The older patient with diabetes: a practical approach.

Type 2 diabetes mellitus is very prevalent among persons aged 60-80 years old. This population is expected to increase in number and is characterized by the presence of comorbidities, long standing diabetes, frailty, high rate of cognitive impairment and limited life expectancy. These characteristics have a significant impact on diabetes and treatment among the elderly, much as diabetes predisposes to these conditions. In this article we will describe mechanisms that may lead to insulin resistance and diabetes among the elderly and also how these conditions contribute to the development of frailty and cognitive impairment. Hypoglycemia and it's consequences are important considerations when planning the treatment of diabetes. Treatment options in light of new goals and the danger of hypoglycemia will be detailed.

Age related microsatellite instability in T cells from healthy individuals.

Many immune functions decline with age and may jeopardize the elderly, as illustrated, for example by the significantly higher mortality rate from influenza in old age. Although innate and humoral immunity are affected by aging, it is the T cell compartment, which manifests most alterations. The mechanisms behind these alterations are still unclear, and several explanations have been offered including thymic involution and Telomere attrition leading to cell senescence. Age related accumulation of mutations has been documented and could serve as an additional mechanism of T cell dysfunction. One effective repair mechanism capable of rectifying errors in DNA replications is the mismatch repair (MMR) system. We previously reported a comparative examination of individual DNA samples from blood cells obtained at 10 year intervals from young and old subjects. We showed significantly higher rates of microsatellite instability (MSI), an indicator of MMR dysfunction in older subjects, compared to young. In the present study we confirm this result, using direct automated sequencing and in addition, we demonstrate that as CD8 lymphocytes from aged individuals, undergo repeated population doublings (PDs) in culture, they develop MSI. CD4 clones that also undergo repeated PDs in culture develop significant MSI as well. Elucidation of this previously unexplored facet of lymphocyte dynamics in relation to aging may help identify novel mechanisms of immunosenescence and pathways that could serve as targets for interventions to restore immune function.