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Significance of brain glucose hypometabolism and of altered insulin signal transduction in an experimental model of amiotrophic lateral esclerosis (ALE)

Amyotrophic Lateral Sclerosis (ALS) and Multiple Sclerosis (MS): Molecular Etiology and Novel Treatments

Senior Researcher : Enrique Blázquez Fernández

Research Centre or Institution : Universidad Complutense de Madrid

Abstract

Certain neurodegenerative disorders such as, Alzheimer (AD), Parkinson (PD) and Huntington (HD) diseases, as well as Epilepsy, Type 2 Diabetes Mellitus (T2DM), Schizophrenia and Major Depressive Disorder (MDD) show common pathogenic manifestations although they have a different ethiological origin.They are cerebral glucose hypometabolism, oxidative stress, neuroinflammation, resistance to the action of insulin and/or modifications in the transduction of signals induced by this hormone. Neuroinflammation appears in response to astrogliosis and microglial activation that induce the release of cytokines, neural dysfunction and cell death. Despite it was believed that insulin lack of biological effects on the brain, now we know that it play an important role in the health and in certain neurodegenerative diseases. Also, in patients with AD and PD, the brain glucose hypometabolism precede to the clinical manifestations of the disease and, in this way may be considered as an early marker of both diseases. In addition, alterations of glucose and insulin metabolism have been reported in Epilepsy, AD, HD, PD, MDD and Schizophrenia. Taking into account these facts we suggest the role of insulin in several neurodegenerative diseases and in others than still have not been analyzed, which reinforce the interest of its study because their scientific, sanitary, economical and social relevance.Accordingly we propose the study of the possible metabolic alterations in the Esclerosis Lateral Amiotrophy (ELA) by using the transgenic mice TDP-43, experimental model of this disease, in which we will determine the brain glucose metabolism, expression of the genes implied and the resistance to the insulin action.

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