Journal
NEUROBIOLOGY OF AGING
Volume 50, Issue -, Pages 25-29Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2016.09.024
Keywords
Aging; Thermoregulation; Tau; Alzheimer's disease; Body temperature
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Funding
- Alzheimer Society of Canada [1502]
- Canadian Institutes of Health Research [MOP 102532, IAO 74443]
- Canadian Foundation for Innovation [34480]
- Fonds de Recherche en sante du Quebec (FRQ-S)
- Fonds d'Enseignement et de la Recherche (FER)
- Faculty of Pharmacy, Laval University
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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 degrees 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 3 beta 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. (C) 2016 Elsevier Inc. All rights reserved.
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