conduritol/atrofie

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LidwoordKlinische proevenOctrooien

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[Experimental [corrected] study of hypoglycemic activity of conduritol A of stems of Gymnema sylvestre].

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OBJECTIVE To investigates the mechanism of hypooglycemic effect of conduritol A of stems of Gymnema sylvestre. METHODS Fourteen days later after administration, observation is taken on the change of these mice and rats weight, the FBG, TG, CHO, SOD, MDA, INS, TNF in serum were also detected with

Dependence of reversibility and progression of mouse neuronopathic Gaucher disease on acid beta-glucosidase residual activity levels.

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Genetic and chemically induced neuronopathic mouse models of Gaucher disease were developed to facilitate understanding of the reversibility and/or progression of CNS involvement. The lethality of the skin permeability barrier defect of the complete gene knock out [gba, (glucocerebrosidase) GCase]

Differential effects of glycolipid biosynthesis inhibitors on ceramide-induced cell death in neuroblastoma cells.

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An in vitro model of Gaucher's disease in murine neuroblastoma x rat glioma NG108-15 cells was used to investigate the physiological effects of two specific inhibitors of glucosylceramide synthase, d,l-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (d,l-PDMP) and N-butyldeoxynojirimycin

Sustained Systemic Glucocerebrosidase Inhibition Induces Brain α-Synuclein Aggregation, Microglia and Complement C1q Activation in Mice.

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OBJECTIVE Loss-of-function mutations in GBA1, which cause the autosomal recessive lysosomal storage disease, Gaucher disease (GD), are also a key genetic risk factor for the α-synucleinopathies, including Parkinson's disease (PD) and dementia with Lewy bodies. GBA1 encodes for the lysosomal

Inhibition of β-Glucocerebrosidase Activity Preserves Motor Unit Integrity in a Mouse Model of Amyotrophic Lateral Sclerosis.

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Recent metabolomic reports connect dysregulation of glycosphingolipids, particularly ceramide and glucosylceramide, to neurodegeneration and to motor unit dismantling in amyotrophic lateral sclerosis at late disease stage. We report here altered levels of gangliosides in the cerebrospinal fluid of

Development and biochemical characterization of a mouse model of Parkinson's disease bearing defective glucocerebrosidase activity.

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GBA1 gene encodes for the lysosomal membrane protein glucocerebrosidase (GCase). GBA1 heterozygous mutations profoundly impair GCase activity and are currently recognized as an important risk factor for the development of Parkinson's disease (PD). Deficits in lysosomal degradation pathways may

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