Microglia immune cells in the brain can slow down Alzheimer’s progression, according to research from Lund University.
Microglia cells can be found in the central nervous system. They are known as “big eaters” and are known to kill viruses, damaged cells and infectious agents responsible for Alzheimer’s progression. It has been established that microglial cells can be activated in several ways via a range of neurological diseases such as Alzheimer’s and Parkinson’s diseases.
Depending on their activation, these cells can drive and slow disease development. Researchers from Lund University and Karolinska Institutet have worked together to show how certain types of activation of the microglial cells can trigger protective inflammatory mechanisms in the immune system.
The study has been published in the journal Nature Aging.
Inflammation can halt Alzheimer’s progression
“Most people probably think that inflammation in the brain is something bad and that you should inhibit the inflammatory system in case of illness. But inflammation does not just have to be negative,” said Joana B Pereira, a researcher at Lund University and Karolinska Institutet, and the study’s first author.
TREM2 is a protein that sits on the surface of microglial cells. The risk of developing Alzheimer’s increases when unusual mutations occur in this protein. However, when the protein is activated, it can become protective.
TREM 2 receptors are seemingly able to sense residual products of disintegrating cells in the brain which triggers the protein. The researchers found less of the thread-like structures formed by the protein in the brain cells once TREM2 was activated.
“This in turn means that the development of the disease is slower and the deterioration of the patient’s cognitive abilities is slowed down,” said Oskar Hansson, professor of neurology at Lund University and senior physician at Skåne University Hospital.
Creating treatments to activate microglial cells
It has been previously observed in a series of animal models that microglial cells can “eat” tau proteins, essentially cleaning up any abnormal occurrences in the brain and inhibiting Alzheimer’s progression.
The researchers believe this could be the same effects could be present in humans, as observed in their study. The researchers also feel their findings are particularly interesting as several pharmaceutical companies are now developing antibodies that can activate TREM2. It is hoped the new research will be used to create new treatment methods to slow Alzheimer’s progression.
“In addition to trying to find therapies to reduce the proteins beta-amyloid and tau, I see this as a third treatment principle. Perhaps in the future patients can receive a cocktail of drugs that, in addition to reducing beta-amyloid, also boost TREM2 antibodies and thus slow down the course of the disease,” concluded Oskar Hansson.