{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:46:48Z","timestamp":1791406008596,"version":"4.3.3"},"reference-count":22,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,3,8]],"date-time":"2013-03-08T00:00:00Z","timestamp":1362700800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain Pathology"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We quantified vascular changes in the frontal lobe and basal ganglia of four inherited small vessel diseases (<jats:styled-content style=\"fixed-case\">SVDs<\/jats:styled-content>) including cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (<jats:styled-content style=\"fixed-case\">CADASIL<\/jats:styled-content>), pontine autosomal dominant microangiopathy and leukoencephalopathy (<jats:styled-content style=\"fixed-case\">PADMAL<\/jats:styled-content>), hereditary multi\u2010infarct dementia of<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>wedish type (<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>wedish h<jats:styled-content style=\"fixed-case\">MID<\/jats:styled-content>), and hereditary endotheliopathy with retinopathy, nephropathy, and stroke (<jats:styled-content style=\"fixed-case\">HERNS<\/jats:styled-content>). Vascular pathology was most severe in<jats:styled-content style=\"fixed-case\">CADASIL<\/jats:styled-content>, and varied with marginally greater severity in the basal ganglia compared to the frontal lobe. The overall sclerotic index values in frontal lobe were in the order<jats:styled-content style=\"fixed-case\">CADASIL<\/jats:styled-content>\u2009\u2265\u2009<jats:styled-content style=\"fixed-case\">HERNS<\/jats:styled-content>\u2009&gt;\u2009<jats:styled-content style=\"fixed-case\">PADMAL<\/jats:styled-content>\u2009&gt;\u2009<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>wedish h<jats:styled-content style=\"fixed-case\">MID<\/jats:styled-content>\u2009&gt;\u2009sporadic<jats:styled-content style=\"fixed-case\">SVD<\/jats:styled-content>, and in basal ganglia<jats:styled-content style=\"fixed-case\">CADASIL<\/jats:styled-content>\u2009&gt;\u2009<jats:styled-content style=\"fixed-case\">HERNS<\/jats:styled-content>\u2009&gt;\u2009<jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>wedish h<jats:styled-content style=\"fixed-case\">MID<\/jats:styled-content>\u2009&gt;\u2009<jats:styled-content style=\"fixed-case\">PADMAL<\/jats:styled-content>&gt; sporadic<jats:styled-content style=\"fixed-case\">SVD<\/jats:styled-content>. The subcortical white matter was almost always more affected than any gray matter. We observed glucose transporter\u20101 (<jats:styled-content style=\"fixed-case\">GLUT<\/jats:styled-content>\u20101) protein immunoreactivities were most affected in the white matter indicating capillary degeneration whereas collagen<jats:styled-content style=\"fixed-case\">IV<\/jats:styled-content>(<jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>4) immunostaining was increased in<jats:styled-content style=\"fixed-case\">PADMAL<\/jats:styled-content>cases in all regions and tissue types. Overall,<jats:styled-content style=\"fixed-case\">GLUT<\/jats:styled-content>\u20101\u2009:\u2009<jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>4 ratios were higher in the basal ganglia indicating modifications in capillary density compared to the frontal lobe. Our study shows that the extent of microvascular degeneration varies in these genetic disorders exhibiting common end\u2010stage pathologies but is the most aggressive in<jats:styled-content style=\"fixed-case\">CADASIL<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/bpa.12041","type":"journal-article","created":{"date-parts":[[2013,2,6]],"date-time":"2013-02-06T13:07:08Z","timestamp":1360156028000},"page":"547-557","source":"Crossref","is-referenced-by-count":56,"title":["Quantitative Vascular Pathology and Phenotyping Familial and Sporadic Cerebral Small Vessel Diseases"],"prefix":"10.1111","volume":"23","author":[{"given":"Lucinda J. L.","family":"Craggs","sequence":"first","affiliation":[{"name":"Centre for Brain Ageing and Vitality Institute for Ageing and Health Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Hagel","sequence":"additional","affiliation":[{"name":"Institute of Neuropathology University Medical Center Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregor","family":"Kuhlenbaeumer","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurobiology Institute of Experimental Medicine University of Kiel Kiel Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne","family":"Borjesson\u2010Hanson","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience and Physiology Sahlgrenska Academy at G\u00f6teborg University Goteborg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oluf","family":"Andersen","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience and Physiology Sahlgrenska Academy at G\u00f6teborg University Goteborg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matti","family":"Viitanen","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences Karolinska Institute Huddinge Hospital Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannu","family":"Kalimo","sequence":"additional","affiliation":[{"name":"Department of Neuropathology Helsinki University Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catriona A.","family":"McLean","sequence":"additional","affiliation":[{"name":"Anatomical Pathology Department The Alfred Hospital Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet Y.","family":"Slade","sequence":"additional","affiliation":[{"name":"Centre for Brain Ageing and Vitality Institute for Ageing and Health Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roslyn A.","family":"Hall","sequence":"additional","affiliation":[{"name":"Centre for Brain Ageing and Vitality Institute for Ageing and Health Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur E.","family":"Oakley","sequence":"additional","affiliation":[{"name":"Centre for Brain Ageing and Vitality Institute for Ageing and Health Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yumi","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Centre for Brain Ageing and Vitality Institute for Ageing and Health Newcastle University Newcastle upon Tyne 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