Skip to main content
Frontiers in Autism Research: New Horizons for Diagnosis and Treatment

The epigenetics of Autism-Running beyond the bases

Publication ,  Chapter
Gregory, SG
January 1, 2014

Previous studies have established that there is a strong genetic component to the development of ASD, but these genetic risks do not account for all of the heritability of the disorder. This raises the prospect that alternative, epigenetic mechanisms may play a role in ASD development. Epigenetic mechanisms facilitate temporal and spatial regulation of gene expression, but are independent of changes to the underlying DNA sequence. Because epigenetic profi les are labile, they represent an intriguing mechanism whereby environmental infl uences, which are not severe enough to alter the DNA sequence of a cell, may alter gene expression and cellular response and contribute to ASD. In this chapter, we discuss the role of DNA methylation and histone modifi cations in the development of ASD.

Duke Scholars

DOI

Publication Date

January 1, 2014

Start / End Page

303 / 333
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Gregory, S. G. (2014). The epigenetics of Autism-Running beyond the bases. In Frontiers in Autism Research: New Horizons for Diagnosis and Treatment (pp. 303–333). https://doi.org/10.1142/9789814602167_0013
Gregory, S. G. “The epigenetics of Autism-Running beyond the bases.” In Frontiers in Autism Research: New Horizons for Diagnosis and Treatment, 303–33, 2014. https://doi.org/10.1142/9789814602167_0013.
Gregory SG. The epigenetics of Autism-Running beyond the bases. In: Frontiers in Autism Research: New Horizons for Diagnosis and Treatment. 2014. p. 303–33.
Gregory, S. G. “The epigenetics of Autism-Running beyond the bases.” Frontiers in Autism Research: New Horizons for Diagnosis and Treatment, 2014, pp. 303–33. Scopus, doi:10.1142/9789814602167_0013.
Gregory SG. The epigenetics of Autism-Running beyond the bases. Frontiers in Autism Research: New Horizons for Diagnosis and Treatment. 2014. p. 303–333.

DOI

Publication Date

January 1, 2014

Start / End Page

303 / 333