In August last year, Unity released interim results showing that its drug was probably ineffective in treating study patients suffering from osteoarthritis.
Its stock price plummeted as a consequence, but Dr de Grey remains hopeful that “soon we might have drugs that actively cause these cells to die”.
While Dr de Grey is excited to see much of the life extension research he helped develop come to fruition, some thinkers are raising concerns about the implications of an extended human lifespan.
Mesenchymal stem cells derived from adipose tissue appear to reverse some effects of aging in nearby somatic cells.
A new study published in the FASEB Journal shows how mesenchymal stem cells derived from adipose tissue (ADSCs) reverse some effects of aging in nearby cells.
It’s not the cells themselves, it’s what they secrete
The original and ongoing main purpose of stem cell therapies is to directly combat stem cell exhaustion: to replenish the body’s regenerative capability by introducing fresh stem cells, which divide into somatic cells in order to repair tissues and organs.
To understand how the clones can create millions of copies of themselves and yet remain functional, Oldroyd and his team compared the genomes of Cape honeybee workers with those of their queen and her offspring.
After forcing the Cape queen to reproduce asexually by fitting her with surgical tape that prevented her from mating, the team examined certain DNA sequences of both the Cape queen and the 25 larvae she produced. Then, they did the same for four Cape honeybee workers and their 63 larvae.
The team discovered that the asexually reproduced offspring of the queen had levels of recombination (DNA mixing) 100 times greater than the genetically identical cloned offspring of the workers — a finding that suggests the Cape worker bees have evolved a mutation that prevents recombination. Without the risk of a one-third loss of genetic material caused by the asexual reshuffling process, the workers are free to continually create perfect copies of themselves.
“At first, we had a hard time believing the results. Many of these genes are classical hallmarks of aging and yet our results suggested that their activity is more a function of the presence of bacteria rather than the aging process,” said Dr. Shukla.
Notably, this included genes that control stress and immunity. The researchers tested the impact that the antibiotics had on these genes by starving some flies or infecting others with harmful bacteria and found no clear trend. At some ages, the antibiotics helped flies survive starvation or infection longer than normal whereas at other ages the drugs either had no effect or reduced the chances of survival.
NIH scientists discover that bacteria may drive activity of many hallmark aging genes in flies.
To better understand the role of bacteria in health and disease, National Institutes of Health researchers fed fruit flies antibiotics and monitored the lifetime activity of hundreds of genes that scientists have traditionally thought control aging. To their surprise, the antibiotics not only extended the lives of the flies but also dramatically changed the activity of many of these genes. Their results suggested that only about 30% of the genes traditionally associated with aging set an animal’s internal clock while the rest reflect the body’s response to bacteria.
“For decades scientists have been developing a hit list of common aging genes. These genes are thought to control the aging process throughout the animal kingdom, from worms to mice to humans,” said Edward Giniger, Ph.D., senior investigator, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published in iScience. “We were shocked to find that only about 30% of these genes may be directly involved in the aging process. We hope that these results will help medical researchers better understand the forces that underlie several age-related disorders.”
The results happened by accident. Dr. Giniger’s team studies the genetics of aging in a type of fruit fly called Drosophila. Previously, the team showed how a hyperactive immune system may play a critical role in the neural damage that underlies several aging brain disorders. However, that study did not examine the role that bacteria may have in this process.
These results suggest that IL-12 and IFN-γ could one day be measured along with other biomarkers to predict future brain health in cognitively normal people–a tool that doesn’t yet exist in medicine.
Summary: Higher levels of two cytokines were associated with slower cognitive decline in aging adults, a new study reports.
Source: Mass General
Research has previously linked inflammation to Alzheimer’s disease (AD), yet scientists from Massachusetts General Hospital (MGH) and the Harvard Aging Brain Study (HABS) have made a surprising discovery about that relationship.
In a new study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, they report that elevated levels of two chemical mediators of inflammation, known as cytokines, are associated with slower cognitive decline in aging adults.
An aging/longevity link, (not sure how novel)
As life expectancies around the world increase, so are the number of people who will experience age-related cognitive decline. The amount of oxygen in the blood declines with age. Aging in the brain might be naturally held at bay by adenosine receptor A2B (ADORA2B), a protein on the membrane of red blood cells which is known to help release oxygen from the blood cells so it can be used by the body.
Aging in the brain is naturally reduced by ADORA2B, which helps get oxygen to the brain when needed. Further testing will be needed to determine whether ADORA2B levels naturally decline with age and whether treatment with drugs that activate ADORA2B can reduce cognitive decline in normal mice.