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

Research output: Contribution to journalArticlepeer-review

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

ASJC Scopus subject areas

  • General

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