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Cerebrovascular and Brain Morphologic Correlates of Mild Cognitive Impairment in the National Heart, Lung, and Blood Institute Twin Study
Charles DeCarli, MD;
Bruce L. Miller, MD;
Gary E. Swan, PhD;
Terry Reed, PhD;
Philip A. Wolf, MD;
Dorit Carmelli, PhD
Arch Neurol. 2001;58:643-647.
Objective To evaluate the relative risk (RR) of mild cognitive impairment (MCI)
associated with cerebrovascular risk factors and cerebrovascular-related brain
changes.
Design Mild cognitive impairment was determined for the subjects of the prospective
National Heart, Lung, and Blood Institute Twin Study. Quantitative measures
of brain, white matter hyperintensity, cerebral infarction, apolipoprotein
E genotype, and psychometric testing were obtained.
Results Subjects with MCI were older (73.5 ± 3.0 vs 72.1 ± 2.8
years), consumed less alcohol (3.7 ± 5.8 vs 7.0 ± 10.7 drinks
per week), had greater white matter hyperintensity volumes (0.56% ±
0.82% vs 0.25% ± 0.34% of cranial volume), and had an increased prevalance
of apolipoprotein E4 genotype (31.4% vs 19.2%) than normal subjects. White
matter hyperintensity and the presence of the apolipoprotein E4 genotype were
associated with a significantly increased risk for MCI. When all subjects
were included in the analysis, alcohol consumption was associated with a reduced
risk for MCI (RR = 0.93, P<.05). When subjects
with a history of symptomatic cerebrovascular disease were excluded from the
analysis, elevated midlife diastolic blood pressure was associated with an
increased risk for MCI (RR = 1.70, P<.05).
Conclusions Elevated midlife blood pressures, and the resulting increased white
matter hyperintensities, increase the risk for MCI in a group of community-dwelling
older men to at least the same degree as apolipoprotein E4 genotype. Given
the common occurrence of elevations in midlife blood pressure, early and effective
treatment may be warranted to prevent late-life brain abnormalities and MCI.
Moreover, since many individuals with MCI progress to clinical dementia, longitudinal
evaluations of this cohort will be important.
From the Department of Neurology, University of Kansas, Kansas City
(Dr DeCarli); Department of Neurology, University of California at San Francisco
(Dr Miller); Health Sciences Division, SRI International, Menlo Park, Calif
(Drs Swan and Carmelli); Department of Medical and Molecular Genetics, Indiana
University, Indianapolis (Dr Reed); and Department of Neurology, Boston University,
Boston, Mass (Dr Wolf). Dr DeCarli is now with the Department of Neurology,
University of California at Davis.
Corresponding author and reprints: Charles DeCarli, MD, Department
of Neurology, University of California at Davis, 4860 Y St, Suite 3700, Sacramento,
CA 95817 (e-mail: cdecarli{at}ucdavis.edu).
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