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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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