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However, the mechanisms by which end\u2010organ dysfunction arise are poorly understood. Here, we report strikingly diminished cerebral microvascular density in a murine model of disease, and provide a detailed analysis of the accompanying cerebral glycosphingolipidome in these animals, with marked elevations of \u03b2\u2010glucosylsphingosine. Further\n                    <jats:italic>in vitro<\/jats:italic>\n                    studies confirmed a concentration\u2010dependent impairment of endothelial cytokinesis upon exposure to quasi\u2010pathological concentrations of \u03b2\u2010glucosylsphingosine. These findings support a premise for pathogenic disruption of cerebral angiogenesis as an end\u2010organ effect, with potential for therapeutic modulation in neuronopathic Gaucher disease. Copyright \u00a9 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.4992","type":"journal-article","created":{"date-parts":[[2017,10,5]],"date-time":"2017-10-05T10:17:01Z","timestamp":1507198621000},"page":"120-128","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Reduced cerebral vascularization in experimental neuronopathic Gaucher disease"],"prefix":"10.1002","volume":"244","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2409-9239","authenticated-orcid":false,"given":"Nicholas JC","family":"Smith","sequence":"first","affiliation":[{"name":"Department of Neurology and Clinical Neurophysiology Women's and Children's Health Network  Adelaide South Australia Australia"},{"name":"School of Medicine University of Adelaide  Adelaide South Australia Australia"},{"name":"Department of Medicine University of Cambridge  Cambridge 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