Telomere length and hTERT in mania and subsequent remission

Çınar, Rugül Köse

doi:10.1590/1516-4446-2017-2216

Cited by 18 publications

(9 citation statements)

References 38 publications

(47 reference statements)

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“…Most recently, Pisanu et al ( 124 ) reported that BD patients with a history of lithium treatment had longer leukocyte TL compared to those who never had been treated with lithium and similar TL compared to controls ( 124 ). In the only prospective clinical study on lithium’s effect of TL thus far, Köse Çinar ( 125 ) found that manic BD patients had shorter TL than healthy controls and that TL was significantly increased at remission after treatment with lithium and antipsychotics ( 125 ).…”

Section: Telomere Maintenancementioning

confidence: 99%

Lithium and the Interplay Between Telomeres and Mitochondria in Bipolar Disorder

et al. 2020

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Bipolar disorder is a severe psychiatric disorder which affects more than 1% of the world’s population and is a leading cause of disability among young people. For the past 50 years, lithium has been the drug of choice for maintenance treatment of bipolar disorder due to its potent ability to prevent both manic and depressive episodes as well as suicide. However, though lithium has been associated with a multitude of effects within different cellular pathways and biological systems, its specific mechanism of action in stabilizing mood remains largely elusive. Mitochondrial dysfunction and telomere shortening have been implicated in both the pathophysiology of bipolar disorder and as targets of lithium treatment. Interestingly, it has in recent years become clear that these phenomena are intimately linked, partly through reactive oxygen species signaling and the subcellular translocation and non-canonical actions of telomerase reverse transcriptase. In this review, we integrate the current understanding of mitochondrial dysfunction, oxidative stress and telomere shortening in bipolar disorder with documented effects of lithium. Moreover, we propose that lithium’s mechanism of action is intimately connected with the interdependent regulation of mitochondrial bioenergetics and telomere maintenance.

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Section: Telomere Maintenancementioning

confidence: 99%

Lithium and the Interplay Between Telomeres and Mitochondria in Bipolar Disorder

et al. 2020

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“…The majority of studies published so far explored peripheral TL in BD, using genomic DNA extracted from leukocytes [47,48,49,50], peripheral blood mononuclear cell (PBMC) [51,52] or buccal smears [53]. Overall, findings suggest that BD patients have a significant decrease of peripheral TL, compared with healthy controls [47,51,52,54]. This effect, also confirmed by a recent meta-analysis [55], seems to be independent from mood state, as shorter telomeres have been reported in BD patients in euthymic, depressed, and manic states [55].…”

Section: Telomeres and Mood Disordersmentioning

confidence: 99%

“…Two recent studies compared early- or late-stage BD patients. The study by Kose Cinar and colleagues [54], showed shorter LTL in late-stage BD patients compared to early-stage and healthy controls ( p < 0.001). Early-stage patients were defined as those with less than five episodes, while late-stage were those with more than 10 episodes.…”

Section: Telomeres and Mood Disordersmentioning

confidence: 99%

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Mood Disorders, Accelerated Aging, and Inflammation: Is the Link Hidden in Telomeres?

Squassina

Pisanu

Vanni

2019

Cells

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Mood disorders are associated with an increased risk of aging-related diseases, which greatly contribute to the excess morbidity and mortality observed in affected individuals. Clinical and molecular findings also suggest that mood disorders might be characterized by a permanent state of low-grade inflammation. At the cellular level, aging translates into telomeres shortening. Intriguingly, inflammation and telomere shortening show a bidirectional association: a pro-inflammatory state seems to contribute to aging and telomere dysfunction, and telomere attrition is able to induce low-grade inflammation. Several independent studies have reported shorter telomere length and increased levels of circulating inflammatory cytokines in mood disorders, suggesting a complex interplay between altered inflammatory–immune responses and telomere dynamics in the etiopathogenesis of these disorders. In this review, we critically discuss studies investigating the role of telomere attrition and inflammation in the pathogenesis and course of mood disorders, and in pharmacological treatments with psychotropic medications.

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“…Lithium, which inhibits GSK‐3, has been FDA approved since the 1970s for bipolar disorder and, although its therapeutic index is low, its safety and toxicity profile are well known. Furthermore, it is approved for use in pediatric patients, it stimulates granulopoiesis, it shows potential utility in the treatment of AA, and observational studies suggest that lithium leads to telomere lengthening in bipolar patients, indicating that telomeres are impacted by clinically relevant doses of the drug (although we caution that the conclusion related to telomere lengthening might be viewed as tentative, because it relies primarily on case–control studies and on a qPCR‐based telomere measurement technique that can suffer from inaccuracy and imprecision) . Therefore, lithium should be considered as a candidate for a clinical trial to test for potential benefits in DC spectrum patients, although it would be helpful to first study the consequences of lithium in additional tissues in mice and human culture models of DC pathology.…”

Section: The Therapeutic Potential Of Wnt Pathway Agonists In Telomermentioning

confidence: 99%

A regulatory loop connecting WNT signaling and telomere capping: possible therapeutic implications for dyskeratosis congenita

Fernández

Johnson

2018

Annals of the New York Academy of Sciences

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The consequences of telomere dysfunction are most apparent in rare inherited syndromes caused by genetic deficiencies in factors that normally maintain telomeres. The principal disease is known as dyskeratosis congenita (DC), but other syndromes with similar underlying genetic defects share some clinical aspects with this disease. Currently, there are no curative therapies for these diseases of telomere dysfunction. Here, we review recent findings demonstrating that dysfunctional (i.e., uncapped) telomeres can downregulate the WNT pathway, and that restoration of WNT signaling helps to recap telomeres by increasing expression of shelterins, proteins that naturally bind and protect telomeres. We discuss how these findings are different from previous observations connecting WNT and telomere biology, and discuss potential links between WNT and clinical manifestations of the DC spectrum of diseases. Finally, we argue for exploring the use of WNT agonists, specifically lithium, as a possible therapeutic approach for patients with DC.

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Telomere length and hTERT in mania and subsequent remission

Abstract: TL and hTERT gene expression might reflect a novel aspect of BD pathophysiology and TL might represent a novel biomarker for BD staging.

Cited by 18 publications

References 38 publications

Lithium and the Interplay Between Telomeres and Mitochondria in Bipolar Disorder

Lithium and the Interplay Between Telomeres and Mitochondria in Bipolar Disorder

Mood Disorders, Accelerated Aging, and Inflammation: Is the Link Hidden in Telomeres?

A regulatory loop connecting WNT signaling and telomere capping: possible therapeutic implications for dyskeratosis congenita

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