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CSF-ApoER2 fragments as a read-out of reelin signaling: Distinct patterns in sporadic and autosomal-dominant Alzheimer disease


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Title:
CSF-ApoER2 fragments as a read-out of reelin signaling: Distinct patterns in sporadic and autosomal-dominant Alzheimer disease
Authors:
Lopez-Font, Inmaculada  
Iborra Lázaro, Guillermo  
Sánchez-Valle, Raquel
Molinuevo, José Luis  
Cuchillo-Ibañez, Inmaculada
Sáez-Valero, Javier  
Editor:
Elsevier
Issue Date:
2018-12-12
URI:
https://hdl.handle.net/11000/31210
Abstract:
Reelin is a glycoprotein associated with synaptic plasticity and neurotransmission. The malfunctioning of reelin signaling in the brain is likely to contribute to the pathogenesis of Alzheimer's disease (AD). Reelin binding to Apolipoprotein E receptor 2 (ApoER2) activates downstream signaling and induces the proteolytic cleavage of ApoER2, resulting in the generation of soluble fragments. To evaluate the efficiency of reelin signaling in AD, we have quantified the levels of reelin and soluble ectodomain fragments of ApoER2 (ectoApoER2) in the cerebrospinal fluid (CSF). CSF from sporadic AD patients (sAD; n = 14, age 54-83 years) had lower levels of ecto-ApoER2 (~31% reduction; p = .005) compared to those in the age-matched controls (n = 10, age 61-80), and a higher reelin/ecto-ApoER2 ratio. In contrast, autosomal dominant AD patients, carriers of PSEN1 mutations (ADAD; n = 7, age 31-49 years) had higher ecto-ApoER2 levels (~109% increment; p = .001) and a lower reelin/ecto-ApoER2 ratio than the non-mutation carriers from the same families (n = 7, age 25-47 years). Our data suggest that the levels of ecto-ApoER2 in CSF could be a suitable read-out of an impaired reelin signaling in AD, but also indicate differences between sAD and ADAD.
Keywords/Subjects:
Reelin
ApoER2
Autosomal-dominant AD
CSF
Proteolytic fragment
Sporadic AD
Type of document:
application/pdf
Access rights:
info:eu-repo/semantics/closedAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
DOI:
https://doi.org/10.1016/j.cca.2018.12.012
Appears in Collections:
Instituto de Neurociencias



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