Cited by 202Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Progression of corpus callosum atrophy in Alzheimer disease

Teipel, Stefan J., Bayer, Wolfram, Alexander, Gene E., Zebuhr, York, Teichberg, Diane, Kulic, Luka, Schapiro, Marc B., Möller, Hans-Jürgen +2 more·2002·Archives of Neurology

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). 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.

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Crossref · 10.1001/archneur.59.2.243

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  • Major fibre tracts such as the forceps major and forceps minor, inferior fronto-occipital fasciculus as well as the posterior cingulum show white matter alterations in Alzheimer's disease dementia.

    “In particular, major fibre tracts such as the forceps major and forceps minor, inferior fronto-occipital fasciculus as well as the posterior cingulum show white matter alterations in Alzheimer’s disease dementia (Taylor et al., 2001; Teipel et al., 2002; Douaud et al., 2011; Mito et al., 2018).”

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Authors
Teipel, S. J., Bayer, W., Alexander, G. E., Zebuhr, Y., Teichberg, D., Kulic, L., Schapiro, M. B., Möller, H.-J., Rapoport, S. I., & Hampel, H.
Affiliations
  • Ludwig-Maximilians-Universität München (DE)
  • National Institutes of Health (US)
  • Cincinnati Children's Hospital Medical Center (US)
Venue
Archives of Neurology
Published
2002-02-01
Volume
59
Issue
2
Pages
243
ISSN
0003-9942 (ISSN-L)
OpenAlex
W1993812357
Cited by
202
References
25
Citations by year
2026: 4 · 2025: 11 · 2024: 9 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 5 · 2019: 4 · 2018: 8 · 2017: 5 · 2016: 10 · 2015: 6 · 2014: 7 · 2013: 12 · 2012: 10
FWCI
6.20
Type
journal article
Language
en
Open access
closed
Locations
  • Archives of Neurology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
corpus callosum atrophy, Alzheimer's disease, dementia severity, subcortical lesions, white matter hyperintensities, splenium, rostrum, longitudinal MRI, surrogate markers, drug efficacy
MeSH terms
Aged, Alzheimer Disease, Atrophy, Corpus Callosum, Cross-Sectional Studies, Female, Humans, Male, Severity of Illness Index, Biomarkers, Disease Progression

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