Aged garlic extract suppresses lipid peroxidation induced by beta -Amyloid in PC12 cells

• Published in: In vitro cellular & developmental biology. Animal Vol. 36; no. 5; pp. 279 - 280
• Main Authors: Griffin, B, Selassie, M, Gwebu, E T
• Format: Journal Article
• Language: English
• Published: 01.05.2000
• Subjects: 4-hydroxynonenal; Allium sativum; malondialdehyde
• ISSN: 1071-2690; 1543-706X
• DOI: 10.1290/1071-2690(2000)036(0279:AGESLP)2.0.CO;2

Alzheimer's disease (AD) is a progressively debilitating disease of the brain that leads to intellectual failure and memory impairment in the elderly. About 5 million Americans are affected by AD. The precise cause of this disease is still unknown. Several lines of evidence support the role of oxidative stress, including increased lipid peroxidation, in the pathogenesis of AD. Beta-amyloid sub(1-40) peptide plays a crucial role in this pathogenesis. Its internal fragment, beta-amyloid sub(25-35) (A beta ), generates toxic free radicals, which induce lipid peroxidation and other cellular dysfunction. Lipid peroxidation has been suggested as a potential cause of neuronal damage in AD. Indeed, A beta -induced lipid peroxidation products, 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), have been detected in AD. It is suggested that neuronal death caused by A beta is mediated via 4-HNE. 4-HNE is increased in the brains in AD, especially in the amygdala and hippocampus regions, which show the most pronounced histopathological alterations in AD.