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Dominantly inherited\n CADASIL<\/jats:styled-content>\n is caused by mutations (n\u2009>\u2009230) in\n \n NOTCH<\/jats:italic>\n <\/jats:styled-content>\n 3<\/jats:italic>\n gene, which encodes Notch3 receptor expressed in vascular smooth muscle cells (\n VSMC<\/jats:styled-content>\n ). Notch3 extracellular domain (\n N<\/jats:styled-content>\n 3\n ECD<\/jats:styled-content>\n ) accumulates in arterial walls followed by\n VSMC<\/jats:styled-content>\n degeneration and subsequent fibrosis and stenosis of arterioles, predominantly in cerebral white matter, where characteristic ischemic\n MRI<\/jats:styled-content>\n changes and lacunar infarcts emerge. The likely pathogenesis of\n CADASIL<\/jats:styled-content>\n is toxic gain of function related to mutation\u2010induced unpaired cysteine in\n N<\/jats:styled-content>\n 3\n ECD<\/jats:styled-content>\n . Definite diagnosis is made by molecular genetics but is also possible by electron microscopic demonstration of pathognomonic granular osmiophilic material at\n VSMC<\/jats:styled-content>\n s or by positive immunohistochemistry for\n N<\/jats:styled-content>\n 3\n ECD<\/jats:styled-content>\n in dermal arteries.\n <\/jats:p>\n \n In rare, recessively inherited\n CARASIL<\/jats:styled-content>\n the clinical picture and white matter changes are similar as in\n CADASIL<\/jats:styled-content>\n , but cognitive decline begins earlier. In addition, gait disturbance, low back pain and alopecia are characteristic features.\n CARASIL<\/jats:styled-content>\n is caused by mutations (presently n\u2009=\u200910) in high\u2010temperature requirement. A serine peptidase 1 (\n \n HTRA<\/jats:italic>\n <\/jats:styled-content>\n 1<\/jats:italic>\n ) gene, which result in reduced function of\n HTRA<\/jats:styled-content>\n 1 as repressor of transforming growth factor\u2010\u03b2 (\n TGF<\/jats:styled-content>\n \u03b2) \u2010signaling. Cerebral arteries show loss of\n VSMC<\/jats:styled-content>\n s and marked hyalinosis, but not stenosis.\n <\/jats:p>","DOI":"10.1111\/bpa.12181","type":"journal-article","created":{"date-parts":[[2014,10,16]],"date-time":"2014-10-16T08:39:58Z","timestamp":1413448798000},"page":"525-544","source":"Crossref","is-referenced-by-count":185,"title":["CADASIL<\/scp>\n and\n CARASIL<\/scp>"],"prefix":"10.1111","volume":"24","author":[{"given":"Saara","family":"Tikka","sequence":"first","affiliation":[{"name":"Protein Chemistry Unit, Institute of Biomedicine\/Anatomy University of Helsinki Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Baumann","sequence":"additional","affiliation":[{"name":"Protein Chemistry Unit, Institute of Biomedicine\/Anatomy University of Helsinki Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maija","family":"Siitonen","sequence":"additional","affiliation":[{"name":"Department of 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