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Pesquisa : C10.228.140.163.100.362.375 [Categoria DeCS]
Referências encontradas : 268 [refinar]
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[PMID]:28101991
[Au] Autor:Mendes MI; Smith DE; Pop A; Lennertz P; Fernandez Ojeda MR; Kanhai WA; van Dooren SJ; Anikster Y; Baric I; Boelen C; Campistol J; de Boer L; Kariminejad A; Kayserili H; Roubertie A; Verbruggen KT; Vianey-Saban C; Williams M; Salomons GS
[Ad] Endereço:Department of Clinical Chemistry, Metabolic Unit, VU University Medical Center, Amsterdam Neuroscience, Amsterdam, The Netherlands.
[Ti] Título:Clinically Distinct Phenotypes of Canavan Disease Correlate with Residual Aspartoacylase Enzyme Activity.
[So] Source:Hum Mutat;38(5):524-531, 2017 May.
[Is] ISSN:1098-1004
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe 14 patients with 12 novel missense mutations in ASPA, the gene causing Canavan disease (CD). We developed a method to study the effect of these 12 variants on the function of aspartoacylase-the hydrolysis of N-acetyl-l-aspartic acid (NAA) to aspartate and acetate. The wild-type ASPA open reading frame (ORF) and the ORFs containing each of the variants were transfected into HEK293 cells. Enzyme activity was determined by incubating cell lysates with NAA and measuring the released aspartic acid by LC-MS/MS. Clinical data were obtained for 11 patients by means of questionnaires. Four patients presented with a non-typical clinical picture or with the milder form of CD, whereas seven presented with severe CD. The mutations found in the mild patients corresponded to the variants with the highest residual enzyme activities, suggesting that this assay can help evaluate unknown variants found in patients with atypical presentation. We have detected a correlation between clinical presentation, enzyme activity, and genotype for CD.
[Mh] Termos MeSH primário: Amidoidrolases/metabolismo
Doença de Canavan/diagnóstico
Doença de Canavan/enzimologia
Fenótipo
[Mh] Termos MeSH secundário: Adolescente
Alelos
Amidoidrolases/química
Criança
Pré-Escolar
Análise Mutacional de DNA
Ativação Enzimática
Genótipo
Seres Humanos
Lactente
Masculino
Modelos Moleculares
Mutação
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.5.- (Amidohydrolases); EC 3.5.1.15 (aspartoacylase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1002/humu.23181


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[PMID]:28077719
[Au] Autor:Sohn J; Bannerman P; Guo F; Burns T; Miers L; Croteau C; Singhal NK; McDonough JA; Pleasure D
[Ad] Endereço:Institute for Pediatric Regenerative Medicine, University of California, Davis, Sacramento, California 95817, and.
[Ti] Título:Suppressing N-Acetyl-l-Aspartate Synthesis Prevents Loss of Neurons in a Murine Model of Canavan Leukodystrophy.
[So] Source:J Neurosci;37(2):413-421, 2017 Jan 11.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canavan disease is a leukodystrophy caused by aspartoacylase (ASPA) deficiency. The lack of functional ASPA, an enzyme enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates brain NAA and causes "spongiform" vacuolation of superficial brain white matter and neighboring gray matter. In children with Canavan disease, neuroimaging shows early-onset dysmyelination and progressive brain atrophy. Neuron loss has been documented at autopsy in some cases. Prior studies have shown that mice homozygous for the Aspa nonsense mutation Nur7 also develop brain vacuolation. We now report that numbers of cerebral cortical and cerebellar neurons are decreased and that cerebral cortex progressively thins in Aspa mice. This neuronal pathology is prevented by constitutive disruption of Nat8l, which encodes the neuronal NAA-synthetic enzyme N-acetyltransferase-8-like. SIGNIFICANCE STATEMENT: This is the first demonstration of cortical and cerebellar neuron depletion and progressive cerebral cortical thinning in an animal model of Canavan disease. Genetic suppression of N-acetyl-l-aspartate (NAA) synthesis, previously shown to block brain vacuolation in aspartoacylase-deficient mice, also prevents neuron loss and cerebral cortical atrophy in these mice. These results suggest that lowering the concentration of NAA in the brains of children with Canavan disease would prevent or slow progression of neurological deficits.
[Mh] Termos MeSH primário: Ácido Aspártico/análogos & derivados
Doença de Canavan/metabolismo
Modelos Animais de Doenças
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácido Aspártico/biossíntese
Ácido Aspártico/deficiência
Ácido Aspártico/genética
Doença de Canavan/genética
Doença de Canavan/patologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neurônios/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
30KYC7MIAI (Aspartic Acid); 997-55-7 (N-acetylaspartate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2013-16.2016


