Depression in residential care: A UK primary care perspective

Abstract

Since Aaron Beck proposed his cognitive model of depression, biased attention, biased processing, and biased rumination (different phases of biased cognition) have been considered as the key elements consistently linked with depression. Increasing evidence suggests that the functional failures in the “emotional processing system (EPS)” underlie the neurological foundation of the biased cognition of depression. Light therapy, a non-intrusive approach, exerts powerful effects on emotion and cognition and affects the activity, functional connectivity, and plasticity of multiple brain structures. Although numerous studies have reported its effectiveness in treating depression, the findings have not been integrated with Beck’s cognitive model and EPS, and the neurobiological mechanisms of antidepressant light therapy remain largely unknown. In this review, integrated with the classical theories of Beck’s cognitive model of depression and EPS, we identified the key neural circuits and abnormalities involved in the cognitive bias of depression and, accordingly, identified and depicted several light-sensitive circuits (LSCs, neural circuits in the EPS that are responsive to light stimulation) that may underlie the antidepressant neural targets of light therapy, as listed below:•Retina (rods/cones)–thalamic regions (LGN, pulvinar, and SC)–visual cortex.•ipRGCs hypothalamic (SCN, PVN, DMH, SPVZ, LH)–preoptic areas (DMH–VLPO)–brainstem (DMH–LC)/other regions (pituitary and pineal gland).•ipRGCs–limbic regions (LHb and amygdala).•ipRGCs–thalamic regions (vLGN/IGL and OPN)–LHb.•Thalamic region/brainstem region/hypothalamic region–amygdala, amygdala–mPFC–PFC, amygdala–ACC–PFC, brainstem (VTA/LC)–ACC–PFC.In summary, the LSCs above narrow down the research scope of identifying the neural targets of antidepressant light therapy and help elucidate the neuropsychological mechanism of antidepressant light therapy.