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Progression of Corpus Callosum Atrophy in Alzheimer Disease
Stefan J. Teipel, MD;
Wolfram Bayer, MD;
Gene E. Alexander, PhD;
York Zebuhr, MD;
Diane Teichberg;
Luka Kulic, MD;
Marc B. Schapiro, MD;
Hans-Jürgen Möller, MD;
Stanley I. Rapoport, MD;
Harald Hampel, MD
Arch Neurol. 2002;59:243-248.
Background Atrophy of the corpus callosum in the absence of primary white matter
degeneration reflects loss of intracortical projecting neocortical pyramidal
neurons in Alzheimer disease (AD).
Objectives To determine individual rates of atrophy progression of the corpus callosum
in patients with AD and to correlate rates of atrophy progression with clinical
disease severity and subcortical disease.
Methods Magnetic resonance imaging–derived measurements of corpus callosum
size were studied longitudinally in 21 patients clinically diagnosed as having
AD (mean observation time, 17.0 ± 8.5 months) and 10 age- and sex-matched
healthy controls (mean observation time, 24.1 ± 6.8 months).
Results Corpus callosum size was significantly reduced in AD patients at baseline.
Annual rates of atrophy of total corpus callosum, splenium, and rostrum were
significantly larger in AD patients (-7.7%, -12.1%, and -7.3%,
respectively) than in controls (-0.9%, -1.5%, and 0.6%, respectively).
Rates of atrophy of the corpus callosum splenium were correlated with progression
of dementia severity in AD patients ( = 0.52, P<.02).
The load of subcortical lesions at baseline (P<.05)
predicted rate of anterior corpus callosum atrophy in healthy controls. Rates
of atrophy of corpus callosum areas were independent of white matter hyperintensity
load in patients with AD.
Conclusions Measurement of corpus callosum size allows in vivo mapping of neocortical
neurodegeneration in AD over a wide range of clinical dementia severities
and may be used as a surrogate marker for evaluation of drug efficacy.
From the Dementia and Neuroimaging Section, Department of Psychiatry,
Ludwig-Maximilian University, Munich, Germany (Drs Teipel, Bayer, Zebuhr,
Kulic, Möller, and Hampel); Arizona Alzheimer's Research Center and Department
of Psychology, Arizona State University, Tempe (Dr Alexander); Brain Physiology
and Metabolism Section, National Institute on Aging, National Institutes of
Health, Bethesda, Md (Ms Teichberg and Dr Rapoport); and Department of Pediatric
Neurology, Children Hospital Medical Center, Cincinnati, Ohio (Dr Schapiro).
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