Inflammation and oxidative stress as biomarkers of premature aging in persons with intellectual disability.

The decline in cognitive ability and physical performance in older adults with intellectual disabilities (ID) is accompanied by less participation in social activities and a sedentary lifestyle; however the pathogenesis is not clear yet. It was recently suggested that chronic disease, adverse drug reactions, and aging create a cascade of events that can be best characterized as an asymptomatic inflammatory process. This cascade of events is mediated by cytokine interleukins 1 and 6 (IL-1α, and IL-6), nitric oxide (NO) and total oxidative stress (OS). Our hypothesis was that chronic inflammation in the bloodstream of persons with ID contributes to their "premature aging". To test this hypothesis, we measured and compared the levels of inflammatory molecules in persons with and without ID. Fifteen adults with, and 15 adults without ID (control group) participated in this study. The levels of NO metabolites (NOx), IL-1α, and IL-6 were obtained from participants' serum. OS markers were drawn from participants' capillary. Western blot, RT-PCR and specific chemical analysis were used as measurement tools. The levels of inflammatory molecules and OS were significantly higher in persons with ID compared to the control group. Asymptomatic inflammation in the bloodstream of the older adults with ID might explain the "premature aging" of these individuals. Monitoring the levels of inflammatory molecules could serve as biomarkers of "premature aging" which may allow early diagnosis and intervention, and improve the quality of care for persons with ID.