Summary: A new study reports people with bipolar disorder may have accelerated epigenetic aging. The findings could explain why people with bipolar are more likely to develop, and even die from, age related diseases.
Source: UT Houston.
Bipolar disorder may involve accelerated epigenetic aging, which could explain why persons with the disorder are more likely to have – and die from – age-related diseases, according to researchers from The University of Texas Health Science Center at Houston (UTHealth).
The findings were published in yesterday’s issue of Translational Psychiatry.
While chronological age is measured in the amount of time that a person has been alive, epigenetic age measures molecular markers of chemical modifications to DNA.
“Bipolar disorder has been previously associated with accelerated aging but the mechanisms are largely unknown,” said Gabriel R. Fries, Ph.D., first author and post-doctoral research fellow in the Department of Psychiatry and Behavioral Sciences at McGovern Medical School at UTHealth. “We aimed to understand from our study the biology of what’s driving the accelerated aging. What we found is that patients with bipolar disorder showed an accelerated epigenetic aging compared to healthy controls.”
The chemical modifications could be precipitated by the disorder itself or by poor lifestyle habits in diet, exercise, tobacco use and illegal substance use.
“Controlling these factors is just as important as taking medications,” Fries said.
Senior author of the study was Joao L. de Quevedo, M.D., Ph.D., professor and director of the Translational Psychiatry Program in the Department of Psychiatry and Behavioral Sciences at McGovern Medical School.
Using blood samples, the researchers compared 22 patients with bipolar disorder, 16 siblings of bipolar patients and 20 healthy controls. They also found that while older bipolar disorder patients had significantly accelerated epigenetic aging compared to controls, no difference was found in younger patients.
“We believe a difference wasn’t detected in younger patients because they haven’t had as much exposure to stressful events,” Fries said. “This gave us a hint that cumulative chronic exposure to stress would relate to accelerated aging. We would see it more in older people who have experienced a lifetime of stress in dealing with the disease.”
Along with the epigenetic clock, the study included two other biologic clocks: telomere length and mitochondrial DNA copy numbers.
“The epigenetic acceleration correlated with the number of copies of mitochondrial DNA, suggesting that the cross-talk between the nucleus and the mitochondria might be underlying the premature aging in bipolar disorder,” Fries said.
McGovern Medical School co-authors were Isabelle Bauer, Ph.D.; Giselli Scaini, Ph.D.; Mon-Ju Wu, Ph.D.; Iram F. Kazimi, M.D.; Giovana Zunta-Soares, M.D.; Consuelo Walss-Bass, Ph.D.; and Jair Soares, M.D., Ph.D. Quevedo, Soares and Walss-Bass are also on the faculty of The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences.
Funding: The study was supported in part by grants from the Pat Rutherford, Jr. Endowed Chair in Psychiatry, John S. Dunn Foundation and the National Institute of Mental Health (R01MH085667), part of the National Institutes of Health.
Source: Verena Müller – UT Houston
Publisher: Organized by NeuroscienceNews.com.
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Original Research: Abstract for “Accelerated epigenetic aging and mitochondrial DNA copy number in bipolar disorder” by Gabriel R. Fries, Isabelle E. Bauer, Giselli Scaini, Mon-Ju Wu, Iram F. Kazimi, Samira S. Valvassori, Giovana Zunta-Soares, Consuelo Walss-Bass, Jair C. Soares & Joao Quevedo in Translational Psychiatry. Published online December 11 2017 doi:10.1038/s41398-017-0048-8
Accelerated epigenetic aging and mitochondrial DNA copy number in bipolar disorder
Bipolar disorder (BD) has been previously associated with accelerated aging; yet, the mechanisms underlying this association are largely unknown. The epigenetic clock has been increasingly recognized as a valuable aging marker, although its association with other biological clocks in BD patients and high-risk subjects, such as telomere length and mitochondrial DNA (mtDNA) copy number, has never been investigated. We included 22 patients with BD I, 16 siblings of BD patients, and 20 healthy controls in this analysis. DNA was isolated from peripheral blood and interrogated for genome-wide DNA methylation, mtDNA copy number, and telomere length. DNA methylation age (DNAm age) and accelerated aging were calculated using the Horvath age estimation algorithm in blood and in postmortem brain from BD patients and nonpsychiatric controls using publicly available data. Older BD patients presented significantly accelerated epigenetic aging compared to controls, whereas no difference was detected among the younger subjects. Patients showed higher levels of mtDNA copy number, while no difference was found between controls and siblings. mtDNA significantly correlated with epigenetic age acceleration among older subjects, as well and with global functioning in our sample. Telomere length did not show significant differences between groups, nor did it correlate with epigenetic aging or mtDNA copy number. These results suggest that BD may involve an accelerated epigenetic aging, which might represent a novel target for treating BD and subjects at risk. In particular, our results suggest a complex interplay between biological clocks to determine the accelerated aging and its consequences in BD.
“Accelerated epigenetic aging and mitochondrial DNA copy number in bipolar disorder” by Gabriel R. Fries, Isabelle E. Bauer, Giselli Scaini, Mon-Ju Wu, Iram F. Kazimi, Samira S. Valvassori, Giovana Zunta-Soares, Consuelo Walss-Bass, Jair C. Soares & Joao Quevedo in Translational Psychiatry. Published online December 11 2017 doi:10.1038/s41398-017-0048-8