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Association between cortical thickness and CSF biomarkers in mild cognitive impairment and Alzheimer’s disease

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  • Sara Mohades, McGill University, Canada
  • Jonathan Dubois, McGill University, Canada
  • Maxime Parent, McGill University, Canada
  • Laksanun Cheewakriengkrai, McGill University, Canada
  • Jared Rowley, McGill University, Canada
  • Monica Shin, McGill University, Canada
  • Thomas Beaudry, McGill University, Canada
  • Simon Fristed Eskildsen
  • Antoine Leuzy, McGill University, Canada
  • Marina Dauar, McGill University, Canada
  • Vladimir Fonov, McGill University, Canada
  • Serge Gauthier, McGill University, Canada
  • Pedro Rosa-Neto, McGill University, Canada
Background: The dynamic biomarker hypothesis predicts that fluid biomarker
abnormalities precede brain morphological changes observed in
AD by many years. However, the link between early CSF abnormalities
and late structural changes remains under debate. Here we investigated
the association between regional cortical thinning (CT) measured by Magnetic
Resonance Imaging (MRI) and brain amyloidosis (measured by CSF
Ab 1-42 concentrations), or tau hyperphosphorylation (tau 181; p-tau) in
Alzheimer’s Disease (AD) and Mild Cognitive Impairment (MCI) patients.
We test the hypothesis that the association between cortical thinning, amyloidosis
or tau hyperphosphorylation depends on cortical regions and clinical
stages of AD. Methods: T1-weighed MRIs and associated CSF markers
from individuals with mild cognitive impairment (MCI; 16), Alzheimer Disease
(AD; n¼7) and age-matched cognitively normal subjects (CN; n¼8)
were obtained from the Alzheimer’s Disease Neuroimaging Initiative
(ADNI) cohort. Cortical surface reconstruction and group registration were generated using Freesurfer. A general linear model was used to conduct
regressions between CSF markers and cortical thickness. Results: Correlation
analyses in the MCI group showed a positive correlation between
CT and Ab 1-42 measures predominantly in the temporo-parietal regions,
namely the precuneus (peak r¼0.67; p<0.01) and the fusiform (peak
r¼0.85; p<0.0001). Similar but smaller effects were present in AD, with additional
clusters in the frontal cortex (peak r¼0.94; p¼0.0001). In both MCI
and AD groups, significant clusters of negative correlations between CTand
p-tau were mainly found in medio-temporal and dorso-lateral prefrontal
areas. In the CN group, no relationship was observed between cortical thickness
and either CSF biomarkers. Conclusions: Although limited by sample
sizes, our results suggest a posterior-anterior gradient of structural vulnerability
to A b 1-42. Alternatively, weaker temporo-parietal effect between CT
and Ab 1-42 in AD relative to MCI, likely results from a ceiling effect of Ab
1-42 levels in the ADgroup. Conversely, a frontal effect can only be found in
the AD group, which possibly corresponds to a later stage of Ab 1-42
-driven neurodegeneration.
Original languageEnglish
Publication yearJul 2013
Number of pages1
Publication statusPublished - Jul 2013
EventAlzheimer's Association International Conference - Boston, United States
Duration: 13 Jul 201318 Jul 2013


ConferenceAlzheimer's Association International Conference
CountryUnited States

    Research areas

  • Alzheimer, cortical thickness, CSF, MCI

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