| Literature DB >> 17177147 |
C G Janson1, S W J McPhee, J Francis, D Shera, M Assadi, A Freese, P Hurh, J Haselgrove, D J Wang, L Bilaniuk, P Leone.
Abstract
Canavan disease is a childhood leukodystrophy caused by mutations in the gene for human aspartoacylase ( ASPA), which leads to an abnormal accumulation of the substrate molecule N-acetyl-aspartate (NAA) in the brain. This study was designed to model the natural history of Canavan disease using MRI and proton magnetic resonance spectroscopy ( (1)H-MRS). NAA and various indices of brain structure (morphology, quantitative T1, fractional anisotropy, apparent diffusion coefficient) were measured in white and gray matter regions during the progression of Canavan disease. A mixed-effects statistical model was used to fit all outcome measures. Longitudinal data from 28 Canavan patients were directly compared in each brain region with reference data obtained from normal, age-matched pediatric subjects. The resultant model can be used to non-invasively monitor the natural history of Canavan disease or related leukodystrophies in future studies involving drug, gene therapy, or stem cell treatments.Entities:
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Year: 2006 PMID: 17177147 DOI: 10.1055/s-2006-924734
Source DB: PubMed Journal: Neuropediatrics ISSN: 0174-304X Impact factor: 1.947