Obesity A risk for Alzheimer's disease? I. Common molecular mechanisms
Obesity is a recognized risk factor for cardiovascular diseases and the main responsible for the resistance to the action of insulin, a state that precedes the development of diabetes type 2. In the last years, researches have demonstrated that there are also common molecular mechanisms between obesity and Alzheimer's disease, to be the more likely pathological link a state of insulin resistance, which is mediated by inflammation. If the brain dysfunction in Alzheimer's effectively shares underlying mechanisms with obesity, certain intracellular signaling molecules might be involved in both diseases. Identification of these molecules and their consideration as therapeutic targets would represent a breakthrough in the understanding of the mechanisms of these diseases, and an excellent strategy in the development of new therapies for both pathologic conditions. In this work the last hypothesis linking obesity with Alzheimer's disease are reviewed. Adipose tissue dysfunction and consequent accumulation of ectopic fat as a cause of inflammation and insulin resistance systemic conditions obesity characteristics are described. It also highlights these peripheral systemic pathological states as primarily responsible for neuroinflammation and insulin resistance in the brain that would lead to the neuronal dysfunction and cognitive impairment found in Alzheimer's disease.
| Main Authors: | , |
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| Format: | artículo de revisión biblioteca |
| Language: | English |
| Published: |
Real Academia Nacional de Farmacia (España)
2016
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| Online Access: | http://hdl.handle.net/20.500.12792/3830 http://hdl.handle.net/10261/291066 |
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| Summary: | Obesity is a recognized risk factor for cardiovascular diseases and the main responsible for the resistance to the action of insulin, a state that precedes the development of diabetes type 2. In the last years, researches have demonstrated that there are also common molecular mechanisms between obesity and Alzheimer's disease, to be the more likely pathological link a state of insulin resistance, which is mediated by inflammation. If the brain dysfunction in Alzheimer's effectively shares underlying mechanisms with obesity, certain intracellular signaling molecules might be involved in both diseases. Identification of these molecules and their consideration as therapeutic targets would represent a breakthrough in the understanding of the mechanisms of these diseases, and an excellent strategy in the development of new therapies for both pathologic conditions. In this work the last hypothesis linking obesity with Alzheimer's disease are reviewed. Adipose tissue dysfunction and consequent accumulation of ectopic fat as a cause of inflammation and insulin resistance systemic conditions obesity characteristics are described. It also highlights these peripheral systemic pathological states as primarily responsible for neuroinflammation and insulin resistance in the brain that would lead to the neuronal dysfunction and cognitive impairment found in Alzheimer's disease. |
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