ABSTRACT
BACKGROUND: Bright light therapy (BLT) has been increasingly used as an experimental treatment in non-seasonal unipolar depression. While clinical trials have demonstrated the efficacy of BLT in ameliorating depression for outpatients, studies examining BLT in the psychiatric inpatient setting are currently lacking. AIM: The purpose of this study is to explore whether BLT as adjunctive treatment for depressive symptoms on an acute psychiatric floor is feasible and explore associated changes in depressive symptoms. METHODS: An observational, cross-sectional study was conducted at State University of New York (SUNY) Upstate 4B acute inpatient psychiatric unit. BLT was administered to participating patients as adjunctive therapy to their psychopharmacological and psychotherapy treatments on a daily basis throughout their hospitalization. Beck Depression Inventory-II (BDI-II), Hamilton Rating Scale for Depression (HAM-D), and Outcome Questionnaire-45.2 (OQ-45.2) were administered before commencing BLT and after their last BLT session. Changes to the aforementioned measures before and after BLT treatment, the dose response of measure changes based on number of sessions, and the hospital length of stay along with the secondary factors such as age, gender, other psychiatric comorbidities, social factors, and psychiatric medications were analyzed. RESULTS: BLT is feasible on acute psychiatric inpatient floor with adherence of 94% and has very few side effects. The repeated measures of depression and functioning demonstrated significant decrease in depression and improvement in functioning. Although not statistically significant, clinical meaningful dose-response relationship was found between a number of BLT sessions and improvement in depressive symptoms with five BLT sessions being an optimal amount for depression amelioration. CONCLUSION: BLT combined with the ongoing psychopharmacological treatment was well tolerated and easy to administer. It offers a simple, safe, and cost-effective approach to augmenting depressive treatment on an acute psychiatric floor.
ABSTRACT
Accumulating evidence implicates the transcriptional coactivator peroxisome proliferator activated receptor γ coactivator 1α (PGC-1α) in the pathophysiology of Huntington Disease (HD). Adult PGC-1α (-/-) mice exhibit striatal neurodegeneration, and reductions in the expression of PGC-1α have been observed in striatum and muscle of HD patients as well as in animal models of the disease. However, it is unknown whether decreased expression of PGC-1α alone is sufficient to lead to the motor phenotype and striatal pathology characteristic of HD. For the first time, we show that young PGC-1α (-/-) mice exhibit severe rotarod deficits, decreased rearing behavior, and increased occurrence of tremor in addition to the previously described hindlimb clasping. Motor impairment and striatal vacuolation are apparent in PGC-1α (-/-) mice by four weeks of age and do not improve or decline by twelve weeks of age. The behavioral and pathological phenotype of PGC-1α (-/-) mice can be completely recapitulated by conditional nervous system deletion of PGC-1α, indicating that peripheral effects are not responsible for the observed abnormalities. Evaluation of the transcriptional profile of PGC-1α (-/-) striatal neuron populations and comparison to striatal neuron profiles of R6/2 HD mice revealed that PGC-1α deficiency alone is not sufficient to cause the transcriptional changes observed in this HD mouse model. In contrast to R6/2 HD mice, PGC-1α (-/-) mice show increases in the expression of medium spiny neuron (MSN) markers with age, suggesting that the observed behavioral and structural abnormalities are not primarily due to MSN loss, the defining pathological feature of HD. These results indicate that PGC-1α is required for the proper development of motor circuitry and transcriptional homeostasis in MSNs and that developmental disruption of PGC-1α leads to long-term alterations in motor functioning.
