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, P. C. M., Hock, C., & Unschuld, P. G. Scientific Reports, October, 2016. Environnement, fer![Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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 ε4 (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 \textless 0.001) and APOE-e4 carrier status (p \textless 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.
@article{van_bergen_colocalization_2016,
title = {Colocalization of cerebral iron with {Amyloid} beta in {Mild} {Cognitive} {Impairment}},
volume = {6},
issn = {2045-2322},
url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066274/},
doi = {10.1038/srep35514},
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 ε4 (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 {\textless} 0.001) and APOE-e4 carrier status (p {\textless} 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.},
urldate = {2017-04-12},
journal = {Scientific Reports},
author = {van Bergen, J. M. G. and Li, X. and Hua, J. and Schreiner, S. J. and Steininger, S. C. and Quevenco, F. C. and Wyss, M. and Gietl, A. F. and Treyer, V. and Leh, S. E. and Buck, F. and Nitsch, R. M. and Pruessmann, K. P. and van Zijl, P. C. M. and Hock, C. and Unschuld, P. G.},
month = oct,
year = {2016},
pmid = {27748454},
pmcid = {PMC5066274},
note = {Environnement, fer}
}
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