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, Peter C Van Zijl, C. Hock, P. G. Unschuld

Research output: Contribution to journalArticle

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 languageEnglish (US)
Article number35514
JournalScientific Reports
Volume6
DOIs
StatePublished - Oct 17 2016

Fingerprint

Apolipoprotein E4
Amyloid
Iron
Brain
Alzheimer Disease
Cognition
Disease Progression
Carbon
Alleles
Cognitive Dysfunction

ASJC Scopus subject areas

  • General

Cite this

Van Bergen, J. M. G., Li, X., Hua, J., Schreiner, S. J., Steininger, S. C., Quevenco, F. C., ... Unschuld, P. G. (2016). Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment. Scientific Reports, 6, [35514]. https://doi.org/10.1038/srep35514

Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment. / 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, Peter C; Hock, C.; Unschuld, P. G.

In: Scientific Reports, Vol. 6, 35514, 17.10.2016.

Research output: Contribution to journalArticle

Van Bergen, JMG, Li, X, Hua, J, Schreiner, SJ, Steininger, SC, Quevenco, FC, Wyss, M, Gietl, AF, Treyer, V, Leh, SE, Buck, F, Nitsch, RM, Pruessmann, KP, Van Zijl, PC, Hock, C & Unschuld, PG 2016, 'Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment', Scientific Reports, vol. 6, 35514. https://doi.org/10.1038/srep35514
Van Bergen JMG, Li X, Hua J, Schreiner SJ, Steininger SC, Quevenco FC et al. Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment. Scientific Reports. 2016 Oct 17;6. 35514. https://doi.org/10.1038/srep35514
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, Peter C ; Hock, C. ; Unschuld, P. G. / Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment. In: Scientific Reports. 2016 ; Vol. 6.
@article{398e8cc805414ed795878e708e2dfe07,
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.",
author = "{Van Bergen}, {J. M G} and X. Li and J. Hua and Schreiner, {S. J.} and Steininger, {S. C.} and Quevenco, {F. C.} and M. Wyss and Gietl, {A. F.} and V. Treyer and Leh, {S. E.} and F. Buck and Nitsch, {R. M.} and Pruessmann, {K. P.} and {Van Zijl}, {Peter C} and C. Hock and Unschuld, {P. G.}",
year = "2016",
month = "10",
day = "17",
doi = "10.1038/srep35514",
language = "English (US)",
volume = "6",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment

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, Peter C

AU - Hock, C.

AU - Unschuld, P. G.

PY - 2016/10/17

Y1 - 2016/10/17

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.

UR - http://www.scopus.com/inward/record.url?scp=84992111252&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84992111252&partnerID=8YFLogxK

U2 - 10.1038/srep35514

DO - 10.1038/srep35514

M3 - Article

C2 - 27748454

AN - SCOPUS:84992111252

VL - 6

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 35514

ER -