Astrocytes contribute to neuronal impairment in βA toxicity increasing apoptosis in rat hippocampal neurons

✍ Scribed by Fiorella Malchiodi-Albedi; Maria Rosaria Domenici; Silvia Paradisi; Antonietta Bernardo; Maria Antonietta Ajmone-Cat; Luisa Minghetti

• Book ID: 102224103
• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 166 KB
• Volume: 34
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.1041

✦ Synopsis

Abstract

Astrocytosis is a common feature of amyloid plaques, the hallmark of Alzheimer's disease (AD), along with activated microglia, neurofibrillary tangles, and β‐amyloid (βA) deposition. However, the relationship between astrocytosis and neurodegeneration remains unclear. To assess whether βA‐stimulated astrocytes can damage neurons and contribute to βA neurotoxicity, we studied the effects of βA treatment in astrocytic/neuronal co‐cultures, obtained from rat embryonic brain tissue. We found that in neuronal cultures conditioned by βA‐treated astrocytes, but not directly in contact with βA, the number of apoptotic cells increased, doubling the values of controls. In astrocytes, βA did not cause astrocytic cell death, nor did produce changes in nitric oxide or prostaglandin E~2~ levels. In contrast, S‐100β expression was remarkably increased. Our data show for the first time that βA–astrocytic interaction produces a detrimental effect on neurons, which may contribute to neurodegeneration in AD. GLIA 34:68–72, 2001. © 2001 Wiley‐Liss, Inc.