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. 2017 Aug 10;7:7719. doi: 10.1038/s41598-017-08292-4

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Hypothetical model linking our results with other potentially intervening factors. Gray boxes and black solid arrows are based on findings obtained in the current study; while white boxes and gray dashed arrows refer to other potentially intervening elements derived from alternative evidence. Our findings suggest that the relationship between HCY and TAC levels was mediated by poorer sleep quality in MCI, while the impact of HCY on cerebral GM was mediated by the relationship between sleep quality and TAC levels. Based on previous evidence, we hypothesize that the impact of HCY on TAC levels may be further mediated by copper (Cu) accumulation and/or Aβ aggregation in the brain, and that sleep disruptions may be additionally prompted by increased hypoxemia, which in turn has also shown to enhance Aβ burden; whereas the impact of HCY on GM loss may be further mediated by cardiovascular dysfunctions (CVD), which is promoted by multiple factors including elevated HCY, oxidative stress, reduced TAC and low-grade systemic inflammation.