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 (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.
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 ADpatients at baseline. Annual rates of atrophy of total corpus callosum, splenium, and rostrum were significantly larger in ADpatients (-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 ADpatients (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: Leon J Thal; Kejal Kantarci; Eric M Reiman; William E Klunk; Michael W Weiner; Henrik Zetterberg; Douglas Galasko; Domenico Praticò; Sue Griffin; Dale Schenk; Eric Siemers Journal: Alzheimer Dis Assoc Disord Date: 2006 Jan-Mar Impact factor: 2.703
Authors: Peter Harris; Dan A Alcantara; Nina Amenta; Oscar L Lopez; Gudný Eiríksdóttir; Sigurdur Sigurdsson; Villmundur Gudnason; Sarah Madsen; Paul M Thompson; Lenore J Launer; Owen T Carmichael Journal: Neuroimage Date: 2008-07-18 Impact factor: 6.556
Authors: Y Likitjaroen; T Meindl; U Friese; M Wagner; K Buerger; H Hampel; S J Teipel Journal: Eur Arch Psychiatry Clin Neurosci Date: 2011-08-05 Impact factor: 5.270
Authors: A T Du; N Schuff; X P Zhu; W J Jagust; B L Miller; B R Reed; J H Kramer; D Mungas; K Yaffe; H C Chui; M W Weiner Journal: Neurology Date: 2003-02-11 Impact factor: 9.910