TY  - JOUR
PY  - 2019//
TI  - Accelerated extrinsic epigenetic aging and increased natural killer cells in blood of suicide completers
JO  - Progress in neuro-psychopharmacology and biological psychiatry
A1  - Okazaki, Satoshi
A1  - Otsuka, Ikuo
A1  - Horai, Tadasu
A1  - Hirata, Takashi
A1  - Takahashi, Motonori
A1  - Ueno, Yasuhiro
A1  - Boku, Shuken
A1  - Sora, Ichiro
A1  - Hishimoto, Akitoyo
SP  - ePub
EP  - ePub
VL  - ePub
IS  - ePub
N2  - BACKGROUND: Studies suggest aberrant DNA methylation in victims of suicide. Recently, DNA methylation profiles have been developed for determining "epigenetic age," which is the most accurate estimate of biological age. Subsequently, two refined measures of epigenetic age acceleration have been expanded for blood samples as intrinsic and extrinsic epigenetic age acceleration (IEAA and EEAA, respectively). IEAA involves pure epigenetic aging independent of blood cell composition, whereas EEAA involves immunosenescence in association with blood cell composition. <br><br>METHODS: We investigated epigenetic age acceleration using two independent DNA methylation datasets: a brain dataset from 16 suicide completers and 15 non-psychiatric controls and a blood dataset compiled using economical DNA pooling technique from 56 suicide completers and 60 living healthy controls. In the blood dataset, we considered IEAA and EEAA, as well as DNA methylation-based blood cell composition. <br><br>RESULTS: There was no significant difference in universal epigenetic age acceleration between suicide completers and controls in both brain and blood datasets. Blood of suicide completers exhibited an increase in EEAA, but not in IEAA. We additionally found that suicide completers had more natural killer cells but fewer granulocytes compared to controls. <br><br>CONCLUSION: This study provides novel evidence for accelerated extrinsic epigenetic aging in suicide completers and for the potential application of natural killer cells as a biomarker for suicidal behavior.<br><br>Copyright © 2019. Published by Elsevier Inc.<p />  <p>Language: en</p>
LA  - en
SN  - 0278-5846
UR  - http://dx.doi.org/10.1016/j.pnpbp.2019.109805
ID  - ref1
ER  -