beta-amyloid controls altered Reelin expression and processing in Alzheimer's disease.
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beta-amyloid controls altered Reelin expression and processing in Alzheimer's disease.

Neurobiol Dis. 2009 Dec 15;

Authors: Botella-López A, Cuchillo-Ibáñez I, Cotrufo T, Mok SS, Li QX, Barquero MS, Dierssen M, Soriano E, Sáez-Valero J

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 Down's syndrome (DS), where the extra copy of chromosome 21 leads to overexpression of beta-amyloid. In cortical extracts of 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 Abeta42 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 Abeta42-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.

PMID: 20025970 [PubMed - as supplied by publisher]

Read the complete post at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&db=PubMed&cmd=Retrieve&list_uids=20025970&dopt=Abstract

Posted 23 Dec 2009 4:45 AM by pubmed: neuroblastoma
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