Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

J. M.G. Van Bergen; X. Li; J. Hua; S. J. Schreiner; S. C. Steininger; F. C. Quevenco; M. Wyss; A. F. Gietl; V. Treyer; S. E. Leh; F. Buck; R. M. Nitsch; K. P. Pruessmann; P. C.M. Van Zijl; C. Hock; P. G. Unschuld

doi:10.1038/srep35514

Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

J. M.G. Van Bergen, X. Li, J. Hua, S. J. Schreiner, S. C. Steininger, F. C. Quevenco, M. Wyss, A. F. Gietl, V. Treyer, S. E. Leh, F. Buck, R. M. Nitsch, K. P. Pruessmann, P. C.M. Van Zijl, C. Hock, P. G. Unschuld

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Abstract

Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E Îμ 4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. Carriers of APOE-e4 with normal cognition had higher cortical Aβ-plaque-load than non-carriers. In MCI an association between APOE-e4 and higher Aβ-plaque-load was observable both for cortical and subcortical brain-regions. APOE-e4 and MCI was also associated with higher cortical iron. Moreover, cerebral iron significantly affected functional coupling, and was furthermore associated with increased Aβ-plaque-load (R²-adjusted = 0.80, p < 0.001) and APOE-e4 carrier status (p < 0.001) in MCI. This study confirms earlier reports on an association between increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that disease-progression is conferred by spatial colocalization of brain iron deposits with Aβ-plaques.

Original language	English (US)
Article number	35514
Journal	Scientific reports
Volume	6
DOIs	https://doi.org/10.1038/srep35514
State	Published - Oct 17 2016

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Van Bergen, J. M. G., Li, X., Hua, J., Schreiner, S. J., Steininger, S. C., Quevenco, F. C., Wyss, M., Gietl, A. F., Treyer, V., Leh, S. E., Buck, F., Nitsch, R. M., Pruessmann, K. P., Van Zijl, P. C. M., Hock, C., & Unschuld, P. G. (2016). Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment. Scientific reports, 6, Article 35514. https://doi.org/10.1038/srep35514

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title = "Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment",

abstract = "Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E {\^I}μ 4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. Carriers of APOE-e4 with normal cognition had higher cortical Aβ-plaque-load than non-carriers. In MCI an association between APOE-e4 and higher Aβ-plaque-load was observable both for cortical and subcortical brain-regions. APOE-e4 and MCI was also associated with higher cortical iron. Moreover, cerebral iron significantly affected functional coupling, and was furthermore associated with increased Aβ-plaque-load (R2-adjusted = 0.80, p < 0.001) and APOE-e4 carrier status (p < 0.001) in MCI. This study confirms earlier reports on an association between increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that disease-progression is conferred by spatial colocalization of brain iron deposits with Aβ-plaques.",

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AU - Van Bergen, J. M.G.

AU - Li, X.

AU - Hua, J.

AU - Schreiner, S. J.

AU - Steininger, S. C.

AU - Quevenco, F. C.

AU - Wyss, M.

AU - Gietl, A. F.

AU - Treyer, V.

AU - Leh, S. E.

AU - Buck, F.

AU - Nitsch, R. M.

AU - Pruessmann, K. P.

AU - Van Zijl, P. C.M.

AU - Hock, C.

AU - Unschuld, P. G.

PY - 2016/10/17

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N2 - Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E Îμ 4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. Carriers of APOE-e4 with normal cognition had higher cortical Aβ-plaque-load than non-carriers. In MCI an association between APOE-e4 and higher Aβ-plaque-load was observable both for cortical and subcortical brain-regions. APOE-e4 and MCI was also associated with higher cortical iron. Moreover, cerebral iron significantly affected functional coupling, and was furthermore associated with increased Aβ-plaque-load (R2-adjusted = 0.80, p < 0.001) and APOE-e4 carrier status (p < 0.001) in MCI. This study confirms earlier reports on an association between increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that disease-progression is conferred by spatial colocalization of brain iron deposits with Aβ-plaques.

AB - Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E Îμ 4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects. Carriers of APOE-e4 with normal cognition had higher cortical Aβ-plaque-load than non-carriers. In MCI an association between APOE-e4 and higher Aβ-plaque-load was observable both for cortical and subcortical brain-regions. APOE-e4 and MCI was also associated with higher cortical iron. Moreover, cerebral iron significantly affected functional coupling, and was furthermore associated with increased Aβ-plaque-load (R2-adjusted = 0.80, p < 0.001) and APOE-e4 carrier status (p < 0.001) in MCI. This study confirms earlier reports on an association between increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that disease-progression is conferred by spatial colocalization of brain iron deposits with Aβ-plaques.

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Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

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