As modern medicine and health care help us live longer and longer, the number of older adults is on the rise worldwide. Unfortunately, one of the ailments often encountered at an advanced age is memory loss. Solving or even mitigating this problem would seriously improve the quality of life of many.

Luckily there is some good news in this particular field as UK-based researchers have effectively restored age-related memory loss in mice, paving the way for the development of therapies to counteract memory problems.

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Neuroplasticity concerns the brain's ability to learn and adapt, as well as its capacity to form memories. PNNs (Perineuronal nets) have recently been discovered to play a role in neuroplasticity.

PNNs are cartilage-like structures in the brain that mostly surround inhibitory neurons. Their primary role is to regulate the brain's plasticity. They first occur in humans at the age of five, and they cut off the time of increased plasticity when the brain's connections are optimized. After that, plasticity gets partially disabled, resulting in a more efficient but less plastic brain.

Chondroitin sulfates are chemicals found in PNNs. Some of them, like chondroitin 4-sulfate, block the function of the networks, preventing neuroplasticity; others, like chondroitin 6-sulfate, encourage it.

When we get older, the mixture of the above-mentioned chemicals shifts. As chondroitin 6-sulfate levels drop over time, our capacity to learn and build new memories deteriorates, leading to what is commonly called age-related memory loss.

Now, UK scientists looked into whether changing the chondroitin sulfate content of PNNs may help repair neuroplasticity and reduce age-related memory loss.

To accomplish this, the team looked at 20-month-old mice, which are considered quite old. A series of tests showed that these had memory impairments when compared to six-month-old mice.

In one experiment, for example, the researchers examined if mice could recognize an object. A mouse was placed at the beginning of a Y-shaped maze and given two identical items at the ends of the two arms to investigate. After a brief time, the mouse was placed back in the maze, but this time one arm held a new object, while the other held a duplicate of the previously used object. - The researchers then timed how long the mouse spent investigating each object to determine if it remembered what it had seen in the prior exercise. The elder mice had a considerably lower chance of remembering the item.

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The researchers used a 'viral vector,' a virus capable of restoring the quantity of 6-sulfate chondroitin sulfates to the PNNs, to treat the aging mice, and discovered that this completely restored memory in the older mice to a level comparable to that seen in the younger critters.

According to Dr. Jessica Kwok, one of the researchers, she and her team observed impressive results when treating the older mice. The memory and capacity to learn were restored to levels they would not have seen since they were of young age.

University of Cambridge Professor James Fawcett, lead researcher, stated in a press release that although their study focused only on mice, the same mechanism should operate in humans - the molecules and structures in the human brain are identical to those in rodents. This implies that it may be possible to prevent humans from developing memory loss in old age.

The researchers are now investigating if compounds can also mitigate memory loss in animal models of Alzheimer's disease. The approach taken by Professor Fawcett's team (using viral vectors to deliver the treatment) is starting to be used more often to treat human neurological conditions. A second team of scientists at the Centre for Brain Repair at the University of Cambridge recently published research showing their use for repairing damage caused by glaucoma and dementia.

The researchers published their findings in the science journal Molecular Psychiatry listed below.

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