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We therefore studied whether longstanding cerebral hypoperfusion is associated with Alzheimer pathology in nondemented humans.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Cerebral blood flow and amyloid \u03b2 (<jats:sup>18<\/jats:sup>F\u2010Flutemetamol) positron emission tomography retention were assessed in eleven patients with unilateral occlusion of precerebral arteries resulting in chronic and uneven hypoperfusion. A subset of patients underwent tau (<jats:sup>18<\/jats:sup>F\u2010AV\u20101451) positron emission tomography.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The blood flow was significantly reduced on the affected side of the brain in patients with unilateral occlusion of the internal carotid artery or stenosis of the middle cerebral artery. However, the cortical uptake of <jats:sup>18<\/jats:sup>F\u2010Flutemetamol or <jats:sup>18<\/jats:sup>F\u2010AV\u20101451 was not altered.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>Our results suggest that longstanding cerebral hypoperfusion in humans does not result in accumulation of amyloid \u03b2 fibrils or tau aggregates.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.jalz.2017.06.2265","type":"journal-article","created":{"date-parts":[[2017,7,15]],"date-time":"2017-07-15T13:01:06Z","timestamp":1500123666000},"page":"54-61","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Cerebral hypoperfusion is not associated with an increase in amyloid \u03b2 pathology in middle\u2010aged or elderly people"],"prefix":"10.1002","volume":"14","author":[{"given":"Oskar","family":"Hansson","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences Malm\u00f6, Clinical Memory Research 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