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Gaceta médica de México

versión impresa ISSN 0016-3813

Resumen

MANZANO-LEON, Natalia  y  MAS-OLIVA, Jaime. Oxidate stress β-amiloide peptide and Alzheimer's disease. Gac. Méd. Méx [online]. 2006, vol.142, n.3, pp.229-238. ISSN 0016-3813.

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

Palabras llave : Oxidative stress; β-amyloid peptide; microglial cells; scavenger receptor.

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