Why vision deteriorates with age and memory deteriorates: scientists have found the sources of problems

Vision problems in old age are caused by abnormalities in blood proteins

Studies by scientists were able to establish that vision problems in the elderly in 90% of people are caused by an impaired blood protein, vitronectin. Another study on mice also allowed scientists to discover an enzyme whose accumulation causes elderly people to lose the ability to remember the faces of people with whom they have interacted.

The first study was conducted by biologists from the Sanford Burnham Prebys Research Institute. Scientists led by Professor Francesca Marassi were able to uncover the molecular secrets of macular degeneration (a chronic disease of the retina at the back of the eye, which is responsible for central vision - ed.), which causes almost 90% of all age-related vision loss.

The researchers focused on vitronectin, one of the most abundant proteins. In addition to the fact that it circulates in the blood in high concentrations, this protein is found in the skeletons between cells and is also an important component of cholesterol.

Vitronectin plays a key role in many age-related diseases, but for Marassi's team, the most promising target is macular degeneration, which affects 11 million people in the United States.

"This protein is an important target for macular degeneration because it accumulates in the back of the eye, causing vision loss. Similar deposits appear in the brain in Alzheimer's disease and in the arteries in atherosclerosis," Marassi said.

She noted that the main goal of the research is "to understand why this happens and to use that knowledge to develop new treatments."

By performing biochemical analysis, the researchers found that the protein can change its shape slightly under pressure. These changes make it more easily combine with calcium ions in the blood, which, according to the researchers, leads to the formation of calcified plaques characteristic of macular degeneration and other age-related diseases.

The knowledge gained will help scientists develop antibodies that aim to selectively block calcium binding by a protein without disrupting its other important functions in the body.

"It will take some time to turn this into a clinical treatment, but we hope to have a working antibody as a potential treatment in a few years," Marassi said.

In a second study, researchers at the University of Maryland School of Medicine came close to unraveling the cause of one of the most frustrating aspects of age-related memory impairment: the inability to match the name and face of a person with whom there was a dialogue just hours ago.

Researchers still don't understand why this dysfunction occurs, but they have some important new clues.

During a study conducted on aging mice, researchers identified a new mechanism in neurons that causes memories associated with social interactions to deteriorate with age. In addition, they were able to reverse this memory loss under laboratory conditions.

It is reported that the scientists have discovered a specific target in the brain that could be used in the future to develop therapies that could prevent or reverse memory loss caused by typical aging.

It is worth noting that memory problems with aging are different from those caused by diseases such as Alzheimer's or dementia: an elderly person is able to remember faces and names of people with whom he has interacted for several hours, but he will have difficulty matching the person's face to the name.

An enzyme known as PDE11A is responsible for the proper functioning of the corresponding memory regions. Scientists have found that in both humans and mice, levels of this enzyme increase with age. In particular, it accumulates in the hippocampus, which is responsible for many types of learning and memory. However, the enzyme was not just where it was supposed to be, but accumulated as small strands in compartments of neurons.

As part of the study, scientists monitored whether older mice would taste food they had never eaten, but whose smell they could pick up while "socializing" with other mice. This behavior is the social norm among mice. It turned out that aging mice are unable to relate these two facts and refuse to eat.

After scientists genetically removed the PDE11A enzyme in the aging mice, they began to eat unfamiliar food, which was smelled in the other mouse's breath. Reactivating the enzyme again prevented the mice from eating.

However, scientists cannot simply turn off PDE11 in humans because it is not only involved in memory, but also in preferences about who you prefer to be around. The researchers explained that such an action would ensure that an older person would remember his friends and family, but he might lose attachment to them.

"Thus, our goal is to find a way to target the bad form of PDE11A so as not to interfere with normal, healthy enzyme function."

As OBOZREVATEL reported, earlier Israeli scientists discovered antibodies that can neutralize any type of COVID-19. The effectiveness of such treatment reaches 95%.

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