alexa A Breakthrough in Understanding the Nature of Canavan D
ISSN: 2168-975X

Brain Disorders & Therapy
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Short Communication

A Breakthrough in Understanding the Nature of Canavan Disease, a Human Spongiform Leukodystrophy due to Inborn Errors in the Gene Encoding for Aspartoacylase

Morris H. Baslow* and David N. Guilfoyle
Nathan S. Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Corresponding Author : Morris H. Baslow
Nathan S. Kline Institute for Psychiatric Research
140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Tel: +1-845-398-547
E-mail: [email protected] nki.rfmh.org
Received May 07, 2015; Accepted May 23, 2015; Published May 28, 2015
Citation: Baslow MH, Guilfoyle DN (2014) A Breakthrough in Understanding the Nature of Canavan Disease, a Human Spongiform Leukodystrophy due to Inborn Errors in the Gene Encoding for Aspartoacylase. Brain Disord Ther 4:170. doi:10.4172/2168-975X.1000170
Copyright: © 2013 Baslow MH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Canavan disease (CD) is a rare early-onset progressive spongiform leukodystrophy in brain of both humans and animals and is due to mutations in the gene encoding for aspartoacylase (ASPA), the enzyme that hydrolyzes N-acetyl-L-aspartate (NAA) [1]. In humans, the effects of CD are generally much more profound than in rodents exhibiting this same genetic lesion. The gene for ASPA is an autosomal recessive and human or animal carriers of mutations do not appear to be affected. ASPA is expressed in oligodendrocytes and based on their large fractional cellular volume, these cells are the major source of ASPA in brain. However, ASPA has also been identified in microglia and in several other cellular brain compartments.

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