Journal
NEUROBIOLOGY OF DISEASE
Volume 37, Issue 3, Pages 682-691Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.12.006
Keywords
Alzheimer's disease; Down's syndrome; Amyloid; Reelin; Glycoprotein; Cerebral cortex
Categories
Funding
- Ministerio de Ciencia e Innovacion (MCI) [BFU2008-3980]
- FIS [06/0181]
- Fundacio Obra Social Caixa Catalunya [EU-037627-AnEUploidy]
- CIBERNED
- ISC-III from Spain
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Reelin is a glycoprotein that modulates synaptic function and plasticity in the mature brain, thereby favouring memory formation. We recently reported altered cerebral Reelin expression in Alzheimer's disease (AD). Here we demonstrate pronounced Reelin changes at protein and mRNA levels in the frontal cortex in adult Down's syndrome (DS), where the extra copy of chromosome 21 leads to overexpression of beta-amyloid. In cortical extracts of fetal DS samples we detected increased levels of the full-length Reelin and the 310-kDa fragment. Overexpression of mutant human amyloid precursor protein also led to an increase in levels of Reelin fragments in Tg2576 transgenic mice for human beta-amyloid. Finally, in vitro A beta A2 treatment of SH-SY5Y neuroblastoma cells led to increased Reelin levels. An altered pattern of Reelin glycosylation was detected in extracts from the frontal cortex of AD patients and in A beta 42-treated SH-SY5Y cells, supporting the notion that beta-amyloid triggers altered Reelin processing. These results provide evidence that Reelin expression and processing is altered in several amyloid conditions. (C) 2009 Elsevier Inc. All rights reserved.
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