Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment
Abstract Tremendous progress has been made over the last few years in understanding how sleep and amyloid-β (Aβ) cooperate to speed up the progression of Alzheimer’s disease (AD). However, it remains unknown whether sleep deficits also interact with other risk factors that exacerbate the pathologica...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2017-08-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-017-08292-4 |
| _version_ | 1818425288382480384 |
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| author | Mayely P. Sanchez-Espinosa Mercedes Atienza Jose L. Cantero |
| author_facet | Mayely P. Sanchez-Espinosa Mercedes Atienza Jose L. Cantero |
| author_sort | Mayely P. Sanchez-Espinosa |
| collection | DOAJ |
| description | Abstract Tremendous progress has been made over the last few years in understanding how sleep and amyloid-β (Aβ) cooperate to speed up the progression of Alzheimer’s disease (AD). However, it remains unknown whether sleep deficits also interact with other risk factors that exacerbate the pathological cascade of AD. Based on evidence showing that higher levels of homocysteine (HCY) and sleep loss increase oxidative damage, we here investigate whether the relationship between HCY and total antioxidant capacity (TAC) is mediated by changes in objective sleep in healthy older (HO, N = 21) and mild cognitive impairment (MCI, N = 21) subjects. Results revealed that reduced TAC levels in MCI was significantly correlated with increased HCY, shorter sleep duration, lower sleep efficiency, and reduced volume of temporal regions. However, only the HCY-TAC association showed diagnostic value, and this relationship was mediated by poorer sleep quality in MCI patients. We further showed that HCY-related cerebral volume loss in MCI depended on the serial relationship between poorer sleep quality and lower TAC levels. These findings provide novel insights into how impaired sleep may contribute to maintain the relationship between HCY and oxidative stress in prodromal AD, and offer empirical foundations to design therapeutic interventions aimed to weaken this link. |
| first_indexed | 2024-12-14T14:11:33Z |
| format | Article |
| id | doaj.art-dcbaa1f6c1b64db98537df177efde6b1 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-12-14T14:11:33Z |
| publishDate | 2017-08-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-dcbaa1f6c1b64db98537df177efde6b12022-12-21T22:58:18ZengNature PortfolioScientific Reports2045-23222017-08-01711910.1038/s41598-017-08292-4Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairmentMayely P. Sanchez-Espinosa0Mercedes Atienza1Jose L. Cantero2Laboratory of Functional Neuroscience, Spanish Network of Excellence for Research on Neurodegenerative Diseases (CIBERNED), Pablo de Olavide UniversityLaboratory of Functional Neuroscience, Spanish Network of Excellence for Research on Neurodegenerative Diseases (CIBERNED), Pablo de Olavide UniversityLaboratory of Functional Neuroscience, Spanish Network of Excellence for Research on Neurodegenerative Diseases (CIBERNED), Pablo de Olavide UniversityAbstract Tremendous progress has been made over the last few years in understanding how sleep and amyloid-β (Aβ) cooperate to speed up the progression of Alzheimer’s disease (AD). However, it remains unknown whether sleep deficits also interact with other risk factors that exacerbate the pathological cascade of AD. Based on evidence showing that higher levels of homocysteine (HCY) and sleep loss increase oxidative damage, we here investigate whether the relationship between HCY and total antioxidant capacity (TAC) is mediated by changes in objective sleep in healthy older (HO, N = 21) and mild cognitive impairment (MCI, N = 21) subjects. Results revealed that reduced TAC levels in MCI was significantly correlated with increased HCY, shorter sleep duration, lower sleep efficiency, and reduced volume of temporal regions. However, only the HCY-TAC association showed diagnostic value, and this relationship was mediated by poorer sleep quality in MCI patients. We further showed that HCY-related cerebral volume loss in MCI depended on the serial relationship between poorer sleep quality and lower TAC levels. These findings provide novel insights into how impaired sleep may contribute to maintain the relationship between HCY and oxidative stress in prodromal AD, and offer empirical foundations to design therapeutic interventions aimed to weaken this link.https://doi.org/10.1038/s41598-017-08292-4 |
| spellingShingle | Mayely P. Sanchez-Espinosa Mercedes Atienza Jose L. Cantero Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment Scientific Reports |
| title | Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| title_full | Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| title_fullStr | Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| title_full_unstemmed | Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| title_short | Sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| title_sort | sleep mediates the association between homocysteine and oxidative status in mild cognitive impairment |
| url | https://doi.org/10.1038/s41598-017-08292-4 |
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