Introduction

Introduzione al numero di Functional Neurology che raccoglie i contributi scientifici di un Congresso Internazionale dedicato al decennio del cervello (The Decade of the Brain), tenuto a Pavia il 24-26 Giugno 2001, e breve recensione del contenuto stess

The decade of the brain at the C. Mondino Foundation: ten years of research in experimental neurobiology - Functional Neurology

Volume di Functional Neurology (n.16, suppl. 4), edito dagli autori sopra riportati, che raccoglie i contributi scientifici presentati al Congresso Internazionale "The decade of the brain at the C. Mondino Foundation: ten years of research in experimental neurobiology", Pavia, 24-26 Giugno 200

Overexpression of superoxide dismutase 1 protects against beta-amyloid peptide toxicity:effect of estrogen and copper chelators.

Amyloid peptides (Abeta) are major constituents of senile plaques in Alzheimer’s disease (AD) brain and contribute to neurodegeneration, operating through activation of apoptotic pathways. It has been proposed that Abeta induces death by oxidative stress, possibly through the generation of peroxynitrite from superoxide and nitric oxide. Estrogen is thought to play a protective role against neurodegeneration through a variety of mechanisms including scavenging of reactive oxygen species (ROS). In this study, we have challenged with Abeta, either in the presence or in the absence of 17beta-estradiol, differentiated human neuroblastoma SH-SY5Y cells (named line SH) and the same line overexpressing anti-oxidant enzyme superoxide dismutase 1 (SOD1; named line WT). We have observed that: (1) WT cells are less susceptible than SH cells to Abeta insult; (2) caspase-3, but not caspase-1, is involved in Abeta-induced apoptosis in this system; (3) estrogen protects both lines, without significantly affecting SOD activity; and (4) copper chelators prevent Abeta-induced toxicity. Our results further support the notion that anti-oxidant therapy might be beneficial in the treatment of AD by preventing activation of selected apoptotic pathways