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We previously showed elevated activity of the endothelin and angiotensin pathways in <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>lzheimer's disease (<jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>). We have measured endothelin\u20101 (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101) level and angiotensin\u2010converting enzyme (<jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>) activity in the occipital cortex in <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content> and control brains. We also measured vascular endothelial growth factor (<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>); factor <jats:styled-content style=\"fixed-case\">VIII<\/jats:styled-content>\u2010related antigen (<jats:styled-content style=\"fixed-case\">FVIIIRA<\/jats:styled-content>) to indicate microvessel density; myelin\u2010associated glycoprotein (<jats:styled-content style=\"fixed-case\">MAG<\/jats:styled-content>), a marker of ante\u2010mortem hypoperfusion; total \u03b1\u2010synuclein (\u03b1\u2010syn) and \u03b1\u2010synuclein phosphorylated at <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>er129 (\u03b1\u2010syn\u2010p129). In contrast to findings in <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content> activity and <jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>\u20101 level were unchanged in <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content> compared with controls. <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">FVIIIRA<\/jats:styled-content> levels were, however, significantly lower in <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> correlated positively with <jats:styled-content style=\"fixed-case\">MAG<\/jats:styled-content> concentration (in keeping with a relationship between reduction in <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> and hypoperfusion), and negatively with \u03b1\u2010syn and \u03b1\u2010syn\u2010p129 levels. Both \u03b1\u2010syn and \u03b1\u2010syn\u2010p129 levels increased in human <jats:styled-content style=\"fixed-case\">SH<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">SY<\/jats:styled-content>5<jats:styled-content style=\"fixed-case\">Y<\/jats:styled-content> neuroblastoma cells after oxygen\u2010glucose deprivation (<jats:styled-content style=\"fixed-case\">OGD<\/jats:styled-content>), and <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> level was reduced in <jats:styled-content style=\"fixed-case\">SH<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">SY<\/jats:styled-content>5<jats:styled-content style=\"fixed-case\">Y<\/jats:styled-content> cells overexpressing \u03b1\u2010syn. Taken together, our findings suggest that reduced microvessel density rather than vasoconstriction is responsible for lower occipital blood flow in <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>, and that the loss of microvessels may result from <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> deficiency, possible secondary to the accumulation of \u03b1\u2010syn.<\/jats:p>","DOI":"10.1111\/bpa.12130","type":"journal-article","created":{"date-parts":[[2014,2,13]],"date-time":"2014-02-13T07:04:35Z","timestamp":1392275075000},"page":"334-343","source":"Crossref","is-referenced-by-count":43,"title":["Reduced Vascular Endothelial Growth Factor and Capillary Density in the Occipital Cortex in Dementia with <scp>L<\/scp>ewy Bodies"],"prefix":"10.1111","volume":"24","author":[{"given":"Scott","family":"Miners","sequence":"first","affiliation":[{"name":"Dementia Research Group Institute of Clinical Neurosciences School of Clinical Sciences University 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