期刊
ALZHEIMERS & DEMENTIA
卷 10, 期 -, 页码 S26-S32出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2013.12.004
关键词
Alzheimer's disease; Amyloid-beta oligomers; Insulin resistance; Insulin therapy; GLP-IR agonists
资金
- Human Frontiers Science Program
- National Institute for Translational Neuroscience (INNT/Brazil)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao de Amparo a Pesquisa do Estado do Rio de Janeiro
- CNPq
Compelling preclinical and clinical evidence supports a pathophysiological connection between Alzheimer's disease (AD) and diabetes. Altered metabolism, inflammation, and insulin resistance are key pathological features of both diseases. For many years, it was generally considered that the brain was insensitive to insulin, but it is now accepted that this hormone has central neuromodulatory functions, including roles in learning and memory, that are impaired in AD. However, until recently, the molecular mechanisms accounting for brain insulin resistance in AD have remained elusive. Here, we review recent evidence that sheds light on how brain insulin dysfunction is initiated at a molecular level and why abnormal insulin signaling culminates in synaptic failure and memory decline. We also discuss the cellular basis underlying the beneficial effects of stimulation of brain insulin signaling on cognition. Discoveries summarized here provide pathophysiological background for identification of novel molecular targets and for development of alternative therapeutic approaches in AD. (C) 2014 The Alzheimer's Association. All rights reserved.
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