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of Heat Shock Proteins Protects Cortical Neurons Against Amyloid-Beta Peptide 1–42-Mediated Oxidative Stress and Neurotoxicity: Implications for Alzheimer’s Disease

By Hafiz Mohmmad Abdul, Vittorio Calabrese, Menotti Calvani and D. Allan Butterfield

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by loss of memory and cognition and by senile plaques and neurofibrillary tangles in brain. Amyloid-beta peptide, particularly the 42amino-acid peptide (Ab1–42), is a principal component of senile plaques and is thought to be central to the pathogenesis of the disease. The AD brain is under significant oxidative stress, and Ab1–42 peptide is known to cause oxidative stress in vitro and in vivo. Acetyl-Lcarnitine (ALCAR) is an endogenous mitochondrial membrane compound that helps to maintain mitochondrial bioenergetics and lowers the increased oxidative stress associated with aging. Glutathione (GSH) is an important endogenous antioxidant, and its levels have been shown to decrease with aging. Administration o

Year: 2013
OAI identifier: oai:CiteSeerX.psu:10.1.1.319.5322
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