Next Article in Journal
Spondyloarthritis: Matrix Metalloproteinasesas Biomarkers of Pathogenesis and Response to Tumor Necrosis Factor (TNF) Inhibitors
Next Article in Special Issue
Unbalance between Excitation and Inhibition in Phenylketonuria, a Genetic Metabolic Disease Associated with Autism
Previous Article in Journal
Mitochondrial Genomes Provide Insights into the Phylogeny of Lauxanioidea (Diptera: Cyclorrhapha)
Previous Article in Special Issue
Increased Force Variability Is Associated with Altered Modulation of the Motorneuron Pool Activity in Autism Spectrum Disorder (ASD)
Review

Delineating the Common Biological Pathways Perturbed by ASD’s Genetic Etiology: Lessons from Network-Based Studies

Molecular and Behavioral Neurosciences Lab, Bar-Ilan University, Faculty of Medicine, 13215 Safed, Israel
*
Author to whom correspondence should be addressed.
Academic Editor: Merlin G. Butler
Int. J. Mol. Sci. 2017, 18(4), 828; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18040828
Received: 28 February 2017 / Revised: 3 April 2017 / Accepted: 6 April 2017 / Published: 14 April 2017
In recent decades it has become clear that Autism Spectrum Disorder (ASD) possesses a diverse and heterogeneous genetic etiology. Aberrations in hundreds of genes have been associated with ASD so far, which include both rare and common variations. While one may expect that these genes converge on specific common molecular pathways, which drive the development of the core ASD characteristics, the task of elucidating these common molecular pathways has been proven to be challenging. Several studies have combined genetic analysis with bioinformatical techniques to uncover molecular mechanisms that are specifically targeted by autism-associated genetic aberrations. Recently, several analysis have suggested that particular signaling mechanisms, including the Wnt and Ca2+/Calmodulin-signaling pathways are often targeted by autism-associated mutations. In this review, we discuss several studies that determine specific molecular pathways affected by autism-associated mutations, and then discuss more in-depth into the biological roles of a few of these pathways, and how they may be involved in the development of ASD. Considering that these pathways may be targeted by specific pharmacological intervention, they may prove to be important therapeutic targets for the treatment of ASD. View Full-Text
Keywords: ASD; autism; networks; genetics; Fragile-X Syndrome; Wnt; mTOR; Calmodulin; Calcium; NGF ASD; autism; networks; genetics; Fragile-X Syndrome; Wnt; mTOR; Calmodulin; Calcium; NGF
MDPI and ACS Style

Oron, O.; Elliott, E. Delineating the Common Biological Pathways Perturbed by ASD’s Genetic Etiology: Lessons from Network-Based Studies. Int. J. Mol. Sci. 2017, 18, 828. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18040828

AMA Style

Oron O, Elliott E. Delineating the Common Biological Pathways Perturbed by ASD’s Genetic Etiology: Lessons from Network-Based Studies. International Journal of Molecular Sciences. 2017; 18(4):828. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18040828

Chicago/Turabian Style

Oron, Oded, and Evan Elliott. 2017. "Delineating the Common Biological Pathways Perturbed by ASD’s Genetic Etiology: Lessons from Network-Based Studies" International Journal of Molecular Sciences 18, no. 4: 828. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18040828

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop