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1 for the treatment of patients suffering from Canavan disease.
2 ion aspartoacylase mutations associated with Canavan Disease.
3 ng to preliminary studies in 2 children with Canavan disease.
4 iency of ASPA and should therefore result in Canavan disease.
5 nown patient of African-American origin with Canavan disease.
6 bral cortical thinning in an animal model of Canavan disease.
7 ith aspartoacylase that, when mutated, cause Canavan disease.
8 ial abnormalities such as Leighs disease and Canavans disease.
9  the central nervous system (CNS), result in Canavan Disease, a fatal dysmyelinating disease.
10 n lipids, and defects in this enzyme lead to Canavan disease, a fatal neurological disorder.
11 of the brain and is the established cause of Canavan disease, a fatal progressive leukodystrophy affe
12 oacylase, ASPA, where variants are linked to Canavan disease, a lethal neurological disorder.
13 tion of N-acetyl-l-aspartate, correlate with Canavan Disease, a neurodegenerative disorder usually fa
14 partate (NAA) is a characteristic feature of Canavan disease, a vacuolar leukodystrophy resulting fro
15 ve in vivo gene therapy for the treatment of Canavan disease and other neurological disorders, we dev
16 ral to the understanding the pathogenesis of Canavan disease and to the development of therapeutic st
17                The majority of patients with Canavan disease are from an Ashkenazi Jewish background.
18 ng Alzheimer's disease, Parkinson's disease, Canavan disease, aromatic l-amino acid decarboxylase [AA
19                                              Canavan disease (CD) is a severe, lethal leukodystrophy
20 ligodendrocytes, to deliver gene therapy for Canavan disease (CD), a rare leukodystrophy characterize
21      Mutations in the gene coding ASPA cause Canavan disease (CD), an autosomal recessive neurodegene
22 childhood autosomal recessive leukodystrophy Canavan disease (CD).
23    Aspartoacylase (ASPA)-deficient patients [Canavan disease (CD)] reportedly have increased urinary
24 , eight Gaucher mutations, four mutations in Canavan disease, four mutations in Fanconi anemia, and f
25  was aimed at finding the molecular basis of Canavan disease in 25 independent patients of non-Jewish
26                                              Canavan disease is a fatal neurological disorder caused
27                                              Canavan disease is a leukodystrophy caused by aspartoacy
28                                              Canavan disease is caused by inactivating ASPA (aspartoa
29                                              Canavan disease is inherited as an autosomal recessive t
30 partoacylase (ASPA), the defective enzyme in Canavan disease, is detectable in the brain only in the
31 tion and prevents leukodystrophy in a murine Canavan disease model.
32 P183H, M195R, K213E/G274R, G274R, and F295S) Canavan Disease mutations resulted in undetectable enzym
33                             In children with Canavan disease, neuroimaging shows early-onset dysmyeli
34 neurodegenerative disease in 2 children with Canavan disease to assess the in vivo toxicity and effic
35            The data can be used to interpret Canavan disease variants and provide insight into the re
36 ration of NAA in the brains of children with Canavan disease would prevent or slow progression of neu