  3 / 268 MEDLINE  
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[PMID]:28007430
[Au] Autor:Thangavelu B; Mutthamsetty V; Wang Q; Viola RE
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Toledo, Toledo, OH 43606, United States.
[Ti] Título:Design and optimization of aspartate N-acetyltransferase inhibitors for the potential treatment of Canavan disease.
[So] Source:Bioorg Med Chem;25(3):870-885, 2017 Feb 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Canavan disease is a fatal neurological disorder caused by defects in the metabolism of N-acetyl-l-aspartate (NAA). Recent work has shown that the devastating symptoms of this disorder are correlated with the elevated levels of NAA observed in these patients, caused as a consequence of the inability of mutated forms of aspartoacylase to adequately catalyze its breakdown. The membrane-associated enzyme responsible for the synthesis of NAA, aspartate N-acetyltransferase (ANAT), has recently been purified and examined (Wang et al., Prot Expr Purif. 2016;119:11). With the availability, for the first time, of a stable and soluble form of ANAT we can now report the identification of initial inhibitors against this biosynthetic enzyme, obtained from the screening of several focused compound libraries. Two core structures of these moderate binding compounds have subsequently been optimized, with the most potent inhibitors in these series possessing sub-micromolar inhibition constants (K values) against ANAT. Slowing the production of NAA via the inhibition of ANAT will lower the elevated levels of this metabolite and can potentially serve as a treatment option to moderate the symptoms of Canavan disease.
[Mh] Termos MeSH primário: Acetiltransferases/antagonistas & inibidores
Doença de Canavan/tratamento farmacológico
Desenho de Drogas
Inibidores Enzimáticos/farmacologia
[Mh] Termos MeSH secundário: Acetiltransferases/metabolismo
Doença de Canavan/metabolismo
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.17 (aspartate N-acetyltransferase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE


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[PMID]:27288788
[Au] Autor:Roscoe RB; Elliott C; Zarros A; Baillie GS
[Ad] Endereço:Gardiner Laboratory, Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, Scotland, UK.
[Ti] Título:Non-genetic therapeutic approaches to Canavan disease.
[So] Source:J Neurol Sci;366:116-124, 2016 Jul 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Canavan disease (CD) is a rare leukodystrophy characterized by diffuse spongiform white matter degeneration, dysmyelination and intramyelinic oedema with consequent impairment of psychomotor development and early death. The molecular cause of CD has been identified as being mutations of the gene encoding the enzyme aspartoacylase (ASPA) leading to its functional deficiency. The physiological role of ASPA is to hydrolyse N-acetyl-l-aspartic acid (NAA), producing l-aspartic acid and acetate; as a result, its deficiency leads to abnormally high central nervous system NAA levels. The aim of this article is to review what is currently known regarding the aetiopathogenesis and treatment of CD, with emphasis on the non-genetic therapeutic strategies, both at an experimental and a clinical level, by highlighting: (a) major related hypotheses, (b) the results of the available experimental simulatory approaches, as well as (c) the relevance of the so far examined markers of CD neuropathology. The potential and the limitations of the current non-genetic neuroprotective approaches to the treatment of CD are particularly discussed in the current article, in a context that could be used to direct future experimental and (eventually) clinical work in the field.
[Mh] Termos MeSH primário: Doença de Canavan/terapia
[Mh] Termos MeSH secundário: Animais
Doença de Canavan/fisiopatologia
Terapia Baseada em Transplante de Células e Tecidos/métodos
Seres Humanos
Fármacos Neuroprotetores/farmacologia
Fármacos Neuroprotetores/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neuroprotective Agents)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160612
[St] Status:MEDLINE


