| Περίληψη: | Bipolar disorder (BD) is a mood disorder that manifests itself through manic and
depressive episodes. About 1-2 percent of the population is affected by the
disease. It's been proposed that bipolar disorder (BD) is linked to accelerated
aging and cell senescence. Lithium is the mainstay treatment as a mood
stabilizer in BD, both as an acute treatment for mania and as a prophylactic
intervention. Despite the fact that 30% of patients experience complete
symptom remission with chronic treatment, a large proportion of individuals do
not respond well. In addition, it is widely known that lithium is a drug that has a
narrow therapeutic range and a wide range of mild to severe side effects. The
patient response to lithium appears to have a strong hereditary basis, and
lithium responders appear to have a more uniform disease manifestation.
Individuals with psychiatric diseases, and in particular those with BD, have a
lower life expectancy than people in the general population. This is primarily
caused by three factors: an increase in the prevalence of metabolic and
cardiovascular diseases, as well as an increase in the risk of a suicide attempt.
Elderly people are more likely to develop cardiovascular and metabolic
diseases, and these pathologies are additionally characterized by a persistent
inflammatory state, a trait often present in psychiatric disorders. As a result, we
realize that there is an accelerating aging of the pathogenesis of psychiatric
disorders which is indicated by the increased incidence of age-related
disorders. This conclusion is molecularly supported by modified cell aging
markers, including reduced telomere length. Because of its relationship with
memory function and hippocampus shape, telomere length variation is currently
considered a promising biomarker of susceptibility to neuropsychiatric
diseases. While the evidence supporting shorter telomeres in BD is conflicting,
a recent study found that long-term lithium medication is linked to longer
telomeres in the disease. In our study, we tried to compare telomere length (TL)
between patients treated with BD and healthy controls (HR) and also to explore
if telomere length (TL) differed in clinical responders and non-responders to
lithium (LiRs, non-LiRs). This is the first study exploring if TL differs in cell lines
(LCLs) derived from BD patients with different clinical response to Lithium. Our
findings confirm our previous studies showing that TL does not differ between
R and non-R in lithium. In addition, we suggest that 7 days of treatment may
not be enough to measure any effect of lithium on TL. Thus, not necessarily
excluding, this could take place should the treatment be longer, as in the clinical
setting
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