|Title||Old age potentiates cold-induced tau phosphorylation: linking thermoregulatory deficit with Alzheimer's disease.|
|Publication Type||Journal Article|
|Year of Publication||2017|
|Auteurs||Tournissac, M, Vandal, M, François, A, Planel, E, Calon, F|
|Date Published||2017 Feb|
|Keywords||Adipose Tissue, Brown, Aging, Alzheimer Disease, Animals, Body Temperature, Body Temperature Regulation, Cold Temperature, Glycogen Synthase Kinase 3 beta, Mice, Inbred C57BL, Phosphorylation, tau Proteins|
Thermoregulatory deficits coincide with a rise in the incidence of Alzheimer's disease (AD) in old age. Lower body temperature increases tau phosphorylation, a neuropathological hallmark of AD. To determine whether old age potentiates cold-induced tau phosphorylation, we compared the effects of cold exposure (4 °C, 24 hours) in 6- and 18-month-old mice. Cold-induced changes in body temperature, brown adipose tissue activity, and phosphorylation of tau at Ser202 were not different between 6- and 18-month-old mice. However, following cold exposure, only old mice displayed a significant rise in soluble tau pThr181 and pThr231, which was correlated with body temperature. Inactivation of glycogen synthase kinase 3β was more prominent in young mice, suggesting a protective mechanism against cold-induced tau phosphorylation. These results suggest that old age confers higher susceptibility to tau hyperphosphorylation following a change in body temperature, thereby contributing to an enhanced risk of developing AD.
|Alternate Journal||Neurobiol. Aging|