期刊
AGEING RESEARCH REVIEWS
卷 72, 期 -, 页码 -出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2021.101462
关键词
Alzheimer's disease; Thermoregulation; Brown adipose tissue; Insulin; Metabolism; beta-adrenergic agonist; Body temperature
资金
- Fonds de Recherche du Quebec en Sante (FRQ-S) [253895]
- Alzheimer Society Canada [20-01, 15-02]
- Canadian Institutes of Health Research (CIHR) [PJT 156054, PJT 168927]
- Alzheimer Society of Canada [17-17]
- Fondation du CHU de Quebec
- acceleration MITACS program
- Fonds d'Enseignement et de la Recherche (FER) from the Faculty of Pharmacy, Laval University
- CIHR
- Alberta Innovates - Health Solution Postgraduate Fellowship award
- FRQ-S
Alzheimer's disease (AD) is a complex age-related neurodegenerative disease associated with central and peripheral metabolic anomalies, such as impaired glucose utilization and insulin resistance. Correcting thermoregulatory impairments could slow the progression and delay the onset of AD.
Alzheimer's disease (AD) is a complex age-related neurodegenerative disease, associated with central and peripheral metabolic anomalies, such as impaired glucose utilization and insulin resistance. These observations led to a considerable interest not only in lifestyle-related interventions, but also in repurposing insulin and other anti-diabetic drugs to prevent or treat dementia. Body temperature is the oldest known metabolic readout and mechanisms underlying its maintenance fail in the elderly, when the incidence of AD rises. This raises the possibility that an age-associated thermoregulatory deficit contributes to energy failure underlying AD pathogenesis. Brown adipose tissue (BAT) plays a central role in thermogenesis and maintenance of body temperature. In recent years, the modulation of BAT activity has been increasingly demonstrated to regulate energy expenditure, insulin sensitivity and glucose utilization, which could also provide benefits for AD. Here, we review the evidence linking thermoregulation, BAT and insulin-related metabolic defects with AD, and we propose mechanisms through which correcting thermoregulatory impairments could slow the progression and delay the onset of AD.
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