Researchers at the Massachusetts Institute of Technology’s Picower Institute for Learning and Memory have identified a potential piece of the Alzheimer’s puzzle. They suggest that a mutation can disturb microglia, the brain’s immune-support cells, contributing to the disease. The study’s findings were shared through Wiley Online Library.
The human nervous system relies on two major cell families: neurons and glial cells. Microglia belong to the glial family and reside in the brain and spinal cord. These cells play a defensive role, shaping a microenvironment that helps neurons survive and function properly. In this research, microglia are described as key players in the brain’s response to harmful factors and infections, managing inflammation and coordinating immune activity.
The study centers on the TREM2 gene, focusing on the R47H/+ mutation in the TREM2 protein. This mutation is linked to neuronal damage that may arise when microglial inflammation is altered. Microglia are considered vital to initiating and regulating inflammatory responses in neural tissue when confronted with disease or injury.
Researchers proposed that inflammation in microglia could reduce their capacity to clear amyloid beta protein from the brain. The accumulation of this protein inside affected neurons is widely viewed as a central factor in the development of Alzheimer’s disease.
These findings hold promise for guiding the development of new therapies and drugs aimed at neurodegenerative conditions. They suggest that modulating microglial function and inflammatory pathways might help slow or alter disease progression.
Earlier work by scientists identified a protein linked to improvements in memory and learning, hinting at broader strategies for cognitive health. This new line of inquiry builds on that foundation by exploring how microglial biology interacts with genetic risk factors to shape brain aging and disease risk.