CHARLOTTESVILLE, Va. (WRIC) — Researchers at the University of Virginia have discovered a molecule linked to the body’s immune response to Alzheimer’s disease and multiple sclerosis, foreshadowing the potential for huge leaps in how neurodegenerative diseases will be treated in the future.

According to a release from the university’s website, UVA Health researchers identified a molecule called a kinase, which is crucial to removing plaque buildup linked to Alzheimer’s and presenting debris buildup that causes multiple sclerosis (MS).

It is believed that many neurodegenerative diseases such as Alzheimer’s and MS are caused by the brain’s inability to cleanse itself of toxic buildup. The identified molecule directs the activity of brain cleaners called microglia, which have recently been determined to play a vital role in brain health.

“Our work has described a critical element of microglial function during Alzheimer’s disease and MS,” said researcher Hannah Ennerfelt, one of the authors of a new scientific paper outlining the findings. “Understanding the underlying biology of these cells during neurodegeneration may allow for scientists and doctors to develop increasingly informed and effective therapeutic interventions.”

The researchers found that a lack of the molecule, which they call SYK, resulted in plaque buildup in the brains of mice, causing memory loss. They were also able to reduce the plaque buildup by activating the molecule and microglia. This suggests a potential treatment approach for humans, something that would require much more research and tests.

A lack of the SYK molecule also led to the buildup of damaged myelin, a protective coating on nerve cells, in mice. When myelin cells cannot transmit messages properly, causing symptoms of MS such as muscle spasms and mobility problems. In a new scientific paper, the researchers described the molecule as being “critically involved” in the removal of myelin debris.

“If boosting SYK activity in microglia can decrease the amount of myelin debris in MS lesions, developing new drugs to target SYK could stop the progression of MS and help to reverse the damage,” said Elizabeth L. Frost, PhD, a critical researcher on the project. “This is an especially promising option given that most of the currently available drugs for MS treatment dampen adaptive immunity. These immunosuppressive drugs lead to susceptibility to infection and higher risk of potentially fatal side effects like progressive multifocal leukoencephalopathy. Additionally, some forms of MS do not have a strong involvement of the immune system, and therefore there are currently very limited treatment options for those patients.”

The researchers’ findings were published in the research journal Cell.