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http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17125| Título : | The role of insulin resistance and glucose metabolism dysregulation in the development of Alzheimer's disease |
| Autor: | ISABEL ARRIETA CRUZ ROGER GUTIERREZ JUAREZ |
| Palabras clave : | BIOLOGÍA Y QUÍMICA;Ciencias de la vida;Bioquímica;Enfermedades del sistema nervioso;Enfermedades neurodegenerativas;Tauopatías;Alzheimer, Enfermedad de;Enfermedades metabólicas;Trastornos del metabolismo de la glucosa;Diabetes mellitus;Resistencia a la insulina;Biochemistry;Nervous system diseases;Neurodegenerative diseases;Tauopathies;Alzheimer disease;Metabolic diseases;Glucose metabolism disorders;Diabetes mellitus;Insuline resistance |
| Fecha de publicación: | 2016 |
| Editorial : | Instituto Nacional de Ciencias Medicas y Nutrición Salvador Zubirán |
| Descripción : | Abstract: Alzheimer´s disease is a chronic neurodegenerative disorder affecting millions of people worldwide, characterized by a progressive decline in cognitive functions. Factors involved in the pathogenesis of Alzheimer´s disease include metabolic alterations such as insulin resistance and hyperglycemia, both of which are also hallmarks of type-2 diabetes mellitus. The accumulation of β-amyloid peptides in the brain of Alzheimer´s patients is responsible in part for the neurotoxicity underlying the loss of synaptic plasticity that triggers a cascade of events leading to cell death. A large number of studies revealed the key role of the hippocampus and cerebral cortex in the memory and learning deficits of Alzheimer´s disease. Although ample evidence suggests a link between altered insulin action, the dysregulation of glucose metabolism, and β-amyloid accumulation in animal models and humans with Alzheimer´s, no supporting evidence was available. In this article, we review the potential toxic effects of β-amyloid in the hypothalamus, a brain center involved in the control of insulin action and glucose metabolism. Furthermore, we discuss our recent studies unraveling a novel neurotoxic action of β-amyloid that perturbs hypothalamic glucoregulation, leading to increased hepatic glucose production and hyperglycemia. These findings provide evidence for a link between β-amyloid toxicity and altered glucose metabolism. Conclusions: In conclusion, studies on the molecular and cellular mechanisms involved in the pathophysiology of AD and its relationship with insulin and glucose metabolism support the idea that the metabolic alterations of DM2 are strongly associated to the development of AD. Importantly, our recent studies in rodents provided a piece of evidence supporting the novel concept that AB toxic action in the hypothalamus causes a dysregulation of glucose metabolism directly linking altered insulin action with AD. Further studies are required to better understand the details of this relationship and its causal role, if any, in the onset and progression of AD. |
| URI : | http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17125 |
| Aparece en las colecciones: | 1. Artículos |
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| Fichero | Descripción | Tamaño | Formato | |
|---|---|---|---|---|
| ric_2016_68_2_053-058.pdf | 202.09 kB | Adobe PDF | Visualizar/Abrir |