A groundbreaking study conducted at the lab of Beth Stevens, PhD, at Boston Children's Hospital has revealed that an immune protein impacts neuronal protein synthesis in the aging brain. Previous work from the Stevens lab had uncovered that immune cells in the central nervous system, microglia, help prune synapses in the developing brain by tagging synapses with the immune protein C1q. New research led by Nicole Scott-Hewitt, published in Cell , shows that neurons can also internalize C1q.
C1q seems to influence protein production inside neurons by interacting with ribosomal proteins, RNA-binding proteins, and RNA in the cell's cytoplasm. Additionally, C1q accumulates in neurons over time, suggesting it may play a role in age-related cognitive changes and neurodegenerative conditions. The study, titled "Microglial C1q accumulates in neuronal ribonucleoprotein (RNP) complexes across aging," has been published in Cell, highlighting the following key findings: In adult mice lacking a protein called C1q, there is a significant increase in the production of proteins in neurons and a change in the balance of proteins in the brain, suggesting that C1q may be important for keeping the brain's proteins in check.
These changes are specific to age, with noticeable differences in protein production in adult mice compared to younger ones. Neurons can take in C1q protein from outside the cell. This process depends on endocytosis, a way cells internalize molecules.
The study found that a pa.
