- A Stanford team has figured out how to reverse brain aging and restore mental acuity, a breakthrough that could one day lead to medications that treat medical conditions and cognitive impairment.
- Researchers found a way to block inflammation responsible for age-related cognitive impairment.
- Using drugs adapted to block the link between a specific hormone and a receptor, the researchers restored the normal function of immune cells that collapse with age.
- They observed that mice treated with the drug regained memory and spatial orientation skills, performing as well as younger animals in similar tests.
The aging process is a risk factor in most medical conditions. The bigger the body and mind, the harder it is to do most things, including fighting an infection like the new coronavirus. But several teams of researchers are studying various ways to slow the aging, reverse aging or age reduction of some organs. In the latter category are Stanford researchers, who may have figured out how to reverse brain aging.
It turns out that the immune system is to blame at least in part for the aging of the brain. Scientists discovered a process to reverse mental aging in mice, and the experiments also worked on human cells in laboratory tests. However, these are just the first steps toward creating medications that could one day be used to prevent medical conditions associated with cognitive impairment.
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The team of Dra. Katrin Andreasson published a study in Nature describing his initial work for brain aging. How Stanford Medicine he explains, long ago biologists theorized that inflammation could be responsible for the aging process. Reducing it can slow down the onset of certain conditions, such as loss of mental acuity, or even prevent them completely. Andreasson’s team may have discovered what causes some immune cells to promote inflammatory processes inside the body and how to prevent them.
The team found that a type of immune cell called myeloid cells (such as macrophages) is exceeded as they age and causes inflammation inside tissues, including the brain. Myeloid cells are supposed to clean up debris, provide nutrients to other cells, and control for pathogens. But as they get older, they start to misbehave and this damages the nearby tissue.
The researchers found that blocking the interaction of a specific hormone (PGE2) and a receptor (EP2) is enough to “restore the juvenile metabolism and placid temperament of human and mouse myeloid cells in a dish and in live mice “. Experimental drugs were able to reverse cognitive decline in mice, restoring memory and navigation skills to levels comparable to young mice.
“If you adjust your immune system, you can shrink your brain,” Andreasson said Stanford Medicine.
The problem with the PGE2-EP2 link is “a double”. Myeloid cells, like macrophages, produce more PGE2 than younger ones and have more EP2 receptors on the surface. This leads to an increase in the processes that lead to local inflammation. EP2 is found in immune cells, including myeloid cells, and can initiate inflammatory activity inside cells after binding to PGE2.
Andreasson’s team tested two experimental drugs that blocked the PGE2-EP2 link. This caused the aged myeloid cells to behave in the same way as the younger versions, reversing their inflammatory activities in laboratory tests with incubated mice and human macrophages. As for live mice, older subjects who received the drugs also performed in recovery and space navigation tests such as younger mice, indicating that the drugs may slow the brain. One of the drugs was effective even though it did not penetrate the blood-brain barrier.
While this research looks promising, the team is by no means clinical trials of drugs that can slow or reverse conditions such as dementia or Alzheimer’s. Andreasson said neither test drug could be used in humans, citing possible toxic side effects. But the study could lead to different compounds that could be safe for testing in humans in the future and may eventually help prevent cognitive impairment after a certain age.
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Chris Smith began writing about gadgets as a hobby, and before he knew it, he was sharing his views on technology issues with readers around the world. Whenever he doesn’t write about gadgets, he can’t get away from them, even though he tries desperately. But that’s not necessarily a bad thing.