title: Progression of corpus callosum atrophy in Alzheimer disease.
abstract: 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).
  
  
  OBJECTIVE
  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 (rho = 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.
authors.affiliation: and Harald Hampel, MD, Dementia and Neuroimaging Section, Department of Psychiatry, Ludwig-Maximilian University, Nussbaumstr 7, 80336 Munich, Germany. stt@psy.med.uni-muenchen.de
authors.forename: Stefan J
authors.initials: SJ
authors.lastname: Teipel
authors.forename: Wolfram
authors.initials: W
authors.lastname: Bayer
authors.forename: Gene E
authors.initials: GE
authors.lastname: Alexander
authors.forename: York
authors.initials: Y
authors.lastname: Zebuhr
authors.forename: Diane
authors.initials: D
authors.lastname: Teichberg
authors.forename: Luka
authors.initials: L
authors.lastname: Kulic
authors.forename: Marc B
authors.initials: MB
authors.lastname: Schapiro
authors.forename: Hans-Jürgen
authors.initials: HJ
authors.lastname: Möller
authors.forename: Stanley I
authors.initials: SI
authors.lastname: Rapoport
authors.forename: Harald
authors.initials: H
authors.lastname: Hampel
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000150:complications*; D001284:Atrophy; D015415:Biomarkers; D003337:Corpus Callosum / Q000473:pathology*; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers