Four Patients Test Retinal Implant That Could Stop Age-Related Blindness

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Some parts of getting older are awesome. Retirement. Early bird specials. Free reign to whine about your various aches and pains.

Not so great? Your vision can start to go.

Luckily, a new retinal implant may soon help treat a common cause of age-related vision loss.

Non-neovascular age-related macular degeneration (NNAMD) (also known as “dry” AMD) causes a blurry area right in the middle of a person’s line of vision that can grow as the disease progresses. Sometimes, the previously blurry spot becomes simply blank.

In short, that can be debilitating, making it pretty impossible to live a normal life. After all, you need to be able to see what’s in front of you to do things like drive a car or cook a meal.

Currently, there’s no treatment for the advanced stages of NNAMD, but a research team led by Amir Kashani, an assistant professor of clinical ophthalmology at University of Southern California (USC), is hoping to change that.

NNAMD likely begins with the breakdown of cells in a membrane in the eye called the retinal pigment epithelium (RPE). Kashani and his team designed an implant to mimic the function of this membrane. The implant fits on the retina and is made of human embryonic stem cells placed on a base material.

The team had already tested a version of the implant on rodents, so the next step was to make the leap to humans. So the researchers placed their implant into the eyes of four people with advanced NNAMD. Then, they monitored those people for between four and 12 months.

According to the researchers’ study, published today in Science Translational Medicine, none of the four participants had any negative or severe side effects from the retinal implant, and experienced no vision loss over the course of the trial. Once participant even “demonstrated an observable improvement” in their vision.

When the team took post-operative images of the patients’ eyes, they saw that the stem cells had blended with the existing retinal tissue. That is, the retinas looked like they were regaining their RPEs. A good sign.

Of course, this was an exceptionally small sample size that delivered promising (but not overwhelmingly positive) results. So the researchers’ next step is to test their implant on a larger group.

If it works the way researchers hope, it may someday be a game-changer for thousands of visually-challenged seniors. After all, what good’s a senior discount on movie tickets if you can’t see the screen.

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A Single Gene Could Have a Huge Impact on Age-Related Mental Decline

The Mental Effects of Aging

As animals get older, the electrophysiology of their hippocampal connections begins to degrade. A new study appears to have identified the family of genes that are responsible, demonstrating how a single gene can have a broad effect on age-related decline.

The key component seems to be a protein called FKBP, which is responsible for calcium release within neurons. In the study, rats were injected with viruses engineered to promote overexpression of FKBP1b, and then observed as they attempted to find an underwater platform in a water maze. They were later euthanized so that the researchers could analyze gene expression in their hippocampi.

The rats who received the treatment were found to perform much better than control animals of the same age. What’s more, the hippocampal expression levels of over 800 other genes had been altered as well as the FKBP1b overexpression. The vast majority of these changes caused levels to resemble younger rats more closely than older rats.

Excessive calcium release had already been linked to age-related decline by an earlier study, where increased FKBP expression was seen to increase cognitive function in older rats. The new findings raise further questions, but there are hopes that it could lead to some new ideas in how we respond the mental changes humans experience in old age.

Brain Power

The next step for the researchers involved with this project is to figure out why FKBP levels decrease as animals get older, and what can be done to prevent this from happening. It’s been suggested that metabolic conditions or changes to other cells might be the culprit.

“Another key question is whether Ca2+ dysregulation is why aging is the leading risk factor for Alzheimer’s disease,” wrote the paper’s lead author J.C. Gant in email correspondence with Futurism. “In most neurodegenerative disorders age is a major risk factor and it may be that changes in neuronal calcium are a trigger for multiple diseases. This we do not know, yet.”

Of course, there’s a need for clinical trials to determine whether FKBP expression could be safely manipulated in humans. Gant is hopeful that such trials could take place sooner rather than later, given that we’re already seeing studies using adeno-associated viral vectors to increase gene expression in specific areas of the brain. A microsyringe would be used to inject the virus into the region where it’s needed (in this case the hippocampus).

“Although clinical trials must be run to determine the viability, the debilitating nature of memory loss in normal aging and extreme cases such as Alzheimer’s makes minimally-invasive measures such as this seem more and more viable with respect to alternative consequences of not treating the disease,” explained Gant.

The findings of this study don’t necessarily mean that we have a solution to the way our brains wane as we get older. However, they do offer up some intriguing possibilities when it comes to figuring out what is actually happening inside our bodies that causes this decline to take place.

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Researchers Have Found a New Way to Delay Age-Related Health Decline

“Cellular Time Machine”

Researchers studying middle-aged fruit flies have improved the insects’ health substantially and slowing their aging significantly. They believe their technique could someday pave the way toward delaying the onset of Alzheimer’s disease, Parkinson’s disease, cancer, cardiovascular disease, stroke, and other age-related diseases in humans.

Their approach targets the cellular power houses, called mitochondria, which control the cell growth and death. Mitochondria frequently sustain damage as part of the aging process, and cells can’t always remove these damaged organelles, which then become toxic as they accumulate in the muscles and the brain and other organs. This buildup contributes to a broad variety of age-related diseases.

In this study, published in Nature Communications, the researchers found that the mitochondria in fruit flies changed shape, elongating as the insects hit middle age. The team broke damaged mitochondria up and removed them, which caused the flies to be more energetic and live 12 to 20 percent longer.

Image Credit: Nature Communications/Anil Rana
Fruit flies’ mitochondria (in green) at 10 days (top left), 28 days (top right) and 37 days old (both bottom images). At bottom right, the mitochondria have returned to a more youthful state after UCLA biologists increased the fly’s level of a protein called Drp1. Image Credit: Nature Communications/Anil Rana

“We think the fact that the mitochondria become larger and elongated impairs the cell’s ability to clear the damaged mitochondria,” UCLA professor of integrative biology and physiology and senior author David Walker said in a press release. “And our research suggests dysfunctional mitochondria accumulate with age, rather than being discarded.”

Life Extension

Perhaps even more excitingly, the scientists discovered key cellular components of the process of mitochondrion elongation and removal. When they increased the levels of a protein called Drp1, this broke down the mitochondria, allowing them to be removed through a process controlled by the Atg1 gene. The scientists also switched off a protein called Mfn so the mitochondria were unable to fuse together into larger pieces, which also improving the health and extending the lives of the flies.

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“You can either break up the mitochondria with Drp1 or prevent them from fusing by inactivating Mfn,” UCLA project scientist and lead author Anil Rana said in the press release. “Both have the same effect: making the mitochondria smaller and extending lifespan.”

The results of the study were stunning. “It’s like we took middle-aged muscle tissue and rejuvenated it to youthful muscle,” Walker said during the interview. “We actually delayed age-related health decline. And seven days of intervention was sufficient to prolong their lives and enhance their health.”

These newly discovered cellular mechanisms could potentially be targeted in humans with future anti-aging drugs. The fact that this approach was effective within a short time is particularly significant because long-term use of almost any drug can be harmful. This research joins a host of other studies seeking to extend the human lifespan, which some researchers believe may ultimately be limitless.

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