Journal
NEUROCHEMICAL RESEARCH
Volume 34, Issue 2, Pages 295-303Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-008-9776-8
Keywords
Alzheimer's disease; Amyloid beta-peptide; Organotypic culture; Caspase-3
Categories
Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq/Brazil)
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES/Brazil)
- Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS)
- Pro-Reitoria de Pesquisa da Universidade Federal do Rio Grande do Sul (PROPESQ/UFRGS)
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Accumulation of the neurotoxic amyloid beta-peptide (A beta) in the brain is a hallmark of Alzheimer's disease (AD). Several synthetic A beta peptides have been used to study the mechanisms of toxicity. Here, we sought to establish comparability between two commonly used A beta peptides A beta 1-42 and A beta 25-35 on an in vitro model of A beta toxicity. For this purpose we used organotypic slice cultures of rat hippocampus and observed that both A beta peptides caused similar toxic effects regarding to propidium iodide uptake and caspase-3 activation. In addition, we also did not observe any effect of both peptides on Akt and PTEN phosphorylation; otherwise the phosphorylation of GSK-3 beta was increased. Although further studies are necessary for understanding mechanisms underlying A beta peptide toxicity, our results provide strong evidence that A beta 1-42 and the A beta 25-35 peptides induce neural injury in a similar pattern and that A beta 25-35 is a convenient tool for the investigation of neurotoxic mechanisms involved in AD.
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