"It was surprisingly simple. University of California, Berkeley, scientists inserted a gene for a green-light receptor into the eyes of blind mice and, a month later, they were navigating around obstacles as easily as mice with no vision problems. They were able to see motion, brightness changes over a thousandfold range and fine detail on an iPad sufficient to distinguish letters."
"The researchers say that, within as little as three years, the gene therapy—delivered via an inactivated virus—could be tried in humans who've lost sight because of retinal degeneration, ideally giving them enough vision to move around and potentially restoring their ability to read or watch video."
"You would inject this virus into a person's eye and, a couple months later, they'd be seeing something," said Ehud Isacoff, a UC Berkeley professor of molecular and cell biology and director of the Helen Wills Neuroscience Institute. "With neurodegenerative diseases of the retina, often all people try to do is halt or slow further degeneration. But something that restores an image in a few months—it is an amazing thing to think about."
About 170 million people worldwide live with age-related macular degeneration, which strikes one in 10 people over the age of 55, while 1.7 million people worldwide have the most common form of inherited blindness, retinitis pigmentosa, which typically leaves people blind by the age of 40.
For most people, Juan Ponce de León, comes to the mind for
searching Florida for the Fountain of Youth. He never found it. Perhaps
because, most historians believe that he never went looking for it. The Fountain
of Youth search is a myth, they say. Still, he is credited with exploring the interior of
Florida and mapping the Florida coast.
Well, a few centuries later researchers at the University of
Buffalo weren’t looking for the source of that magic youth elixir either. But
they may have found it or at least its best bud… a gene called CD36.
"Scientists seeking to unlock the secrets of
cellular aging have identified a gene that triggers senescence, a phenomenon in
which cells stop dividing."
"Senescence is a natural occurrence in the life of a cell,
and researchers have sought to learn about it for a couple of reasons. First,
it’s connected to old age: Senescent cells are thought to contribute to heart
disease, arthritis, cataracts and a bevy of other age-linked conditions.
Second, a lack of senescence is a hallmark of cancer cells, which bypass this
process to replicate in an uncontrolled manner."
"The new study — published online on June 20 in Molecular
Omics, a journal of the Royal Society of Chemistry — illuminates genes involved
in cellular senescence, and highlights one in particular that seems tightly
associated with this crucial biological process."
"In experiments, University at Buffalo researchers discovered
that a gene called CD36 is unusually active in older, senescent cells."
“What we found was very surprising,” says Ekin
Atilla-Gokcumen, PhD, an assistant professor of chemistry in the UB College of
Arts and Sciences. “Senescence is a very complex process, and we didn’t expect
that altering expression of one gene could spark it, or cause the same effect
in surrounding cells.”
When I was a boy, my uncle owned some horses. I enjoyed visiting him and riding the horses.
One of my fondest memories is when my cousin and I rode horses to the local swimming pool, tied them to a fence and went in for a swim.
Once I went with my uncle to visit a farrier and bring him back to shoe my uncles’ horses. The farrier was an older Amish man and I remember listening to him talk about horses and taking care of them.
Often, I’d see a horse and buggy tied up waiting for its owner to come back from his trip into the local Lawson’s store, not far from our home on the southeast side of Akron, Ohio.
Thinking back on it, I’m not sure if they were Amish or Mennonite. But, for me, it didn’t matter. I just liked seeing the beautiful horse and buggy.
There’s a point to all this rememberin’, of course.
Scientists at Northwestern University in Chicago have discovered a genetic mutation among an Amish population in Indiana which appears to prolong human life and protect against biological ageing. Their discovery is raising hopes for new treatments to prevent age-related disorders.
I know that has nothing to do with horses, buggies and Lawson's. I just wanted to tell my story.
The discovery of a rare genetic mutation that prolongs human life has raised hopes for new treatments to combat ageing and prevent age-related disorders from heart disease to dementia.
Researchers spotted the mutation in an Amish population in Indiana where carriers were found to have better metabolic health, far less diabetes, and tended to live a decade longer than others in the community.
Scientists studied 177 members of the Old Order Amish in the town of Berne and identified 43 people who had inherited one normal and one mutated version of a gene called Serpine1. Those with the mutated version of the gene typically lived to 85 years old, a full 10 years longer than those who did not carry the mutated form.
“This is a rare genetic mutation that appears to protect against biological ageing in humans,” said Douglas Vaughan, a professor of medicine who led the research at Northwestern University in Chicago.
The Serpine1 gene provides the body with instructions to make a protein called PAI-1 which serves as a brake on a process that destroys any clots that may build up in blood vessels. But the protein also has a hand in a process called senescence, where cells go into a state of suspended animation and steadily build up in the body’s tissues. Senescence is increasingly thought to be a strong driver of the ageing process.
Studies in animals have shown that reducing levels of PAI-1 can protect them against ageing and age-related diseases and even prolong life, but until now, the same effect had not been seen in humans. The Amish group in Indiana are the only known community to carry the mutation that naturally suppresses levels of PAI-1 in the blood.
Writing in the journal Science Advances, the researchers describe how those with the single mutated gene had 50% lower levels of PAI-1 in their blood. The scientists went on to look at biological markers for ageing, known as telomeres, in the individuals. Telomeres are tiny caps that tip the ends of chromosomes and which get shorter with age. Carriers of the mutation had longer telomeres than others, suggesting they had aged more slowly, the scientists report.
Tests found a range of health benefits in those who carried the mutation, including better metabolic health, lower levels of diabetes, and a longer lifespan. More…
Flashback Memory... (when I was just an impressionable kid.) Gene Autry - Back in the Saddle Again (from Back in the Saddle 1941)
