title: Corpus callosum atrophy, white matter lesions, and frontal executive dysfunction in normal aging and Alzheimer's disease. A community-based study: the Tajiri Project.
abstract: OBJECTIVE
  Cerebral MRIs of normal aging and Alzheimer's disease (AD) frequently reveal corpus callosum (CC) atrophy, white matter hyperintensity (WMH), and hippocampal atrophy. However, their relationship or the relationship between these findings and cognitive function has not been fully studied. We investigated the relationship between CC atrophy, WMH, and hippocampal atrophy, together with frontal executive dysfunction in both normal aging and AD.
  
  
  METHODS
  We examined 170 randomly selected residents from a designated community: 99 Clinical Dementia Rating (CDR) 0 (healthy, control group, HC) participants, 54 CDR 0.5 (very mild AD) patients, and 17 CDR 1 & 2 (probable AD) patients. By means of MRI, WMH and CC atrophy were visually rated. Four portions of the CC and the hippocampal width were measured. A Mini-Mental State Examination and Cognitive Abilities Screening Instrument (CASI) were performed to assess global function. For the frontal function, the CASI subitems of attention and word fluency, letter-based fluency, the Digit Symbol test of the WAIS-R, and Trail Making Tests were performed.
  
  
  RESULTS
  Those patients with CDR 1 & 2 had both hippocampal and CC atrophy, whereas the CDR 0.5 patients had only hippocampal atrophy. Frontal executive dysfunction was associated with CC atrophy in both the HC and AD groups. Significant Spearman correlations were noted between CC atrophy and WMH in both groups. The combined effect of CC atrophy and WMH was noted only in the verbal fluency test in the HC group.
  
  
  CONCLUSIONS
  In both groups, CC atrophy was associated with frontal executive dysfunction. The combined effect of CC atrophy and WMH in normal aging was probably due to subclinical ischemic conditions.
authors.affiliation: Division of Neuropsychology, Department of Disability Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. meg@mail.cc.tohoku.ac.jp
authors.forename: Kenichi
authors.initials: K
authors.lastname: Meguro
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Constans
authors.forename: Masumi
authors.initials: M
authors.lastname: Shimada
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: Junichi
authors.initials: J
authors.lastname: Ishizaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ishii
authors.forename: Atshushi
authors.initials: A
authors.lastname: Yamadori
authors.forename: Yasuyoshi
authors.initials: Y
authors.lastname: Sekita
mesh_terms: D000368:Aged; D000375:Aging / Q000473:pathology; D000544:Alzheimer Disease / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology; D001284:Atrophy; D003072:Cognition Disorders / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003337:Corpus Callosum / Q000473:pathology*; D005260:Female; D005625:Frontal Lobe / Q000503:physiopathology*; D006801:Humans; D007807:Language Tests; D008279:Magnetic Resonance Imaging; D008297:Male; D013064:Speech Disorders / Q000209:etiology; D014145:Trail Making Test