Estudio de toxicidad del péptido beta-amiloide en linfocitos humanos

Resumen Introduccion la enfermedad de Alzheimer (EA) es uno de los problemas sociosanitarios mas importantes actualmente. Se considera la toxicidad del peptido beta-amiloide la clave de su patogenia. Cada vez es mas importante conseguir marcadores perifericos de la enfermedad para avanzar en su conocimiento y de sus posibles dianas terapeuticas. Con este estudio pretendemos valorar la idoneidad de los linfocitos como modelo en el que estudiar la toxicidad del beta-amiloide. Material y metodos se recluto a 6 voluntarios sanos, 3 varones y 3 mujeres, con edades comprendidas entre los 25 y 35 anos, sin antecedentes familiares de EA. Se les realizo una extraccion sanguinea de donde se aislaron …

Gender and age-dependent differences in the mitochondrial apoptogenic pathway in Alzheimer's disease

Age-related mitochondrial oxidative stress is highly gender dependent. The aim of this study was to determine the role of gender in the mitochondrial contribution to neuronal apoptosis in Alzheimer's disease (AD). We used mitochondria isolated from brains of Wistar rats to study the toxicity of ss-amyloid peptide (Ass), and found that it increases mitochondrial peroxide production, nitration and oxidation of proteins, and release of cytochrome c. The toxic effects occurred in young males and in old females but not in young females, indicating their resistance to Ass. This resistance was abolished with age. These toxic effects of Ass were prevented by heme. Our findings provide a molecular m…

P1‐278: apoE4, risk factor of Alzheimer's disease, study in young adults

The depletion of nuclear glutathione impairs cell proliferation in 3t3 fibroblasts.

BACKGROUND:Glutathione is considered essential for survival in mammalian cells and yeast but not in prokaryotic cells. The presence of a nuclear pool of glutathione has been demonstrated but its role in cellular proliferation and differentiation is still a matter of debate. PRINCIPAL FINDINGS:We have studied proliferation of 3T3 fibroblasts for a period of 5 days. Cells were treated with two well known depleting agents, diethyl maleate (DEM) and buthionine sulfoximine (BSO), and the cellular and nuclear glutathione levels were assessed by analytical and confocal microscopic techniques, respectively. Both agents decreased total cellular glutathione although depletion by BSO was more sustaine…

Vitamin E Paradox in Alzheimer's Disease: It Does Not Prevent Loss of Cognition and May Even Be Detrimental

There is controversy as to whether vitamin E is beneficial in Alzheimer's disease (AD). In this study, we tested if vitamin E prevents oxidative stress and loss of cognition in AD. Fifty-seven AD patients were recruited and divided in two groups: placebo or treated with 800 IU of vitamin E per day for six months. Of these 57 patients, only 33 finished the study. We measured blood oxidized glutathione (GSSG) and used the following cognitive tests: Mini-Mental State Examination, Blessed-Dementia Scale, and Clock Drawing Test. Of those patients treated with vitamin E, we found two groups. In the first group, "respondents" to vitamin E, GSSG levels were lower after the treatment and scores on t…