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1 aracterize the peripheral neuropathy seen in Krabbe disease.
2  novel target to complement in therapies for Krabbe disease.
3 ychosine, the neurotoxin that accumulates in Krabbe disease.
4 se (GALC), the lysosomal enzyme deficient in Krabbe disease.
5 missense mutation in patients with infantile Krabbe disease.
6 found in nerve samples from a mouse model of Krabbe disease.
7 erability of various neuronal populations in Krabbe disease.
8  aspect for the mechanism of pathogenesis in Krabbe disease.
9  the nervous system causing the neurological Krabbe disease.
10 and ONOO- may play a role in pathogenesis of Krabbe disease.
11 of decreased hyperintensity in patients with Krabbe disease.
12 te-onset GLD and in 1 patient with classical Krabbe disease.
13 ion of neuroinflammation in a mouse model of Krabbe disease.
14 e value of AAV-based combination therapy for Krabbe disease.
15 y directly contribute to the pathogenesis of Krabbe disease.
16 ways in twitcher mice, an authentic model of Krabbe disease.
17 globoid cell leukodystrophy, better known as Krabbe disease.
18  and effective inhibitors of ACDase to treat Krabbe disease.
19  infantile globoid cell leukodystrophy (GLD [Krabbe disease]).
20 nzyme beta-galactocerebrosidase (GALC) cause Krabbe disease, a devastating genetic disorder character
21                                              Krabbe disease, also named globoid cell (GC) leukodystro
22                                              Krabbe disease, an inherited leukodystrophy, is a sphing
23                       In eight patients with Krabbe disease and eight age-matched control subjects, a
24 ent inflammatory response here identified in Krabbe disease and the other neurodegenerative disorders
25 le globoid cell leukodystrophy (GLD) in man (Krabbe disease) and in several other mammalian species,
26  and GM2 gangliosidosis; Fabry, Gaucher, and Krabbe diseases; and metachromatic leukodystrophy).
27 re of abnormal white matter in patients with Krabbe disease, (b) are more sensitive than T2-weighted
28      To determine whether alpha-synuclein in Krabbe disease brain displayed disease-associated pathog
29 formed an observational post-mortem study of Krabbe disease brain tissue (n = 4) compared to infant c
30 rlier with globoid cell leukodystrophy (GLD, Krabbe disease) by his severe deficiency of galactocereb
31                         Approximately 85% of Krabbe disease cases are the infantile subtypes, among w
32 sease, confirming the prion-like capacity of Krabbe disease-derived alpha-synuclein.
33 structurally and functionally compromised in Krabbe disease, even before demyelination, suggesting a
34                    Patients with early-onset Krabbe disease (four girls and three boys) underwent dif
35  Cst7 and Ch25h, correlated with severity of Krabbe disease genetically modelled in the twitcher mous
36        To explore whether alpha-synuclein in Krabbe disease has pathological similarities to that in
37 ve capabilities play no instrumental role in Krabbe disease; however, putative kinase-independent fun
38                                              Krabbe disease is a devastating neurodegenerative diseas
39                                              Krabbe disease is a devastating pediatric leukodystrophy
40         Globoid cell leukodystrophy (GLD) or Krabbe disease is a devastating, degenerative neurologic
41 atrophy of skeletal muscles in patients with Krabbe disease is a major debilitating manifestation tha
42         Globoid cell leukodystrophy (GLD) or Krabbe disease is a neurodegenerative disorder caused by
43                                    Infantile Krabbe disease is a rapidly progressive and fatal disord
44                                              Krabbe disease is a rare neurodegenerative disorder caus
45                                              Krabbe disease is an infantile neurodegenerative disorde
46                                              Krabbe disease is caused by a deficiency of the lysosoma
47                                              Krabbe disease is characterized by GALC deficiency and S
48  work indicates that muscular dysfunction in Krabbe disease is compounded by a pathogenic mechanism i
49  Infantile globoid cell leukodystrophy (GLD, Krabbe disease) is a demyelinating disease caused by the
50  Infantile globoid cell leukodystrophy (GLD, Krabbe disease) is a fatal demyelinating disorder caused
51            Globoid cell leukodystrophy (GLD, Krabbe disease) is a lysosomal storage disease (LSD) cau
52            Globoid cell leukodystrophy (GLD; Krabbe disease) is a progressive, incurable neurodegener
53           Globoid cell leukodystrophy (GLD) (Krabbe disease) is an autosomal recessive, degenerative,
54        The typical infantile disease in man (Krabbe disease) is caused by deficiency of lysosomal gal
55                 Globoid cell leukodystrophy (Krabbe disease) is characterized by the accumulation of
56            Globoid cell leukodystrophy (GLD, Krabbe disease) is diagnosed by measuring galactosylcera
57            Globoid cell leukodystrophy (GLD, Krabbe disease) is due to autosomal recessive mutations
58 oid cell leukodystrophy (GLD), also known as Krabbe disease, is a devastating, degenerative neurologi
59              Globoid cell leukodystrophy, or Krabbe disease, is a severe, autosomal recessive disorde
60                                              Krabbe disease (KD) and metachromatic leukodystrophy (ML
61                                              Krabbe disease (KD) is a lysosomal storage disease (LSD)
62                                              Krabbe disease (KD) is a neurodegenerative lysosomal dis
63                                              Krabbe disease (KD) is caused by a deficiency of galacto
64                      Mutations in GALC cause Krabbe disease (KD), a fatal neurological lysosomal diso
65                 In twitcher mice (a model of Krabbe disease [KD]), a central nervous system (CNS)-pen
66 the disease is the classical infantile form (Krabbe disease), later-onset forms also have been descri
67                                              Krabbe disease or globoid cell leukodystrophy (GLD) is a
68 al abilities of late-infantile patients with Krabbe disease, particularly those who underwent transpl
69                    Differences in RA between Krabbe disease patients and control subjects were signif
70          Our study describes a new aspect of Krabbe disease, placing patients at risk of immune-relat
71 t an important role for neuroinflammation in Krabbe disease progression.
72 xpression of Ripk1 in the authentic model of Krabbe disease strongly resemble those reported in Alzhe
73                                           In Krabbe disease, the brunt of demyelination and neurodege
74  literature that reclassifies late-infantile Krabbe disease to be symptom onset at 12 to 36 months of
75  The inflammasome signature is not unique to Krabbe disease; to varying degrees, this signature is al
76  therapeutic efficacy in the murine model of Krabbe disease (Twitcher).
77 osyl ceramidase, i.e., the enzyme lacking in Krabbe disease, upon psychosine treatment suggest that p
78  changes conducive to muscle degeneration in Krabbe disease using the murine (twitcher mouse) and can
79 ify the role of Ripk1 in the pathogenesis of Krabbe disease, we first explored the contribution of it
80 ants of human globoid cell leukodystrophy or Krabbe disease, were investigated.
81 red as protective in our previous studies on Krabbe disease, which is caused by mutations in both GAL