- A Stanford team has determined how to reverse aging in the brain and restore mental acuity, a breakthrough that could one day lead to medications that treat medical conditions and cognitive decline.
- The researchers found a way to block the inflammation responsible for the cognitive decline with age.
- Using drugs adapted to block the link between a specific hormone and a receptor, the researchers restored normal function in immune cells that disappear with age.
- They noted that mice treated with the drug regained memory and spatial orientation skills, and performed just as well as younger animals in similar tests.
The aging process is a risk factor in most medical conditions. The older the body and mind, the harder it is to do most things, including fighting an infection like the new coronavirus. But several research teams are looking at different ways to slow aging, prevent aging or to age some organs. In the latter category are researchers from Stanford, who may have figured out how to reverse aging in the brain.
It seems that the immune system is at least partially to blame for the aging of the brain. The scientists devised a process to prevent mental aging in mice, and the experiments also worked on human cells in laboratory tests. However, these are just the first steps towards creating medicine that could one day be used to prevent medical conditions associated with cognitive decline.
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Dr. Katrin Andreasson’s team published a study in Earth describe their first job of aging the brain. As Stanford Medicine explained, biologists have long believed that inflammation may be responsible for the aging process. If you reduce it, the onset of certain conditions, such as the loss of mental acuity, may be delayed or even the conditions may occur completely. Andreasson’s team may have determined what causes some immune cells to benefit inflammatory processes in the body and how to prevent them.
The team found that a type of immune cell called myeloid cells (such as macrophages) is transmitted as they age, causing inflammation in tissues, including the brain. The myeloid cells are supposed to clear up debris, give nutrients to other cells and to monitor pathogens. But as they get older, they begin to misbehave and this damages the tissues in the environment.
The researchers found that blocking the interaction between a specific hormone (PGE2) and a receptor (EP2) is enough to ‘the youthful metabolism and restful temperament of mouse and human myeloid cells in a dish and in live mice’ to recover. ‘ The experimental medicine was able to reverse the cognitive decline in mice, restoring memory and navigation skills to levels comparable to young mice.
“If you adjust the immune system, you can age the brain,” Andreasson said. Stanford Medicine.
The problem with the PGE2-EP2 link is “a double hit.” Myeloid cells, such as macrophages, produce more PGE2 than younger ones, and they have more EP2 receptors on their surfaces. This leads to increased processes that cause local inflammation. EP2 occurs on immune cells, including myeloid cells, and it can initiate inflammatory activity in the cells after being bound to PGE2.
Andreasson’s team tried two experimental drugs that blocked the PGE2-EP2 link. This caused aged myeloid cells to behave just like younger versions, and reversed their inflammatory activities in laboratory tests with incubated mice and human macrophages. As for the live mice, the older people who received the medicine also performed in recall and spatial navigation tests than younger mice, and an indication that the drugs could age the brain. One of the drugs was effective, although it did not penetrate the blood-brain barrier.
Although this research sounds promising, the team is nowhere near clinical trials for drugs that can delay or reverse conditions such as dementia or Alzheimer’s. Andreasson said neither of the two test drugs could be used on humans, citing possible toxic side effects. But the study could lead to different compounds that could be safe for human testing in the future, and could ultimately help prevent cognitive decline after a certain age.
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