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Hippocampal volume was estimated by manually drawing regions of interest on relevant scan slices; HA was defined as the lowest quartile of hippocampal volume. Also assessed on the MRI were cortical and subcortical infarcts, lacunes, and white matter hyperintensities. The risk (OR, 95% CI) was estimated for HA associated with systolic (&lt;140 versus \u2265140 mm Hg) and diastolic (&lt;90 versus \u226590 mm Hg) BP and with antihypertensive treatment. Analyses were adjusted for sociodemographic factors, other cardiovascular risk factors, apolipoprotein E allele, and correlated brain pathology. Those never treated with antihypertensive medication had a significantly increased risk for HA (OR 1.7; CI=1.12; 2.65). The nontreated subjects with high systolic BP had an increased risk (OR=1.98; CI=0.89; 4.39) for HA. Results were similar for untreated men with high diastolic BP (OR=3.51; CI=1.26; 9.74). In conclusion, treatment with antihypertensive treatment modifies the association of BP and HA, such that high levels of BP adversely affect the hippocampus in persons never treated with antihypertensives.<\/jats:p>","DOI":"10.1161\/01.hyp.0000132475.32317.bb","type":"journal-article","created":{"date-parts":[[2004,5,24]],"date-time":"2004-05-24T21:03:42Z","timestamp":1085432622000},"page":"29-34","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":204,"title":["Midlife Blood Pressure and the Risk of Hippocampal Atrophy"],"prefix":"10.1161","volume":"44","author":[{"given":"Esther S.C.","family":"Korf","sequence":"first","affiliation":[{"name":"From the Department of Neurology and Alzheimer Center (E.S.C.K., P.S.), Vrije Universiteit Medical Center, Amsterdam, the Netherlands; Pacific Health Research Institute (L.R.W.), Honolulu, Hawaii; and the Laboratory of Epidemiology, Demography, and Biometry (L.J.L.), National Institute on Aging, National Institutes of Health, Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lon R.","family":"White","sequence":"additional","affiliation":[{"name":"From the Department of Neurology and Alzheimer Center (E.S.C.K., P.S.), Vrije Universiteit Medical Center, Amsterdam, the Netherlands; Pacific Health Research Institute (L.R.W.), Honolulu, Hawaii; and the Laboratory of Epidemiology, Demography, and Biometry (L.J.L.), National Institute on Aging, National Institutes of Health, Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip","family":"Scheltens","sequence":"additional","affiliation":[{"name":"From the Department of Neurology and Alzheimer Center (E.S.C.K., P.S.), Vrije Universiteit Medical Center, Amsterdam, the Netherlands; Pacific Health Research Institute (L.R.W.), Honolulu, Hawaii; and the Laboratory of Epidemiology, Demography, and Biometry (L.J.L.), National Institute on Aging, National Institutes of Health, Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lenore J.","family":"Launer","sequence":"additional","affiliation":[{"name":"From the Department of Neurology and Alzheimer Center (E.S.C.K., P.S.), Vrije Universiteit Medical Center, Amsterdam, the Netherlands; Pacific Health Research Institute (L.R.W.), Honolulu, Hawaii; and the Laboratory of Epidemiology, Demography, and Biometry (L.J.L.), National Institute on Aging, National Institutes of Health, Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.16-16-05233.1996"},{"key":"e_1_3_2_2_2","first-page":"19","volume":"21","year":"2000","unstructured":"Convit A, de Asis J, de Leon MJ, Tarshish CY, De Santi S, Rusinek H. 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