Irene Maeve Rea
Queens University, United Kingdom
Biography
Abstract
The question why some people age well and reach ninety years of age in apparent good health while others develop a plethora of age-related disease, remains a perplexing question. But there are some recent signposts and insights into the understanding of the role of inflammation in both healthy aging and age-related diseases. The inflammatory response must be tightly controlled to ensure effective immune protection thorough out life otherwise uncontrolled inflammation can become damaging and destructive. Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, where lose of the fine-control of systemic inflammation seems to be associated with both good quality ageing and age-related disease. The reshaping of the cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called inflammaging and it seems to be associated with most major age-related diseases such as atherosclerosis, diabetes, rheumatoid arthritis and ageing itself. Several common molecular pathways have been associated with low-grade inflammation, and activation of the NF-ï«B cytokine and the IL-1ï¢-mediated inflammatory cascade. The age-related change in redox balance, the increase in age-related senescent cells and senescence-associated secretory phenotype (SASP), and the decline in effective autophagy can trigger the inflammasome, which is central to the inflammatory cascade. Here we will discuss some aspects of the present understanding of the molecular mechanisms that trigger inflammation and related it to findings in various age-related diseases and from long-lived nonagenarian cohorts who exemplify good quality ageing.