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Leptin in Alzheimer's disease

期刊

CLINICA CHIMICA ACTA
卷 450, 期 -, 页码 162-168

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.cca.2015.08.009

关键词

Alzheimer's disease; Leptin; Neuroprotection; Tau; Amyloid-beta protein

资金

  1. Fundacao de Amparo a Pesquisa de Minas Gerais (FAPEMIG)
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)

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Alzheimer's disease (AD) is the most common cause of progressive dementia in the elderly population. AD is histologically characterized by accumulation of amyloid-beta protein (A beta) on extracellular plaques and deposition of hyperphosphorylated tau protein in intracellular neurofibrillary tangles. Several studies have shown that obesity may precede dementia and that lifestyle factors play a critical role in the onset of AD. Furthermore, accumulating evidence indicates that obesity is an independent risk factor for developing AD. In this scenario, the understanding of the role of adipose tissue in brain health is essential to clarify the establishment of demential processes. The objective of this work was to review studies regarding leptin, an anorexigenic peptide hormone synthesized in adipocytes, in the context of dementia. Some authors proposed that leptin evaluation might be a better predictor of dementia than traditional anthropometric measures. Leptin, once established as a biomarker, could enhance the understanding of late-onset AD risk over the life course, as well as the clinical progression of prodromal state to manifested AD. Other studies have proposed that leptin presents neuroprotective activities, which could be explained by inhibiting the amyloidogenic process, reducing the levels of tau protein phosphotylation and improving the cognitive function. (C) 2015 Elsevier B.V. All rights reserved.

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