ライフサイエンスコーパス: Sandhoff disease

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1 rains from this mouse model of Tay-Sachs and Sandhoff disease.

2 storage diseases: NPC, mucolipidosis IV, and Sandhoff disease.

3 ivation also was detected in a human case of Sandhoff disease.

4 -deficient mice, a model of the neuronopathy Sandhoff disease.

5 Sandhoff disease, a GM2 gangliosidosis caused by a defic

6 y and prolonged survival in a mouse model of Sandhoff disease, a lethal gangliosidosis.

7 in neurodegeneration using a mouse model of Sandhoff disease, a prototypical neuronopathic lysosomal

8 ices of postmortem human GM1 gangliosidosis, Sandhoff disease, and Tay-Sachs disease brains.

9 e conditions that include Tay-Sachs disease, Sandhoff disease, and the GM2 activator deficiency.

10 n as the AB variant), Tay-Sachs disease, and Sandhoff disease are the major forms of the GM2 ganglios

11 Tay-Sachs and Sandhoff diseases are caused by mutations in the genes (

12 Tay-Sachs and Sandhoff diseases are lysosomal storage disorders charac

13 The GM2 gangliosidoses, Tay-Sachs and Sandhoff diseases, are caused by mutations in the HEXA (

14 GM2 gangliosidoses, including Tay-Sachs and Sandhoff diseases, are neurodegenerative lysosomal stora

15 GINI was tested on colon cancer and Sandhoff disease cell lines, which contained previously

16 olipid storage diseases, NPC2 deficiency and Sandhoff disease, characterized by sphingolipid traffick

17 he results indicate that the pathogenesis of Sandhoff disease involves an increase in MIP-1alpha that

18 Sandhoff disease is a lysosomal storage disorder charact

19 Sandhoff disease is a prototypical lysosomal storage dis

20 Sandhoff disease is an autosomal recessive disorder caus

21 that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redundancy in the

22 crophage/microglial population in the CNS of Sandhoff disease mice is compounded by the infiltration

23 Bone marrow transplantation of Sandhoff disease mice suppressed both the explosive expa

24 sphingosine kinase 1 (Sphk1) was deleted in Sandhoff disease mice, a milder disease course occurred,

25 In symptomatic Sandhoff disease mice, apoptotic neuronal cell death was

26 otor dysfunction and a prolonged lifespan in Sandhoff disease mice.

27 the terminal stages of neurodegeneration in Sandhoff disease mice.

28 athology together with neuronal apoptosis in Sandhoff disease mice.

29 ganglioside accumulation in a mouse model of Sandhoff disease might be associated with the accumulati

30 is phenotype is not seen in the Tay-Sachs or Sandhoff disease model mice or in the corresponding huma

31 etry to monitor efficacy of this approach in Sandhoff disease model mice.

32 ount of beta-hexosaminidase S present in the Sandhoff disease model mice.

33 ential treatment for these disorders using a Sandhoff disease mouse model.

34 cerebral cortex from a Tay-Sachs patient, a Sandhoff disease patient and a pediatric control.

35 An authentic mouse model of Sandhoff disease (SD) with pathological characteristics

36 ents a 22-month-old girl with infantile type Sandhoff disease that was hospitalized for generalized s

37 exb gene (hexb-/-), a model of Tay-Sachs and Sandhoff disease, versus the functionally normal heteroz

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