{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T19:49:13Z","timestamp":1760384953255},"reference-count":20,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T00:00:00Z","timestamp":1138060800000},"content-version":"vor","delay-in-days":1180,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2002,11]]},"abstract":"<jats:p><jats:bold>A<jats:sc>bstract<\/jats:sc>: <\/jats:bold> Cerebrovascular deposition of the amyloid beta\u2010protein (A\u03b2) is a common pathologic event in patients with Alzheimer's disease (AD) and certain related disorders. Such an A\u03b2 vascular deposition occurs primarily in the medial layer of the cerebral vessel wall in an assembled fibrillar state. These deposits are associated with several pathological responses, including degeneration of the smooth muscle cells in the cerebral vessel wall. Severe cases of cerebrovascular A\u03b2 deposition are also accompanied by loss of vessel wall integrity and hemorrhagic stroke. Although the reasons for this pathological consequence are unclear, altered proteolytic mechanisms within the cerebral vessel wall may be involved. We analyzed cerebral A\u03b2 deposition in brains with AD and Dutch\u2010type hereditary cerebral hemorrhage with amyloidosis (HCHWA\u2010D) on the basis of two amyloid species of A\u03b2<jats:sub>40<\/jats:sub> and A\u03b2<jats:sub>42\/43<\/jats:sub> using specific monoclonal antibodies. Compared to A\u03b2 deposition in senile plaques, the molecular composition of A\u03b2 was distinguishable, indicating that the A\u03b2<jats:sub>40<\/jats:sub> species is the main component for vascular amyloid. Furthermore, we found A\u03b2<jats:sub>42\/43<\/jats:sub> immunoreactivity was also much increased in amyloid angiopathy of all cases with HCHWA\u2010D. Taken together, amyloid angiopathy in HCHWA\u2010D may share an A\u03b2<jats:sub>42<\/jats:sub>\u2010driven deposition mechanism with plaque amyloid, resulting in enhanced A\u03b2<jats:sub>40<\/jats:sub> deposition.<\/jats:p>","DOI":"10.1111\/j.1749-6632.2002.tb04810.x","type":"journal-article","created":{"date-parts":[[2009,7,9]],"date-time":"2009-07-09T19:51:19Z","timestamp":1247169079000},"page":"149-154","source":"Crossref","is-referenced-by-count":11,"title":["Enhanced A\u03b2<sub>40<\/sub> Deposition Was Associated with Increased A\u03b2<sub>42\/43<\/sub> in Cerebral Vasculature with Dutch\u2010Type Hereditary Cerebral Hemorrhage with Amyloidosis (HCHWA\u2010D)"],"prefix":"10.1111","volume":"977","author":[{"given":"K.","family":"OZAWA","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T.","family":"TOMIYAMA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. L.","family":"MAAT\u2010SCHIEMAN","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. A.","family":"ROOS","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"MORI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,1,24]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.16.5991"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004010050793"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00002093-199601040-00008"},{"key":"e_1_2_5_5_2","first-page":"518","article-title":"DNA diagnosis for hereditary cerebral hemorrhage with amyloidosis (Dutch type)","volume":"49","author":"Bakker E.","year":"1991","journal-title":"Am. J. Hum. 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