Reducing the expression of the protein TOM1 in mouse models of Alzheimer's disease increased the pathology, exacerbated cognitive problems, and raised levels of inflammation in the brain. Restoring TOM1 reversed the effects. Findings suggest a new therapeutic target for treating dementia.
Secondary infections and novel inflammatory events, even ones that occur external to the brain, amplify the brain's immune response and detrimentally impact cognition in mouse models of Alzheimer's disease.
A new study sheds light on how the circadian clock controls inflammatory response. By understanding the link between inflammation and circadian rhythm, researchers believe it may be most effective to target specific conditions at certain times of the day. The findings may also explain why those who experience body clock disruptions are more susceptible to inflammatory conditions.
SARM, an ancient immune protein previously implicated in apoptosis, is a key immune regulator in peripheral immune cells. The finding could help in the development of treatments for a range of diseases, including Alzheimer's, cancer and diabetes.