A blood-based discovery as to why humans tend to become frailer after 70 is opening doors to new therapies to manage the decline and disease associated with growing old. Researchers from the Sanger Institute in Cambridge discovered that our blood undergoes a drastic change in older age, which increases our risk of developing diseases and hampers our immune function.
Blood cells and haematopoietic cells – which are young blood cells with the potential to become red or white blood cells or platelets – were taken from 10 humans aged zero to 80+ and analyzed in the study published in Nature. Using these, the researchers were able to sequence the genomes of the 10 people and look for differences in their blood.
It revealed that these stem cells took on an average of 17 mutations per year after birth, as well as losing around 30 base pairs a year from their telomeres. Telomere shortening like this can be influenced by a person’s lifestyle and is associated with aging and the onset of age-related disease.
The genome sequencing also revealed that for adults aged 65 and under, blood is made up of a diverse community of stem cells (in the region of 20,000 to 200,000) who churn out red, white, and platelet cells. However, for people aged 65 and over, there were fewer than 100 different types of stem cell doing the same job.
This lacking diversity is the result of mutated stem cells self-proliferating, something that can happen throughout life but by the age of 70 they have effectively taken over. This means that a person’s blood is being crafted by a small population of faulty stem cells, so not only is it of poorer quality but it also puts older people at higher risk of sickness and slow recovery as well as blood cancers and disorders.
However, it’s not all bad news as establishing a firmer understanding of why this drop off in health occurs at 70 could one day enable us to formulate effective therapies to counter the effect of these selfish, mutant stem cells. Furthermore, it could lead to better support for people undergoing chemotherapy, which appears to have an effect on the body that mirrors aging.
“We predict that these factors also bring forward the decline in blood stem cell diversity associated with ageing,” said joint senior author Dr Elisa Laurenti from the Wellcome-MRC Cambridge Stem Cell Institute to The Guardian.
“It is possible that there are factors that might slow this process down, too. We now have the exciting task of figuring out how these newly discovered mutations affect blood function in the elderly, so we can learn how to minimise disease risk and promote healthy ageing.”