Protein secreted by immune cells may help drive brain aging
Brain-resident immune cells that have reached an old-age state called "senescence" secrete a protein that causes dysfunction in other brain cells, according to a study led by investigators at Weill Cornell Medicine. The discovery sheds light on how aging impairs memory and cognition and makes the brain vulnerable to neurodegenerative disorders.
A study by researchers at Weill Cornell Medicine has revealed that immune cells in the brain may contribute to brain aging through the secretion of a protein called DLK1. In a mouse model of accelerated aging, these brain-resident immune cells, called microglia, enter a state of senescence and begin releasing DLK1, which disrupts other brain cells such as neurons and oligodendrocytes.
This protein-driven dysfunction in the brain may be a crucial mechanism underlying decreased brain function and heightened risk of neurodegenerative diseases as one ages. The senior author of the study, Dr. Li Gan, suggested that neutralizing DLK1 could potentially slow down brain aging. Understanding the mechanisms behind aging-related brain changes, which include shrinkage of key brain areas, reduced neuronal communication, degradation of myelin sheath, and heightened vulnerability to neurodegenerative disorders like Alzheimer's and Parkinson's, has been a mystery until now.
The research team observed a mouse model with telomeres that shorten more quickly than normal, causing accelerated aging. In these mice, brain signs of advanced aging, such as reduced myelination and neuronal dysfunction, were present even in early middle age. Specifically, senescent microglia were found to secrete DLK1, impairing neuronal function and myelin-producing oligodendrocytes.
The researchers also noted a similar pattern in human-derived brain cells, implying that DLK1 may play a role in brain aging and increased susceptibility to neurodegenerative diseases.
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