Researchers at King's College London have shown that adding a molecule involved in the body's inflammatory response to stem cells taken from the hippocampus stops those cells from producing new neurons. The findings, published in Nature Communications, point to a mechanism linking sustained inflammation with the cognitive problems seen in Alzheimer's disease, aging, depression, and the neurological aftermath of viral infections.
The hippocampus is one of the few regions of the adult human brain that continues to generate new neurons, a process called hippocampal neurogenesis. It underpins learning, memory and the regulation of mood, and disruptions to it have already been associated with aging, neurodegenerative disease and mood disorders. The King's team zeroed in on cytokines, the chemical messengers the body releases when it detects a threat such as a virus. Cytokines kick off the wider immune response that fights infection, but persistently high levels are also a signature of chronic inflammation.
That distinction matters. A short burst of cytokine activity during an infection is how the immune system does its job; the concern is what happens when those signals never switch off. This work suggests that under those conditions, the same molecules that mobilise a defence may also shut down the brain's capacity to build new cells in a region critical to memory.
Earlier research had connected viral infection to changes in neuron production in the hippocampus, but the route from infection and inflammatory cytokines to impaired neurogenesis had not been mapped. By demonstrating the effect directly in human hippocampal stem cells, the study fills in part of that gap and gives researchers a specific biological target to investigate as they look for ways to protect cognition in people living with long-running inflammation.