The UK《自然》magazine recently published a new study on aging: Stanford University scientists observed age-related changes in a cell population (neurogenic microenvironment) in which mice can produce new neurons. The study found that the immune system plays a role in the decline of age-related functions in the neurogenesis microenvironment. Relevant results can be used to develop strategies to help the brains of aging mammals to counteract the reduction of neuronal precursor cells.
The mammalian brain is capable of generating new neurons in the neurogenesis microenvironment, which consists of neural stem cells, neural precursor cells, and several other cells. The function of the microenvironment and its ability to produce new neurons decline with age, and this effect is thought to promote a decline in cognitive function. However, it is unclear how this microenvironment changes with age and what factors contribute to these changes.
In order to compare the cellular composition of the young and aging neurogenesis microenvironment, Stanford University Anne Brunette and colleagues brain cells from three young mice (3 months old) and three aged mice (28-29 months old). Characterized. Analysis of the RNA sequence of 14685 single cells revealed age-related changes in the neurogenesis microenvironment, including a decrease in the number of activated neural stem cells and precursor cells, and infiltration of T cells (an immune cell) in the aging brain. T cells from aging brains release a signaling molecule called interferon gamma that has been shown to reduce the proliferation of neural stem cells in vitro.
These results point to one of the reasons for the gradual decrease in neurons during aging, which paves the way for the development of immune strategies for age-related cognitive dysfunction.xx