Do these special plaques protect against Alzheimer’s disease? – Practice healing

What role do plaques really play in Alzheimer’s disease?

Some of the alleged plaques in the brain seem to help immune cells protect against Alzheimer’s disease. Since plaque accumulation is typical of Alzheimer’s disease, it was previously assumed to have a destructive effect, which led to the development of Alzheimer’s disease. However, according to a recent study, some plaques seem to have a more positive effect.

Brain immune cells (microglia) form their own plaques that can help protect against Alzheimer’s disease, according to a study by researchers from the Salk Institute for Biological Studies. The study was published in the Journal of the English Language.Nature’s immunityPublished.

How does Alzheimer’s disease happen?

Alzheimer It is a neurological disorder that causes memory loss, impaired thinking, and behavioral changes, with these effects worsening with age. This disease appears to be caused by abnormal proteins that assemble between brain cells and form distinct plaques that can damage surrounding cells.

Alzheimer’s disease treatment options?

The accumulation of beta-amyloid plaques in the brain is a typical feature of Alzheimer’s disease. The researchers explain that most treatments developed to treat the disease target these plaques, even if these treatment attempts have largely failed in clinical studies.

Differences between panels?

There are many forms of plaque, but the two most common types are referred to as either diffuse or dense. Diffuse plaques are loosely structured amorphous clouds. On the other hand, panels with a dense core have a compact center. Previously, both types of plaques were thought to form spontaneously from the overproduction of a precursor molecule called amyloid precursor protein (APP), the team explains.

The conventional view is that microglia inhibit the growth of plaques by ingesting them with the help of a gas molecule 6. However, as a result of the new research, it is now clear that microglia promote the formation of dense core plaques (dense core plaques). These dense plaques remove thread-like plaque material from nerve cells, where they usually cause cell death.

What causes dense essential plaques?

According to the new study, it is the microglia that form plaques with a dense core of circulating beta-amyloid fibers as part of their cellular cleansing. The finding is based on research from 2016 that found that when a brain cell dies, a fat molecule moves from inside the cell to outside it. In this way, the cell indicates that it is dying and can be consumed.

The dead microglia then consumes the dead cell via surface proteins called TAM receptors with the help of a special intermediate molecule (gas 6). Experts explained that without TAM and gas 6 receptors, microglia cannot attach to and consume dead cells.

The results of the current research show that not only do dead cells show gas and a willingness to signal for consumption, but the same is true of amyloid plaques as well. In studies in mice, the team was able to demonstrate experimentally for the first time that microglia with TAM receptors consume amyloid plaques. The team demonstrates that in mice lacking TAM receptors, the microglia were unable to perform this function.

Diffuse plaques are transformed

In the course of further investigation, the researchers found that the microglia, after ingesting a diffuse plaque, eventually transformed the synaptic beta-amyloid into a highly compact mass. Researchers believe that this is a useful mechanism that turns spreading plaques into plaques with a dense core and removes debris from the intercellular environment. Experts say that dense essential plaque appears to be associated with less harmful effects.

Although it is not yet possible to determine which types of plaque are more harmful in one way or another, new research findings indicate that dense core plaques are milder, study author Youtong Huang of the Salk Institute for Biological Studies explains in one Press release.

Rethinking Alzheimer’s treatment

Study author Professor Greg Lemke of the Salk Institute suggests that the search for a cure for Alzheimer’s disease should stop focusing on breaking down thick plaques and instead develop treatments that either stop the production of beta-amyloid that reduce or facilitate the transfer of beta-amyloid from the body. brain.

“We show that dense primary plaques do not form spontaneously. We think they are made by microglia as a defense mechanism, so it is best to leave them alone,” adds the professor. Previous treatment approaches may be counterproductive here. (Such as)