AI Article Synopsis
- Microglia, the brain's resident immune cells, can self-renew, but how they age and are replaced is still unclear.
- In zebrafish, two sources of microglia are identified: early short-lifespan ones from the rostral blood island (RBI) and later long-lifespan ones from the aorta-gonad-mesonephros (AGM).
- The study finds that the decline of RBI microglia is linked to their poor competition for a key growth factor (Il34), and that age affects the overall maintenance and elimination of microglia through a process called cell competition.
Article Abstract
Microglia are brain-resident macrophages capable of long-term maintenance through self-renewal. Yet the mechanism governing the turnover and lifespan of microglia remains unknown. In zebrafish, microglia arise from two sources, rostral blood island (RBI) and aorta-gonad-mesonephros (AGM). The RBI-derived microglia are born early but have a short lifespan and diminish in adulthood, while the AGM-derived microglia emerge later and are capable of long-term maintenance in adulthood. Here, we show that the attenuation of RBI microglia is due to their less competitiveness for neuron-derived interleukin-34 (Il34) caused by age-dependent decline of colony-stimulating factor-1 receptor a (). Alterations of Il34/Csf1ra levels and removal of AGM microglia revamp the proportion and lifespan of RBI microglia. The expression in zebrafish AGM-derived microglia and murine adult microglia also undergo age-dependent decline, leading to the elimination of aged microglia. Our study reveals cell competition as a general mechanism controlling the turnover and lifespan of microglia.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10275588 | PMC |
| http://dx.doi.org/10.1126/sciadv.adf9790 | DOI Listing |
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