Microglial dormancy in depression challenges conventional understanding centered on inflammation, but highlights the immune cell's crucial role in neu
Chronic inflammation is a dominant feature in people who have depression, suggesting that an overactive immune response drives the disease’s symptoms. But a new study demonstrates something counterintuitive in spite of that: Immune cells in the brain called microglia are less active in people with depression, impairing their ability to clear damaged neuronal connections, undermining neurotrophic support, and driving the disease.
Researchers studied gene expression in the microglia of brain tissues collected during autopsies of 13 people with depression and 10 healthy people. They also examined gene expression of neuronal factors that regulate microglial function.
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They found that the expression of genes in the microglia of people with depression was markedly lower than that of healthy people, especially genes involved in immune responses and phagocytosis (which facilitates the clearance of damaged cells). In addition, the expression of factors involved in immune suppression (CD200 and CD47) was higher.
These findings suggest that people with depression have a distinct disease-associated microglia gene expression profile that impairs microglia activity. Microglia play critical roles in the development, homeostasis, and diseases of the central nervous system and contribute to neuronal plasticity in the healthy brain. Microglial changes are common features of many neuropsychiatric disorders, including schizophrenia, autism spectrum disorder, and bipolar disorder. Learn more about microglia suppression in depression in this clip featuring Dr. Charles Raison.