Leptin: A novel therapeutic strategy for Alzheimer's disease

Nikolaos Tezapsidis, Jane M. Johnston, Mark A. Smith, J. Wesson Ashford, Gemma Casadesus, Nikolaos K. Robakis, Benjamin Wolozin, George Perry, Xiongwei Zhu, Steven J. Greco, Sraboni Sarkar

Research output: Contribution to journalReview articlepeer-review

107 Scopus citations

Abstract

Adipocyte-derived leptin appears to regulate a number of features defining Alzheimer's 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.

Original languageEnglish
Pages (from-to)731-740
Number of pages10
JournalJournal of Alzheimer's Disease
Volume16
Issue number4
DOIs
StatePublished - 2009
Externally publishedYes

Keywords

  • AICAR
  • AMP-activated kinase
  • Amyloid-β
  • Glycogen synthase kinase-3
  • Leptin
  • Tau

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