Estrés oxidativo, péptido β-amiloide y enfermedad de Alzheimer

摘要: SUMMARY Alzheimers disease, the leading cause of dementia in elderly is characterized by presence brain senile plaques formed insoluble fibrillar deposits β-amyloid peptide. This peptide normally produced a monomeric soluble form and it present low concentrations blood spinal fluid. At physiological concentrations, this neurotrophic neuroprotector factor; nevertheless, with aging particularly disease accumulates, favors formation fibrils causes neurotoxicity. toxicity has been associated generation free radicals that turn promote lipid peroxidation protein oxidation. Through recognition specific receptors such as scavenger receptor, β- amyloid becomes internalized aggregates. Independently way enters cell, generates oxidative stress eventually triggers state neurotoxicity cell death. Recent studies our laboratory have shown effect caused an extracellular upon internalization receptor. We also demonstrated process translation molecules implicated mechanism endocytosis through case β-adaptin, arrested microglial cells treated β-amyloid.