The acute neurotoxic effect of β-amyloid on mature cultures of rat hippocampal neurons is attenuated by the anti-oxidant U-78517F

Abstract

The neuropathological characteristics of Alzheimer's disease include the selective loss of neurons and the development of senile plaques and neurofibrillary tangles. These plaques and tangles are invariably associated with deposits of an insoluble protein, β-amyloid, and the hypothesis that the β-amyloid is responsible for the neuronal loss in Alzheimer's disease has received considerable support. The neurotoxic action of β-amyloid has been demonstrated in primary cultures of cortical and hippocampal neurons and in PC-12 cells. The present study reports that the neurotoxicity of β-amyloid is reduced by the antioxidant drug U-78517F. On the basis of this observation, we suggest that the neurotoxic effect of β-amyloid is mediated by oxygen free radicals. The clinical use of antioxidant interventions may reduce neurodegeneration and the progression of the symptoms in patients with Alzheimer's disease.

Key Words:

• J-amyloid
• neurotoxicity
• hippocampal neurons
• free radicals
• neuroprotection
• lazaroid