This explores the association between TL as a molecular marker of aging and diagnosis of LLD, the severity of depressive symptoms, and cognitive performance in older adults.
Several hypotheses have been proposed to explain the emergence of a prematurely aged phenotype in late-life depression, such as glucocorticoid cascade dysregulation, increased allostatic load, and telomere shortening.
This study was a randomized controlled trial (RCT) based on the measurement of the questionnaire and physical activity scores and blood sample analyses were performed at baseline and after six months of follow-up in all study participants.
Linear regression analyses were performed to identify whether early subjective depressive symptoms, cognitive complaints, and several blood biomarkers are associated with TL.
Altogether, 137 relatively healthy elderly individuals (60-79 years old) were enrolled in this prospective RCT. The team observed an approximate decrease of 0.06 and 0.11−0.14 kbps of TL per one-point increase in the geriatric depression scale and cognitive complaint interview scores, respectively, at baseline and after six months of follow-up.
They also found an approximate decrease of 0.08−0.09 kbps of TL per one-point increase in interleukin (IL)-6 levels at baseline and after six months of follow-up.
They showed that both early subjective depressive symptoms and cognitive complaints in relatively healthy elderly individuals were associated with a relatively shorter TL in the randomized controlled prospective study.
In addition, a shorter TL was associated with increased IL-6 levels in our study participants. These findings make researchers believe that IL-6, an inflammatory cytokine, plays an important role in the relationship of shortening TL with early subjective depressive mood and cognitive complaints.
Although the results will need to be verified through a large-scale RCT in the future, they believe that these findings will help prevent and treat depression and cognitive impairment in the healthy elderly.
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