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Descargar Solucionario Del Libro Calculo Integral Moises Lazaro
Descargar Solucionario Del Libro Calculo Integral Moises Lazaro
Descargar Solucionario Del Libro Calculo Integral Moises Lazaro
Descargar Solucionario Del Libro Calculo Integral Moises Lazaro
Descargar Solucionario Del Libro Calculo Integral Moises LazaroAlzheimer’s disease (AD) is a neurodegenerative disease characterized by a progressive deterioration of cognitive functions, including memory. The cause of AD is unknown, but at late stages of the disease the patient has a substantial loss of neurons in the brain regions important for cognition. Although the exact mechanisms of AD are still unknown, we propose to examine the basic mechanisms which underlie the pathogenesis of cognitive impairment in AD. This proposal is based on the idea that although progressive loss of neurons plays a major role in the AD brain, the expression of neurogenesis in the adult brain also plays an important role. In recent studies we have found that expression of the brain derived neurotrophic factor (BDNF) and the NMDA receptor subunit 1 (NR1) in the dentate gyrus is significantly increased in the CA1 and subiculum, brain areas known to be severely affected in AD. We hypothesize that an increased expression of these neurotrophic factors may contribute to the pathogenesis of cognitive impairment in AD. First we will study the mechanisms underlying the increased expression of BDNF and NR1 in the hippocampus. This includes examining the mechanisms regulating these factors in the hippocampus and testing the effects of the increased BDNF and NR1 in the hippocampus. Second, we will study the regulation of BDNF expression in the hippocampus in other pathological models of AD. Third, we will study the effects of activation of BDNF and NR1 in the hippocampus. We will examine the immediate early genes c-fos and Zif 268, as well as the immediate effects of BDNF and NR1, such as c-fos-IR and NR1 synaptic targeting. Fourth, we will examine the effects of activation of BDNF on cognitive functions. AIM 1: To examine the mechanisms underlying the increased expression of BDNF and NR1 in the hippocampus. AIM 2: To determine if increased expression of BDNF in the hippocampus plays an important role in the pathogenesis of cognitive impairment in AD. AIM 3: To examine the regulation of BDNF expression in
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