Abstract
Short telomere length (TL) occurs in individuals under psychological stress, and with various psychiatric diseases. Recent studies have also reported mitochondrial DNA copy number (mtDNAcn) alterations under several neuropsychiatric conditions. However, no study has examined whether aberrant TL or mtDNAcn occur in completed suicide, one of the most serious outcomes of mental illnesses. TL and mtDNAcn in post-mortem samples from 528 suicide completers without severe physical illness (508 peripheral bloods; 20 brains) and 560 samples from control subjects (peripheral bloods from 535 healthy individuals; 25 post-mortem brains) were analysed by quantitative polymerase chain reaction. Suicide completers had significantly shorter TL and higher mtDNAcn of peripheral bloods with sex/age-dependent differences (shorter TL was more remarkably in female/young suicides; higher mtDNAcn more so in male/elderly suicides). The normal age-related decline of TL and mtDNAcn were significantly altered in suicide completers. Furthermore, shorter TL and lower mtDNAcn of post-mortem prefrontal cortex were seen in suicide completers compared to controls. This study shows the first association of aberrant telomeres and mtDNA content with suicide completion. Our results indicate that further research on telomere shortening and mitochondrial dysfunction may help elucidate the molecular underpinnings of suicide-related pathophysiology.
Highlights
Suicide is a significant public health problem that accounts for nearly 1 million deaths worldwide each year
We found significantly shorter telomere length (TL) and higher mitochondrial DNA copy number (mtDNAcn) in blood samples from suicide completers, which remained significant after excluding subjects with psychiatric disorders and/or psychotropic medication use
Our results were similar to prior findings of shortened TL and increased mtDNAcn in cohorts with major depressive disorder (MDD) or other neuropsychiatric conditions[30, 31]
Summary
Suicide is a significant public health problem that accounts for nearly 1 million deaths worldwide each year. The involvement of genetic factors has been demonstrated in suicidal behaviour by family studies, twin and adoption studies, candidate gene analyses and genome-wide association studies (GWAS)[3, 4]. These diverse pieces of evidence suggest that suicide is caused by the accumulation of stress, traumatic events, and/or illnesses in individuals with neurobiological changes and genetic risk. Biological insights into suicidal behaviour lag behind those of other mental problems, and no useful genetic biomarker of suicide risk has been found. Telomere shortening to a critical length triggers genomic instability and cellular apoptosis. Two reports showed evidence that shorter TL and higher mtDNAcn occurred in the same cohorts with MDD or other neuropsychiatric conditions (e.g., childhood adversity)[30, 31]
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