AI Article Synopsis
- The study utilized 7 Tesla MRI and PET scans to explore how brain iron levels relate to Amyloid beta (Aβ) plaque accumulation, focusing on individuals at heightened risk for Alzheimer’s disease (AD) due to the APOE-e4 allele and mild cognitive impairment (MCI).
- Carriers of the APOE-e4 allele showed greater Aβ plaque levels in their brains, regardless of their cognitive status, and this association was even more significant in individuals with MCI.
- Additionally, increased levels of brain iron were linked to both higher Aβ plaque loads and functional brain connectivity issues, suggesting that the buildup of iron in the brain might contribute to the progression of neurocognitive dysfunction in Alzheimer’s disease.
Article 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 (R-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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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066274 | PMC |
| http://dx.doi.org/10.1038/srep35514 | DOI Listing |
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