Biological and Chronological Ageing Population

Biological and Chronological Ageing Population

International research collaboration between the Buck Institute, Stanford 1000 Immunome Project, HLPO.Life and KCL looking at:

Age-dependent and Independent Symptoms and Comorbidities Predictive of COVID-19 Hospitalization

We use advanced bioinformatics techniques to identify features that predict disease severity and can be utilised to inform severe cases of COVID-19 even in younger individuals who may not be labelled as high risk. Continued rise in the number of cases, as societies struggle to balance reopening the economy and ‘flattening the curve’, places an enormous burden on healthcare systems around the world. Knowing the signs of possible severe cases like the ones derived in this study could help healthcare systems devote resources to intervening in potentially severe cases before they become costly to manage. The fact that, in our preliminary analysis, age-associated variables outperform age in the prediction of patient hospitalization indicates that biological age or immunological age could be appropriate measures in assessing an individual’s prognosis.

Download the preprint here (.pdf)

This work uses data provided by participants of the COVID-19 Symptoms Study, developed by ZOE Global Limited with scientific and clinical input from King’s College London. We would also like to acknowledge all data providers who made anonymised data available for research. We wish to acknowledge the input of ZOE Global Limited and King’s College London in their development and sharing of the data, and their input into the understanding and contextualisation of data for COVID-19 research.

SARS-Cov2 and the Aging Immune System 

In this work, we focus on the role of the aging immune system on its ability to respond to SARS-Cov2. As we age, our immune system undergoes age-related immune decline in a process termed immunosenescence. Immunosenescence is characterised by an increase in senescent anti-apoptotic cells and accumulation of senescent-associated secretory phenotype (SASP). New science of ageing suggests that these processes enable a more sustained low grade chronic sterile inflammation that increases the chances of cardiometabolic disease and over time leads to deranged lipid profiles, pro-coagulant state and dysglycemia that is often followed by the development of cardiovascular disease, type 2 diabetes, dementia and certain cancers – disease that become more common with increasing age. Moreover, it may make the immune system of the biologically older patients more likely to form dysregulated reactions and less likely to mount an effective immune response and produce antibodies to vaccines, including potentially the future Covid-19 vaccine. We hope this work could inform scientists around to world to develop interventions that target immunosenescence as immune system boosters might be required together with the vaccine to protect the elderly from the infection.



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