期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 16, 期 4, 页码 731-740出版社
IOS PRESS
DOI: 10.3233/JAD-2009-1021
关键词
AICAR; AMP-activated kinase; amyloid-beta; glycogen synthase kinase-3; leptin; tau
资金
- National Institute on Aging [SBIR-1R43AG029670]
- New Jersey Commission on Science and Technology
- NATIONAL INSTITUTE ON AGING [R43AG029670, R37AG017926] Funding Source: NIH RePORTER
Adipocyte-derived leptin appears to regulate a number of features defining Alzheimerfls disease (AD) at the molecular and physiological level. Leptin has been shown to reduce the amount of extracellular amyloid beta, both in cell culture and animal models, as well as to reduce tau phosphorylation in neuronal cells. Importantly, chronic administration of leptin resulted in a significant improvement in the cognitive performance of transgenic animal models. In AD, weight loss often precedes the onset of dementia and the level of circulating leptin is inversely proportional to the severity of cognitive decline. It is speculated that a deficiency in leptin levels or function may contribute to systemic and CNS abnormalities leading to disease progression. Furthermore, a leptin deficiency may aggravate insulin-controlled pathways, known to be aberrant in AD. These observations suggest that a leptin replacement therapy may be beneficial for these patients.
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