Our neurons communicate with each other via junctions called synapses. In neurodegenerative diseases like Alzheimer’s, the number of synapses in the brain decreases dramatically, contributing to cognitive decline. It’s believed that the mechanism for synapse loss involves brain cells called microglia, which engulf and destroy the synapse in a process known as phagocytosis.
A paper published earlier this year in the journal Glia announced the discovery of a new type of microglia in mice called dark microglia. These cells’ unusually dark color comes from oxidative stress that leads to condensing of fluids in the cell. They are relatively uncommon under normal conditions but become more prevalent in mice that are old, exposed to chronic stress, genetically predisposed to Alzheimer’s disease, or deficient in a microglia signaling molecule called fractalkine. Dark microglia are more phagocytically active than their normal counterparts, often devouring entire synapses whole. The authors suggested that these cells might be a future therapeutic target in Alzheimer’s disease.
Dr. Marie-Eve Tremblay, who led the team that discovered dark microglia, presented an update on her research at the recent Translational Neuroimmunology conference in Big Sky, Montana. She announced that they had identified dark microglia in human brains for the first time. Tremblay’s team examined the postmortem brain of a 45-year-old person who’d had early-onset Alzheimer’s disease. They found that there were around twice as many dark microglia compared to a healthy brain from a person of the same age.
It’s not clear yet what causes dark microglia to appear at higher concentrations, and further research is needed to determine whether they play a causative role in neurodegenerative diseases. Nonetheless, Tremblay’s team’s discovery opens the door to exciting new possibilities for the immunological mechanisms of Alzheimer’s and could one day lead to novel therapeutic approaches.