The aims of this study are to examine differences in depressive symptoms, measures of negative affective responding, and measures of positive affective responding as a function of insomnia and inflammatory challenge. To test this hypothesis, this protocol paper describes a placebo-controlled, randomized, double-blind study of low dose endotoxin in older adults (n = 160 60–80 y) with insomnia vs. This study hypothesizes that insomnia serves as a vulnerability factor for inflammation-related depression older adults with insomnia will show heightened inflammatory- and affective responding to inflammatory challenge as compared to those without insomnia. In turn, inflammatory challenge induces depressive symptoms, which correlate with activation of brain regions implicated in depression.
Sleep disturbance activates inflammatory signaling and primes immune responses to subsequent inflammatory challenge. Yet, it is not known how insomnia gets converted into biological- and affective risk for depression, which is critical for identification of molecular targets for pharmacologic interventions, and for refinement of insomnia treatments that target affective responding to improve efficacy. Insomnia predicts depression recurrence and is a modifiable target to prevent incident and recurrent depression in older adults. Because of the burgeoning population of older adults, the enormous burden of late-life depression, and the limited efficacy of current antidepressants in older adults, biologically plausible models that translate into selective depression prevention strategies are needed. Depression, one of the most common diseases in older adults, carries significant risk for morbidity and mortality.
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