It examines the relationship between TL as a molecular marker of aging and LLD diagnosis, depressive symptom severity, and cognitive performance in older adults.
Several hypotheses have been proposed to explain the emergence of a premature aging phenotype in late-life depression, such as dysregulation of the glucocorticoid cascade, increased allostatic load, and telomere shortening.
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This study was a randomized controlled trial (RCT) based on questionnaire measurements, and physical activity scores and blood sample analyzes were performed at baseline and at six-month follow-up in all study participants.
Linear regression analyzes were performed to determine whether early subjective depressive symptoms, cognitive complaints, and several blood biomarkers were associated with TL.
In total, 137 relatively healthy elderly (60–79 years) were included in this prospective RCT. The team observed decreases in TL of approximately 0.06 and 0.11−0.14 kbps for a one-point increase in geriatric depression scale and cognitive complaints interview scores, respectively, at baseline and at six-month follow-up.
They also found that TL decreased by approximately 0.08−0.09 kbps for a one-point increase in interleukin (IL)-6 levels at baseline and at six-month follow-up.
They showed both In relatively healthy older individuals, early subjective depressive symptoms and cognitive complaints were associated with relatively shorter TL. in a randomized controlled prospective study.
Furthermore, a shorter TL was associated with increased IL-6 levels in our study participants. These findings lead researchers to believe that IL-6, an inflammatory cytokine, plays an important role in the association of TL shortening with early subjective depressive mood and cognitive complaints.
Although the results need to be verified by a large-scale RCT in the future, they believe that these findings will help prevent and treat depression and cognitive impairment in healthy older adults.
Source: Eurekalert
