia has been detected in the aged and diseased brain.
Cytomegalovirus (CMV) stimulates age-like immune changes and CMV reactivation has been related with increased levels of IL-6 and TNF and premature mortality. Reports have shown that very young and old having CMV infection results in similar alterations to CD8+ T cell subset surface phenotypes. As a conclusion, that age-associated changes could rather be due to age-associated increases in prevalence of CMV infection. This suggests an overwhelming impact of CMV on the aging T cell immune system.