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Published in: Molecular Autism 1/2012

Open Access 01-12-2012 | Review

A review of the evidence for the canonical Wnt pathway in autism spectrum disorders

Author: Hans Otto Kalkman

Published in: Molecular Autism | Issue 1/2012

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Abstract

Microdeletion and microduplication copy number variations are found in patients with autism spectrum disorder and in a number of cases they include genes that are involved in the canonical Wnt signaling pathway (for example, FZD9, BCL9 or CDH8). Association studies investigating WNT2, DISC1, MET, DOCK4 or AHI1 also provide evidence that the canonical Wnt pathway might be affected in autism. Prenatal medication with sodium-valproate or antidepressant drugs increases autism risk. In animal studies, it has been found that these medications promote Wnt signaling, including among others an increase in Wnt2 gene expression. Notably, the available genetic information indicates that not only canonical Wnt pathway activation, but also inhibition seems to increase autism risk. The canonical Wnt pathway plays a role in dendrite growth and suboptimal activity negatively affects the dendritic arbor. In principle, this provides a logical explanation as to why both hypo- and hyperactivity may generate a similar set of behavioral and cognitive symptoms. However, without a validated biomarker to stratify for deviant canonical Wnt pathway activity, it is probably too dangerous to treat patients with compounds that modify pathway activity.
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Metadata
Title
A review of the evidence for the canonical Wnt pathway in autism spectrum disorders
Author
Hans Otto Kalkman
Publication date
01-12-2012
Publisher
BioMed Central
Published in
Molecular Autism / Issue 1/2012
Electronic ISSN: 2040-2392
DOI
https://doi.org/10.1186/2040-2392-3-10

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