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1 Krabbe disease (KD) and metachromatic leukodystrophy (ML
2 Krabbe disease (KD) is a lysosomal storage disease (LSD)
3 Krabbe disease (KD) is a neurodegenerative lysosomal dis
4 Krabbe disease (KD) is caused by a deficiency of galacto
5 Krabbe disease is a devastating neurodegenerative diseas
6 Krabbe disease is a devastating pediatric leukodystrophy
7 Krabbe disease is a rare neurodegenerative disorder caus
8 Krabbe disease is an infantile neurodegenerative disorde
9 Krabbe disease is caused by a deficiency of the lysosoma
10 Krabbe disease is characterized by GALC deficiency and S
11 Krabbe disease or globoid cell leukodystrophy (GLD) is a
12 Krabbe disease, also named globoid cell (GC) leukodystro
13 Krabbe disease, an inherited leukodystrophy, is a sphing
14 Krabbe's disease is an infantile neurodegenerative disea
15 Krabbe's disease or globoid cell leukodystrophy is a rar
16 ases psychosine accumulation in cells from a Krabbe patient and prolongs the life span of the twitche
19 oid cell leukodystrophy (GLD), also known as Krabbe disease, is a devastating, degenerative neurologi
23 nzyme beta-galactocerebrosidase (GALC) cause Krabbe disease, a devastating genetic disorder character
26 data, together with a lack of therapies for Krabbe's disease, prompted the current preclinical study
28 the disease is the classical infantile form (Krabbe disease), later-onset forms also have been descri
31 rlier with globoid cell leukodystrophy (GLD, Krabbe disease) by his severe deficiency of galactocereb
32 Infantile globoid cell leukodystrophy (GLD, Krabbe disease) is a demyelinating disease caused by the
33 Infantile globoid cell leukodystrophy (GLD, Krabbe disease) is a fatal demyelinating disorder caused
38 thogenic mutations on GALC function in human Krabbe variants and a compelling explanation for the sev
42 structurally and functionally compromised in Krabbe disease, even before demyelination, suggesting a
44 changes conducive to muscle degeneration in Krabbe disease using the murine (twitcher mouse) and can
45 work indicates that muscular dysfunction in Krabbe disease is compounded by a pathogenic mechanism i
46 itcher, has a nonsense mutation not found in Krabbe patients, although it is similar to the human 30
47 ent inflammatory response here identified in Krabbe disease and the other neurodegenerative disorders
48 osyl ceramidase, i.e., the enzyme lacking in Krabbe disease, upon psychosine treatment suggest that p
52 ve capabilities play no instrumental role in Krabbe disease; however, putative kinase-independent fun
59 literature that reclassifies late-infantile Krabbe disease to be symptom onset at 12 to 36 months of
61 unrelated donors in newborns with infantile Krabbe's disease favorably altered the natural history o
62 (age range, 142 to 352 days) with infantile Krabbe's disease underwent transplantation of umbilical-
64 le globoid cell leukodystrophy (GLD) in man (Krabbe disease) and in several other mammalian species,
70 evidence of the expression of iNOS in CNS of Krabbe patient and show that the iNOS-expressing cells i
73 xpression of Ripk1 in the authentic model of Krabbe disease strongly resemble those reported in Alzhe
77 rapy known as fingolimod in a mouse model of Krabbe's disease (namely, the twitcher mouse model) sign
79 ify the role of Ripk1 in the pathogenesis of Krabbe disease, we first explored the contribution of it
83 Cst7 and Ch25h, correlated with severity of Krabbe disease genetically modelled in the twitcher mous
84 formed an observational post-mortem study of Krabbe disease brain tissue (n = 4) compared to infant c
85 P receptors as drug targets for treatment of Krabbe's disease.SIGNIFICANCE STATEMENT This study demon
86 red as protective in our previous studies on Krabbe disease, which is caused by mutations in both GAL
88 We report the presentation of late-onset Krabbe's disease in 2 siblings, a 17-year-old boy and hi
95 ation in each glial cell type contributes to Krabbe pathogenesis, we used conditional Galc-floxed mic
96 The inflammasome signature is not unique to Krabbe disease; to varying degrees, this signature is al
100 atrophy of skeletal muscles in patients with Krabbe disease is a major debilitating manifestation tha
101 re of abnormal white matter in patients with Krabbe disease, (b) are more sensitive than T2-weighted
102 al abilities of late-infantile patients with Krabbe disease, particularly those who underwent transpl