Microglia and the new hope for Alzheimer’s disease research
Researchers are looking at how microglia behave differently in the brains of people with Alzheimer’s disease and with that knowledge develop new treatments.
As many as 6.7 million Americans were living with Alzheimer’s disease in 2023 according to the Center for Disease Control and Prevention. The number of people in the US suffering from this debilitating ailment of the brain is predicted to rise to 14 million by 2060.
Scientists have made incredible stridesover the years in understanding the effects of Alzheimer’s on the brain. The Food and Drug Administration recently approved the first drug for early onset of the disease, Leqembi, which can moderately slow cognitive decline. However, two new studies looking at Microglia show promise for even more and potentially more effective treatments to combat this devastating neurodegenerative disease.
Microglia and the new hope for Alzheimer’s disease research
Microglia are immune cells in the central nervous system and are the first responders and main defenders in the struggle to keep our brains healthy. They remove damaged or unnecessary neurons, prune synapses during development and fight off infections so that our grey cells continue to function normal.
They also clear away damaging plaques formed by sticky amyloid proteins, that are thought to be cause of Alzheimer’s when there are abnormal build-ups of them in the brain. New immunotherapies that can help the body utilize microglia or make sure they are functioning correctly could be a more effective way to fight Alzheimer’s and other neurodegenerative conditions.
Microglia appears not to function correctly in brains with Alzheimer’s disease
Research headed up by neuroscientists Katherine Prater and Kevin Green at the University of Washington using brain autopsies compared those of individuals with Alzheimer’s to those of a healthy control group. Science Alert reports that the investigators found microglia were in a pre-inflammatory state more frequently in the brains of people with Alzheimer’s disease.
This made them less likely to be protective and more likely to produce inflammatory molecules potentially damaging brain cells. It’s not clear what role they play in the devastating neurodegenerative disease but by contributing to the death of brain cells, improperly functioning microglia may help with the progression of Alzheimer’s.
Another study supported in part by National Institutes of Health and reported in Science Translational Medicine looked at how a protein called apolipoprotein E (APOE) interacts with microglia. APOE is a key component of amyloid plaques but can also inactivate microglia by binding to a LILRB4 receptor found on the immune cells’ surfaces.
Their findings, which looked at brain tissue of people who died with Alzheimer’s and then carried out research on mice with a potential treatment, were promising. The results suggest that by using an antibody they were able to block the interaction between APOE proteins and LILRB4 receptors. This allowed the microglia to go about their work removing amyloid plaques.