Irene Maeve Rea

Queens University, United Kingdom



Biography

Irene Maeve Rea has completed her Medical degree at Queens
University, Belfast before carrying out research towards her
MD Postgraduate research at Stanford University, School of
Medicine. She is a Consultant Physician in Geriatric Medicine,
an Emeritus Professor at Queens University Belfast, and a Visiting
Professor at the University of Ulster in the Northern Ireland
Centre for Stratified Medicine. Both her clinical and research interests
are in the areas of immunology and genetics specializing
in the ‘Oldest Old’ members of the population in innovative
studies of 90-year-old siblings with support by an EU-funded
European collaboration (Genetics of Healthy Ageing) and the
Wellcome Trust.

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-B cytokine and the IL-1-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.