| Literature DB >> 31794880 |
Carley R Corado1, Jason Pinkstaff2, Xuntian Jiang3, Evelyn M Galban4, Samantha J Fisher4, Oriane Scholler1, Chris Russell1, Jessica H Bagel4, Patricia A ODonnell4, Daniel S Ory3, Charles H Vite4, Allison M Bradbury5.
Abstract
Globoid cell leukodystrophy (GLD, Krabbe disease, Krabbe's disease) is caused by genetic mutations in the gene encoding, galactosylceramidase (GALC). Deficiency of this enzyme results in central and peripheral nervous system pathology, and is characterized by loss of myelin and an infiltration of globoid cells. The canine model of GLD provides a translational model which faithfully recapitulates much of the human disease pathology. Targeted lipidomic analysis was conducted in serum and cerebrospinal fluid (CSF) over the lifetime of GLD affected and normal canines, and in brain tissue at humane endpoint to better understand disease progression and identify potential biomarkers of disease. Psychosine, a substrate of GALC and primary contributor to the pathology in GLD, was observed to be significantly elevated in the serum and CSF by 2 or 4 weeks of age, respectively, and steadily increased over the lifetime of affected animals. Importantly, psychosine concentration strongly correlated with disease severity. Galactosylceramide, glucosylceramide, and lactosylceramide were also found to be elevated in the CSF of affected animals and increased with age. Psychosine and galactosylceramide were found to be significantly increased in brain tissue at humane endpoint. This study identified several biomarkers which may be useful in the development of therapeutics for GLD.Entities:
Keywords: Brain lipids; Canine model; Ceramides; Globoid cell leukodystrophy; Liquid chromatography; Mass spectrometry; Sphingolipids
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Year: 2019 PMID: 31794880 PMCID: PMC7032565 DOI: 10.1016/j.mcn.2019.103451
Source DB: PubMed Journal: Mol Cell Neurosci ISSN: 1044-7431 Impact factor: 4.314