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[PMID]:27039844
[Au] Autor:Ahmed SS; Schattgen SA; Frakes AE; Sikoglu EM; Su Q; Li J; Hampton TG; Denninger AR; Kirschner DA; Kaspar B; Matalon R; Gao G
[Ad] Endereço:Horae Gene Therapy Center, University of Massachusetts Medical School, Worcester, Massachusetts, USA; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
[Ti] Título:rAAV Gene Therapy in a Canavan's Disease Mouse Model Reveals Immune Impairments and an Extended Pathology Beyond the Central Nervous System.
[So] Source:Mol Ther;24(6):1030-1041, 2016 Jun.
[Is] ISSN:1525-0024
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aspartoacylase (AspA) gene mutations cause the pediatric lethal neurodegenerative Canavan disease (CD). There is emerging promise of successful gene therapy for CD using recombinant adeno-associated viruses (rAAVs). Here, we report an intracerebroventricularly delivered AspA gene therapy regime using three serotypes of rAAVs at a 20-fold reduced dose than previously described in AspA(-/-) mice, a bona-fide mouse model of CD. Interestingly, central nervous system (CNS)-restricted therapy prolonged survival over systemic therapy in CD mice but failed to sustain motor functions seen in systemically treated mice. Importantly, we reveal through histological and functional examination of untreated CD mice that AspA deficiency in peripheral tissues causes morphological and functional abnormalities in this heretofore CNS-defined disorder. We demonstrate for the first time that AspA deficiency, possibly through excessive N-acetyl aspartic acid accumulation, elicits both a peripheral and CNS immune response in CD mice. Our data establish a role for peripheral tissues in CD pathology and serve to aid the development of more efficacious and sustained gene therapy for this disease.
[Mh] Termos MeSH primário: Amidoidrolases/genética
Doença de Canavan/terapia
Sistema Nervoso Central/patologia
Terapia Genética/métodos
[Mh] Termos MeSH secundário: Animais
Doença de Canavan/genética
Doença de Canavan/patologia
Sistema Nervoso Central/metabolismo
Dependovirus/genética
Modelos Animais de Doenças
Vetores Genéticos/administração & dosagem
Seres Humanos
Camundongos
Especificidade de Órgãos
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.5.- (Amidohydrolases); EC 3.5.1.15 (aspartoacylase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE


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[PMID]:26992473
[Au] Autor:Gowda VK; Bhat MD; Srinivasan VM; Prasad C; Benakappa A; Faruq M
[Ad] Endereço:Department of Pediatric Neurology, Indira Gandhi Institute of Child Health, Bangalore, India. Electronic address: drknvraju@hotmail.com.
[Ti] Título:A case of Canavan disease with microcephaly.
[So] Source:Brain Dev;38(8):759-62, 2016 Sep.
[Is] ISSN:1872-7131
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Canavan disease is an autosomal recessive disorder with spongy degeneration of white matter of the brain. It presents with developmental delay, visual problems and macrocephaly. PATIENT DESCRIPTION: We report a ten-month old boy with Canavan disease who presented with global developmental delay, seizures, abnormal eye movements and microcephaly. RESULTS: MRI brain revealed diffuse involvement of the supra tentorial white matter, globus pallidi, thalami, dentate nuclei and brainstem with sparing of the corpus callosum. The genetic testing revealed homozygous mutation of aspartoacylase gene [c.859 G>A (p.Ala287Thr)] in Exon 6. CONCLUSION: Possibility of Canavan disease should be considered even in the presence of microcephaly.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Doença de Canavan/diagnóstico
Microcefalia/diagnóstico
[Mh] Termos MeSH secundário: Amidoidrolases/genética
Doença de Canavan/genética
Doença de Canavan/fisiopatologia
Deficiências do Desenvolvimento/diagnóstico
Deficiências do Desenvolvimento/genética
Deficiências do Desenvolvimento/fisiopatologia
Diagnóstico Diferencial
Seres Humanos
Lactente
Imagem por Ressonância Magnética
Masculino
Microcefalia/genética
Microcefalia/fisiopatologia
Convulsões/diagnóstico
Convulsões/genética
Convulsões/fisiopatologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.5.- (Amidohydrolases); EC 3.5.1.15 (aspartoacylase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160320
[St] Status:MEDLINE


