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Linking cortical atrophy to white matter hyperintensities of presumed vascular origin

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Linking cortical atrophy to white matter hyperintensities of presumed vascular origin. / Mayer, Carola; Frey, Benedikt M; Schlemm, Eckhard; Petersen, Marvin; Engelke, Kristin; Hanning, Uta; Jagodzinski, Annika; Borof, Katrin; Fiehler, Jens; Gerloff, Christian; Thomalla, Götz; Cheng, Bastian.

in: J CEREBR BLOOD F MET, Jahrgang 41, Nr. 7, 07.2021, S. 1682-1691.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Mayer, C, Frey, BM, Schlemm, E, Petersen, M, Engelke, K, Hanning, U, Jagodzinski, A, Borof, K, Fiehler, J, Gerloff, C, Thomalla, G & Cheng, B 2021, 'Linking cortical atrophy to white matter hyperintensities of presumed vascular origin', J CEREBR BLOOD F MET, Jg. 41, Nr. 7, S. 1682-1691. https://doi.org/10.1177/0271678X20974170

APA

Mayer, C., Frey, B. M., Schlemm, E., Petersen, M., Engelke, K., Hanning, U., Jagodzinski, A., Borof, K., Fiehler, J., Gerloff, C., Thomalla, G., & Cheng, B. (2021). Linking cortical atrophy to white matter hyperintensities of presumed vascular origin. J CEREBR BLOOD F MET, 41(7), 1682-1691. https://doi.org/10.1177/0271678X20974170

Vancouver

Mayer C, Frey BM, Schlemm E, Petersen M, Engelke K, Hanning U et al. Linking cortical atrophy to white matter hyperintensities of presumed vascular origin. J CEREBR BLOOD F MET. 2021 Jul;41(7):1682-1691. https://doi.org/10.1177/0271678X20974170

Bibtex

@article{2c92e5a08fc24add9cd2e14dd817d5d9,
title = "Linking cortical atrophy to white matter hyperintensities of presumed vascular origin",
abstract = "We examined the relationship between white matter hyperintensities (WMH) and cortical neurodegeneration in cerebral small vessel disease (CSVD) by investigating whether cortical thickness is a remote effect of WMH through structural fiber tract connectivity in a population at increased risk of CSVD. We measured cortical thickness on T1-weighted images and segmented WMH on FLAIR images in 930 participants of a population-based cohort study at baseline. DWI-derived whole-brain probabilistic tractography was used to define WMH connectivity to cortical regions. Linear mixed-effects models were applied to analyze the relationship between cortical thickness and connectivity to WMH. Factors associated with cortical thickness (age, sex, hemisphere, region, individual differences in cortical thickness) were added as covariates. Median age was 64 [IQR 46-76] years. Visual inspection of surface maps revealed distinct connectivity patterns of cortical regions to WMH. WMH connectivity to the cortex was associated with reduced cortical thickness (p = 0.009) after controlling for covariates. This association was found for periventricular WMH (p = 0.001) only. Our results indicate an association between WMH and cortical thickness via connecting fiber tracts. The results imply a mechanism of secondary neurodegeneration in cortical regions distant, yet connected to subcortical vascular lesions, which appears to be driven by periventricular WMH.",
author = "Carola Mayer and Frey, {Benedikt M} and Eckhard Schlemm and Marvin Petersen and Kristin Engelke and Uta Hanning and Annika Jagodzinski and Katrin Borof and Jens Fiehler and Christian Gerloff and G{\"o}tz Thomalla and Bastian Cheng",
year = "2021",
month = jul,
doi = "10.1177/0271678X20974170",
language = "English",
volume = "41",
pages = "1682--1691",
journal = "J CEREBR BLOOD F MET",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "7",

}

RIS

TY - JOUR

T1 - Linking cortical atrophy to white matter hyperintensities of presumed vascular origin

AU - Mayer, Carola

AU - Frey, Benedikt M

AU - Schlemm, Eckhard

AU - Petersen, Marvin

AU - Engelke, Kristin

AU - Hanning, Uta

AU - Jagodzinski, Annika

AU - Borof, Katrin

AU - Fiehler, Jens

AU - Gerloff, Christian

AU - Thomalla, Götz

AU - Cheng, Bastian

PY - 2021/7

Y1 - 2021/7

N2 - We examined the relationship between white matter hyperintensities (WMH) and cortical neurodegeneration in cerebral small vessel disease (CSVD) by investigating whether cortical thickness is a remote effect of WMH through structural fiber tract connectivity in a population at increased risk of CSVD. We measured cortical thickness on T1-weighted images and segmented WMH on FLAIR images in 930 participants of a population-based cohort study at baseline. DWI-derived whole-brain probabilistic tractography was used to define WMH connectivity to cortical regions. Linear mixed-effects models were applied to analyze the relationship between cortical thickness and connectivity to WMH. Factors associated with cortical thickness (age, sex, hemisphere, region, individual differences in cortical thickness) were added as covariates. Median age was 64 [IQR 46-76] years. Visual inspection of surface maps revealed distinct connectivity patterns of cortical regions to WMH. WMH connectivity to the cortex was associated with reduced cortical thickness (p = 0.009) after controlling for covariates. This association was found for periventricular WMH (p = 0.001) only. Our results indicate an association between WMH and cortical thickness via connecting fiber tracts. The results imply a mechanism of secondary neurodegeneration in cortical regions distant, yet connected to subcortical vascular lesions, which appears to be driven by periventricular WMH.

AB - We examined the relationship between white matter hyperintensities (WMH) and cortical neurodegeneration in cerebral small vessel disease (CSVD) by investigating whether cortical thickness is a remote effect of WMH through structural fiber tract connectivity in a population at increased risk of CSVD. We measured cortical thickness on T1-weighted images and segmented WMH on FLAIR images in 930 participants of a population-based cohort study at baseline. DWI-derived whole-brain probabilistic tractography was used to define WMH connectivity to cortical regions. Linear mixed-effects models were applied to analyze the relationship between cortical thickness and connectivity to WMH. Factors associated with cortical thickness (age, sex, hemisphere, region, individual differences in cortical thickness) were added as covariates. Median age was 64 [IQR 46-76] years. Visual inspection of surface maps revealed distinct connectivity patterns of cortical regions to WMH. WMH connectivity to the cortex was associated with reduced cortical thickness (p = 0.009) after controlling for covariates. This association was found for periventricular WMH (p = 0.001) only. Our results indicate an association between WMH and cortical thickness via connecting fiber tracts. The results imply a mechanism of secondary neurodegeneration in cortical regions distant, yet connected to subcortical vascular lesions, which appears to be driven by periventricular WMH.

U2 - 10.1177/0271678X20974170

DO - 10.1177/0271678X20974170

M3 - SCORING: Journal article

C2 - 33259747

VL - 41

SP - 1682

EP - 1691

JO - J CEREBR BLOOD F MET

JF - J CEREBR BLOOD F MET

SN - 0271-678X

IS - 7

ER -