Aart Spilt, MD Annelies W. E. Weverling- Rijnsburger, MD Huub A. M. Middelkoop, PhD Wiesje M. van Der Flier, PhD Jacobijn Gussekloo, MD Anton J. M. de Craen, PhD Eduard L. E. M. Bollen, MD Gerard J. Blauw, MD Mark A. van Buchem, MD Rudi G. J. Westendorp, MD Published online before print 10.1148/radiol.2363041454 Radiology 2005; 236:990 –995 Abbreviation: MTR = magnetization transfer ratio 1 From the Departments of Radiology (A.S., M.A.v.B.), General Internal Medi- cine (A.W.E.W., J.G., A.J.M.d.C., G.J.B., R.G.J.W.) and Neurology (H.A.M.M., W.M.v.d.F., E.L.E.M.B.), Leiden Univer- sity Medical Center, Albinusdreef, C2-S, 2333 ZA Leiden, the Netherlands.Re- ceived August 23, 2004; revision re- quested October 29; revision received November 26; accepted January 5, 2005. Address correspondence to A.S. (e-mail: A.Spilt@LUMC.nl). Authors stated no financial relation- ship to disclose. Author contributions: Guarantors of integrity of entire study, A.S., M.A.v.B.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript re- vision for important intellectual con- tent, all authors; approval of final version of submitted manuscript, all au- thors; literature research, A.S., E.L.E.M.B., G.J.B., R.G.J.W.; clinical studies, A.S., A.W.E.W., H.A.M.M., J.G., E.L.E.M.B., G.J.B., R.G.J.W.; experimental studies, A.S., G.J.B.; statistical analysis, A.S., H.A.M.M., A.J.M.d.C., E.L.E.M.B., G.J.B., R.G.J.W.; manuscript editing, A.S., H.A.M.M., W.M.v.d.F., A.J.M.d.C., E.L.E.M.B., G.J.B., M.A.v.B., R.G.J.W. © RSNA, 2005 Late-Onset Dementia: Structural Brain Damage and Total Cerebral Blood Flow 1 PURPOSE: To prospectively compare indicators of structural brain damage and total cerebral blood flow in patients with late-onset dementia, subjects of the same age with optimal cognitive function, and young subjects. MATERIALS AND METHODS: The institutional ethics committee approved the studies, and all participants (or their guardians) gave informed consent. The test group included 17 patients older than 75 years (four men, 13 women; median age, 83 years) and with a diagnosis of dementia according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The control group included 16 subjects (four men, 12 women; median age, 87 years) with optimal cognitive function, who were selected from among 599 elderly subjects enrolled in a popu- lation-based follow-up study, and 15 young healthy subjects (seven men, eight women; median age, 29 years). Measurements of intracranial and total brain volumes, structural brain damage, and cerebral blood flow were obtained with magnetic resonance imaging. Mean values were compared with the t test; medians, with the Mann-Whitney U test. RESULTS: Values for total brain volume were significantly smaller in elderly subjects (P  .001) but did not differ significantly between patients with dementia and subjects of the same age with optimal cognitive function (P = .69). Among the elderly, significantly higher scores for number and extent of white matter areas of signal hyperintensity (P = .028) and lower magnetization transfer ratios (P = .016) indicated greater structural brain damage in those with dementia. Cerebral blood flow was 246 mL/min lower (P  .001) in elderly subjects than in young subjects. In patients with dementia, cerebral blood flow was 108 mL/min lower than that in subjects of the same age with optimal cognitive function (551 vs 443 mL/min, P  .001). CONCLUSION: The combined observations of more structural brain damage and lower cerebral blood flow in demented elderly individuals than in subjects of the same age with optimal cognitive function support the hypothesis that vascular factors contribute to dementia in old age. © RSNA, 2005 The incidence of dementia and cerebrovascular disease rapidly increases after the age of 70 years. The association between the two disorders has been debated for more than 100 years. The notion that cerebrovascular disease might cause dementia goes back to Binswanger in the beginning of the 20th century (1). At that time, this notion competed with Alzheimer’s interpretation of the cause of dementia (2). Amyloid plaques are now considered the cause of dementia in patients with a familial type of dementia. In most of these patients, a mutation in the presenilin gene is responsible for the occurrence of dementia before the age of 70 (3). It is assumed that these abnormal presenilin genes lead to amyloid depositions through an impaired -secretase function (4). This familial type of early-onset dementia, however, accounts for the disease in less than 5% of the total number of patients with dementia. Therefore, this mechanism is unlikely to be the cause of disease in the majority of patients with late-onset dementia. Autopsy in a consecutive series of patients with late-onset dementia from the general population showed that amyloid plaque was present in only one of three patients, 990 R adiology