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[PMID]:26791240
[Au] Autor:Kamate M; Kabate V; Malhotra M
[Ad] Endereço:KLE University's J N Medical College, Belgaum, Karnataka State, India; Child Development Clinic, KLES Prabhakar Kore Hospital, Belgaum, Karnataka State, India. Electronic address: drmaheshkamate@gmail.com.
[Ti] Título:Spongy White Matter: A Novel Neuroimaging Finding in Canavan Disease.
[So] Source:Pediatr Neurol;56:92-93, 2016 Mar.
[Is] ISSN:1873-5150
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença de Canavan/diagnóstico por imagem
Doença de Canavan/patologia
Neuroimagem
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Seres Humanos
Lactente
Imagem por Ressonância Magnética
Espectroscopia de Ressonância Magnética
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160122
[St] Status:MEDLINE


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[PMID]:26586007
[Au] Autor:Sarret C; Boespflug-Tanguy O; Rodriguez D
[Ad] Endereço:Image-Guided Clinical Neuroscience and Connectomics (IGCNC), EA7282, University of Auvergne, Clermont-Ferrand University Hospital, 58 rue Montalembert, 63003, Clermont-Ferrand, cedex, France. csarret@chu-clermontferrand.fr.
[Ti] Título:Atypical clinical and radiological course of a patient with Canavan disease.
[So] Source:Metab Brain Dis;31(2):475-9, 2016 Apr.
[Is] ISSN:1573-7365
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canavan disease (CD) is a rare metabolic disorder caused by aspartoacylase (ASPA) deficiency. It leads to severe neurological degeneration with spongiform brain degeneration. Accumulation of N-acetylaspartate (NAA) in brain and urine is specific to the disease and guides diagnosis. Magnetic resonance imaging (MRI) usually shows diffuse white matter abnormalities with involvement of the basal ganglia. Mild forms of the disease with a more favorable clinical course and radiological involvement of the basal ganglia without white matter abnormalities have also been reported. Here we report an atypical case of a girl aged nine years with CD. The disease started at the classical age of five months. Classical elevation of NAA in brain and urine was present and genetic analysis identified mutations in the ASPA gene. However, clinical evolution was milder than typical CD, with partial motor impairment and relatively well-preserved cognitive skills. MRI was also atypical with low white matter involvement and unusual topography and evolution of abnormalities in the basal ganglia.
[Mh] Termos MeSH primário: Encéfalo/patologia
Encéfalo/fisiopatologia
Doença de Canavan/patologia
Imagem por Ressonância Magnética
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Ácido Aspártico/análogos & derivados
Ácido Aspártico/metabolismo
Doença de Canavan/diagnóstico
Criança
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
30KYC7MIAI (Aspartic Acid); 997-55-7 (N-acetylaspartate); EC 3.5.- (Amidohydrolases); EC 3.5.1.15 (aspartoacylase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151121
[St] Status:MEDLINE
[do] DOI:10.1007/s11011-015-9767-9


