Abstract：
: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 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.
journal_name
Neurobiol Disjournal_title
Neurobiology of diseaseauthors
Botella-López A,Cuchillo-Ibáñez I,Cotrufo T,Mok SS,Li QX,Barquero MS,Dierssen M,Soriano E,Sáez-Valero Jdoi
10.1016/j.nbd.2009.12.006subject
Has Abstractpub_date
2010-03-01 00:00:00pages
682-91issue
3eissn
0969-9961issn
1095-953Xpii
S0969-9961(09)00348-9journal_volume
37pub_type
杂志文章abstract：:Multiple sclerosis (MS) is a chronic, inflammatory autoimmune disease that affects the central nervous system (CNS) for which there is no cure. In MS, encephalitogenic T cells infiltrate the CNS causing demyelination and neuroinflammation; however, little is known about the role of regulatory T cells (Tregs) in CNS ti...
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