{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T20:44:25Z","timestamp":1761597865741,"version":"3.41.2"},"reference-count":51,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2017,10,16]],"date-time":"2017-10-16T00:00:00Z","timestamp":1508112000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2017,11]]},"abstract":"Abstract<\/jats:title>Objectives<\/jats:title>Cerebral microbleeds (CMB<\/jats:styled-content>s) are often observed in memory clinic patients. It has been generally accepted that deep CMB<\/jats:styled-content>s (D\u2010CMB<\/jats:styled-content>s) result from hypertensive vasculopathy (HV<\/jats:styled-content>), whereas strictly lobar CMB<\/jats:styled-content>s (SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s) result from cerebral amyloid angiopathy (CAA<\/jats:styled-content>) which frequently coexists with Alzheimer's disease (AD<\/jats:styled-content>). Mixed CMB<\/jats:styled-content>s (M\u2010CMB<\/jats:styled-content>s) have been partially attributed to HV<\/jats:styled-content> and also partially attributed to CAA<\/jats:styled-content>. The aim of this study was to elucidate the differences between SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s and M\u2010CMB<\/jats:styled-content>s in terms of clinical features and regional distribution.<\/jats:p><\/jats:sec>Materials<\/jats:title>We examined 176 sequential patients in our memory clinic for clinical features and CMB<\/jats:styled-content> location using susceptibility\u2010weighted images obtained on a 3T\u2010MRI<\/jats:styled-content>. The number of lobar CMB<\/jats:styled-content>s in SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s and M\u2010CMB<\/jats:styled-content>s was counted in each cerebral lobe and their regional density was adjusted according to the volume of each lobe.<\/jats:p><\/jats:sec>Results<\/jats:title>Of the total 176 patients, 111 patients (63.1%) had CMB<\/jats:styled-content>s. Within the patients who had CMB<\/jats:styled-content>s, M\u2010CMB<\/jats:styled-content>s were found in 54 patients (48.6%), followed by SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s in 35 (31.5%) and D\u2010CMB<\/jats:styled-content>s in 19 (17.1%). The SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content> group showed a significantly higher prevalence of family history of dementia, whereas the M\u2010CMB<\/jats:styled-content> group showed an increasing trend toward hypertension and smoking. The prevalence of AD<\/jats:styled-content> was significantly higher in the SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s group, whereas the prevalence of AD<\/jats:styled-content> with cerebrovascular disease was higher in the M\u2010CMB<\/jats:styled-content>s group. The regional density of lobar CMB<\/jats:styled-content>s was significantly higher in the occipital lobe in the M\u2010CMB<\/jats:styled-content> group, whereas the SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content> group showed higher regional density between regions an increasing tendency in the parietal and occipital lobe.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>The between\u2010group differences in clinical features and regional distribution indicate there to be an etiological relationship of SL<\/jats:styled-content>\u2010CMB<\/jats:styled-content>s to AD<\/jats:styled-content> and CAA<\/jats:styled-content>, and M\u2010CMB<\/jats:styled-content>s to both HV<\/jats:styled-content> and CAA<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1002\/brb3.856","type":"journal-article","created":{"date-parts":[[2017,10,16]],"date-time":"2017-10-16T07:04:57Z","timestamp":1508137497000},"source":"Crossref","is-referenced-by-count":11,"title":["Background and distribution of lobar microbleeds in cognitive dysfunction"],"prefix":"10.1002","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9137-562X","authenticated-orcid":false,"given":"Hirofumi","family":"Matsuyama","sequence":"first","affiliation":[{"name":"Department of Neurology Mie University Graduate School of Medicine Tsu Mie Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuichiro","family":"Ii","sequence":"additional","affiliation":[{"name":"Department of Neurology Mie University Graduate School of Medicine Tsu Mie Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masayuki","family":"Maeda","sequence":"additional","affiliation":[{"name":"Department of Advanced Diagnostic Imaging Mie University Graduate School of Medicine Tsu Mie Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maki","family":"Umino","sequence":"additional","affiliation":[{"name":"Department of Radiology Mie University Graduate School of Medicine Tsu 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