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Study suggests scientists may need to rethink which genes control aging

“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.

Scientists may need to rethink which genes control aging

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 . These genes are thought to control the aging process throughout the , 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.

Inflammatory Proteins May Slow Cognitive Decline in Aging Adults

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.

Anti-aging Protein in Blood Cells Helps Slow Cognitive Decline

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.

Scientists Develop New Gene Therapy Strategy to Delay Aging and Extend Lifespan

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Cellular senescence, a state of permanent growth arrest, has emerged as a hallmark and fundamental driver of organismal aging. It is regulated by both genetic and epigenetic factors. Despite a few previously reported aging-associated genes, the identity and roles of additional genes involved in the regulation of human cellular aging remain to be elucidated. Yet, there is a lack of systematic investigation on the intervention of these genes to treat aging and aging-related diseases.

How many aging-promoting genes are there in the human genome? What are the molecular mechanisms by which these genes regulate aging? Can gene therapy alleviate individual aging? Recently, researchers from the Chinese Academy of Sciences have shed new light on the regulation of aging.

Recently, researchers from the Institute of Zoology of the Chinese Academy of Sciences (CAS), Peking University, and Beijing Institute of Genomics of CAS have collaborated to identify new human senescence-promoting genes by using a genome-wide CRISPR/Cas9 screening system and provide a new therapeutic approach for treating aging and aging-related pathologies.

Asymmetrex Publishes the First Report of Immortal DNA Strands in Human Stem Cells

BOSTON (PRWEB) November 18, 2020

What does it mean for multiplying cells in the body to be immortal? The cell DNA is being replicated over and over again while being divided equally between new cells produced by cell divisions. All the new cell components produced by the DNA code are mixing with the old cell components and being divided between the new cells. So, every cell is a new cell. There is nothing really immortal about any of them. Right?

Not quite. Stem cells responsible for renewing other mature body cells are different. For a long time, tissue cell scientists had a somewhat nebulous idea that stem cells had a special longevity in organs and tissues – that they were immortal cells, lasting for as long as the human lifespan. However, no one had a molecular concept for this idea of stem cell immortality until John Cairns, a pioneer of DNA replication, started thinking about DNA mutations and cancer in the 1970’s.

NASA inches closer to printing artificial organs in space

In America, at least 17 people a day die waiting for an organ transplant. But instead of waiting for a donor to die, what if we could someday grow our own organs?

Last week, six years after NASA announced its Vascular Tissue Challenge, a competition designed to accelerate research that could someday lead to artificial organs, the agency named two winning teams. The challenge required teams to create thick, vascularized human organ tissue that could survive for 30 days.

The two teams, named Winston and WFIRM, both from the Wake Forest Institute for Regenerative Medicine, used different 3D-printing techniques to create lab-grown liver tissue that would satisfy all of NASA’s requirements and maintain their function.

“We did take two different approaches because when you look at tissues and vascularity, you look at the body doing two main things,” says Anthony Atala, team leader for WFIRM and director of the institute.

The two approaches differ in the way vascularization—how blood vessels form inside the body—is achieved. One used tubular structures and the other spongy tissue structures to help deliver cell nutrients and remove waste. According to Atala, the challenge represented a hallmark for bioengineering because the liver, the largest internal organ in the body, is one of the most complex tissues to replicate due to the high number of functions it performs.


Researchers used 3D-printing to create human liver tissue that could soon be tested on the International Space Station.

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