Abstract
Accelerated cellular aging, evidenced by shortened leukocyte telomere length (LTL), has been reported in Major Depressive Disorder (MDD), and may convey an increased risk for somatic co-morbidity. Shortened LTL reflects a cell’s mitotic history, cellular “age” and cumulative exposure to inflammation and oxidation, as well as the availability of telomerase, a telomere-lengthening enzyme. Telomere shortening leads to replicative senescence and cellular malfunctions including oxidative stress, mitochondrial damage, and apoptosis. Here we present data linking indices of accelerated cellular aging to worse antidepressant treatment response in MDD.
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