Mechanism linking chronic inflammation to reduced brain regeneration identified

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Left: cells that did not have TNF-α added to them (control), right: 1ng/ml TNF-α was added to these cells. Blue marker shows the nuclei of all cells (DAPI), including stem cells. Green (MAP2) and yellow (DCX) shows proteins that are markers of neuron maturation. Scale bar (white line) shows 100 μm. Credit: King's College London

A King's College London study, published in Nature Communications, offers insight into how long-term inflammation may contribute to cognitive decline in disorders such as Alzheimer's disease, aging, depression and the lingering neurological effects of viral infections.

The scientists discovered that adding a molecule involved in the inflammatory response to stem cells from the hippocampus prevents the development of new neurons. The formation of new neurons in this region, known as hippocampal neurogenesis, is essential for learning, memory and mood regulation. It is one of the few parts of the human brain where new neurons are made in adults. Altered adult hippocampal neurogenesis is associated with aging, neurodegeneration and mood disorders such as depression.

The study focused on cytokines, which are chemical signals released by the body in response to a threat such as a viral infection. Cytokines ultimately act as triggers for the rest of the immune response, which helps the body fight the infection. High cytokine levels are also a hallmark of chronic inflammation.

Viral infection has previously been linked to changes in the ability to create new neurons in part of the hippocampus. However, exactly how infection and inflammatory cytokines affect the creation of new neurons was previously unknown.

Stem cells shift into immune mode

When researchers added one particular cytokine, called TNF-α, to human hippocampal stem cells, it prevented them from developing into neurons. Instead, they switched into an "immune alert" state, releasing signals that can attract key immune cells, known as T cells, that drive inflammation while simultaneously reducing the production of new nerve cells.

First author Dr. Tinne A. D. Nissen, who completed the research as part of her Ph.D. at King's College London, said, "What surprised us most was that the stem cells were not simply impaired by inflammation, they actively adopted behaviors that could potentially sustain immune responses in the brain."

Co-corresponding author, Professor Sandrine Thuret, professor of neuroscience at King's College London, said, "Our findings reveal a new link between chronic inflammation and the brain's reduced ability to generate new neurons.

"Inflammatory signals can effectively redirect hippocampal stem cells away from their normal role of producing neurons and toward supporting immune activity instead."

Blocking interferons partly reversed damage

The researchers also identified an unexpected signaling pathway behind this effect involving type I interferons, molecules typically associated with the body's antiviral defense. By blocking interferon signaling with an existing therapeutic antibody, some of the effects of inflammation were reversed—restoring the production of new neurons and preventing the attraction of T cells involved in the immune response.

Co-corresponding author, Professor Linda S. Klavinskis, professor of viral immunology at King's College London, added, "Our work uncovers a new mechanism that may help explain why ongoing inflammation is so damaging to brain health. Importantly, it also points to possible treatments to protect or restore the brain's regenerative capacity."

Publication details

Tinne A. D. Nissen et al, TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells, Nature Communications (2026). DOI: 10.1038/s41467-026-74104-x

Journal information: Nature Communications

Key medical concepts

Interferon Type IAlzheimer's Disease

Clinical categories

NeurologyAllergy and immunologyPsychology & Mental health Provided by King's College London Who's behind this story?

Sadie Harley

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