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[PMID]:26511242
[Au] Autor:Maier H; Wang-Eckhardt L; Hartmann D; Gieselmann V; Eckhardt M
[Ad] Endereço:Institute of Biochemistry and Molecular Biology and.
[Ti] Título:N-Acetylaspartate Synthase Deficiency Corrects the Myelin Phenotype in a Canavan Disease Mouse Model But Does Not Affect Survival Time.
[So] Source:J Neurosci;35(43):14501-16, 2015 Oct 28.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canavan disease (CD) is a severe, lethal leukodystrophy caused by deficiency in aspartoacylase (ASPA), which hydrolyzes N-acetylaspartate (NAA). In the brains of CD patients, NAA accumulates to high millimolar concentrations. The pathology of the disease is characterized by loss of oligodendrocytes and spongy myelin degeneration in the CNS. Whether accumulating NAA, absence of NAA-derived acetate, or absence of any unknown functions of the ASPA enzyme is responsible for the pathology of the disease is not fully understood. We generated ASPA-deficient (Aspa(nur7/nur7)) mice that are also deficient for NAA synthase Nat8L (Nat8L(-/-)/Aspa(nur7/nur7)). These mice have no detectable NAA. Nevertheless, they exhibited normal myelin content, myelin sphingolipid composition, and full reversal of spongy myelin and axonal degeneration. Surprisingly, although pathology was fully reversed, the survival time of the mice was not prolonged. In contrast, Aspa(nur7/nur7) mice with only one intact Nat8L allele accumulated less NAA, developed a less severe pathology, phenotypic improvements, and, importantly, an almost normal survival time. Therefore, inhibition of NAA synthase is a promising therapeutic option for CD. The reduced survival rate of Nat8L(-/-)/Aspa(nur7/nur7) mice, however, indicates that complete inhibition of NAA synthase may bear unforeseeable risks for the patient. Furthermore, we demonstrate that acetate derived from NAA is not essential for myelin lipid synthesis and that loss of NAA-derived acetate does not cause the myelin phenotype of Aspa(nur7/nur7) mice. Our data clearly support the hypothesis that NAA accumulation is the major factor in the development of CD.
[Mh] Termos MeSH primário: Acetiltransferases/genética
Ácido Aspártico/análogos & derivados
Doença de Canavan/patologia
Bainha de Mielina/patologia
[Mh] Termos MeSH secundário: Acetiltransferases/metabolismo
Amidoidrolases/genética
Amidoidrolases/metabolismo
Animais
Ácido Aspártico/metabolismo
Axônios/patologia
Comportamento Animal
Doença de Canavan/tratamento farmacológico
Doença de Canavan/genética
Inibidores Enzimáticos/uso terapêutico
Feminino
Genótipo
Gliose/genética
Gliose/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Bainha de Mielina/metabolismo
Degeneração Neural/patologia
Esfingolipídeos/metabolismo
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Sphingolipids); 30KYC7MIAI (Aspartic Acid); 997-55-7 (N-acetylaspartate); EC 2.3.1.- (Acetyltransferases); EC 3.5.- (Amidohydrolases); EC 3.5.1.15 (aspartoacylase)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:151029
[Lr] Data última revisão:
151029
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1056-15.2015


  10 / 268 MEDLINE  
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[PMID]:26245283
[Au] Autor:De Bernardo G; Giordano M; Sordino D; Buono S
[Ad] Endereço:Department of Emergency, NICU, AORN Santobono Pausilipon, Naples, Italy.
[Ti] Título:Early diagnosis of Canavan syndrome: how can we get there?
[So] Source:BMJ Case Rep;2015, 2015 Aug 05.
[Is] ISSN:1757-790X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Canavan syndrome is a rare genetic disorder characterised by progressive severe leukodystrophy involving the degeneration of white matter. Currently, there is no effective therapy, but after recent studies using early gene therapy, the outcome has appeared to improve. It is of fundamental importance to recognise signs of neonatal Canavan syndrome early on. We describe a case of neonatal Canavan syndrome in which diagnosis was made only at the fourth month of age.
[Mh] Termos MeSH primário: Ácido Aspártico/análogos & derivados
Doença de Canavan/diagnóstico
Doença de Canavan/genética
Diagnóstico Precoce
[Mh] Termos MeSH secundário: Ácido Aspártico/urina
Terapia Genética
Seres Humanos
Lactente
Espectroscopia de Ressonância Magnética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
30KYC7MIAI (Aspartic Acid); 997-55-7 (N-acetylaspartate)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170806
[Lr] Data última revisão:
170806
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150807
[St] Status:MEDLINE



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