Discovery of the trigger of inflammation leads to hope for longer, healthier lives

Inflammation is behind many age-related diseases such as arthritis, gout, Alzheimer’s disease and diabetes. Even when it doesn’t cause disease it can still lead to loss of function and reduces healthspan (the portion of our lives spent relatively free of serious illness).

But a team from the Yale School of Medicine has discovered a vital trigger of inflammation: sensor Nlrp3 inflammasome. It means that instead of tackling each age-dependent disease separately, experts could umbrella them together, says the team in Cell Metabolism.

Tests on healthy mice found that Nlrp3 inflammasome is activated in response to ageing. Mice with lower Nlrp3 activation were protected from age-related disorders such as dementia, bone loss, glucose intolerance and cataracts. They performed better, were less frail, and ran for longer durations.

“This is the first study to show that inflammation is causally linked to functional decline in aging,” says Prof Vishwa Deep Dixit. “There are multiple cellular triggers of inflammation throughout the body, but we’ve pinpointed Nlrp3 as the specific sensor that activates inflammation with age.

“Now that we’ve identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation. This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability.”

More studies will look at if the Nlrp3 mechanism can be safely manipulated without impairing the immune system.