BackgroundBreast cancer is the most common cancer in women. Among the survivors, depression is one of the most common psychiatric comorbidities. This paper reports the point prevalence of major depressive disorder among breast cancer patients and the association between family support and major depressive disorder.MethodsClinical data were collected from a breast cancer clinic of a general hospital in central Taiwan. Participants included 300 patients who were older than 18 years and diagnosed with breast cancer. Among these individuals, we used Mini International Neuropsychiatric Interview (a structural diagnostic tool for psychiatric disorders) to ascertain if they had major depressive disorder. We also used the Family Adaptability, Partnership, Growth, Affection, and Resolve score to assess the family support.ResultsThe point prevalence of major depressive disorder among breast cancer patients was 8.33%, and this was positively associated with insomnia, psychiatric family history, pain severity, and radiotherapy and negatively associated with menopause, cancer duration, hormone therapy, and family support. Family support (adjusted odds ratio =0.87, 95% CI: 0.78–0.98) was found to be an associated factor for major depressive disorder in breast cancer patients after controlling for potential risk factors.ConclusionMajor depressive disorder is a common comorbidity among breast cancer patients. Family support is an important associated factor for these patients. Health care professionals should evaluate mood problems and family support while treating these patients.

Health care providers should make use of community-oriented intervention programmes that aim to strengthen psychosocial functioning. Particularly, programmes that enhance health status and mutuality should be identified and developed for both individuals with schizophrenia and their families.

Huntington’s disease (HD) is an autosomal-dominant brain disorder caused by mutant huntingtin (mHtt). Although the detailed mechanisms remain unclear, the mutational expansion of polyglutamine in mHtt is proposed to induce protein aggregates and neuronal toxicity. Previous studies have shown that the decreased insulin sensitivity is closely related to mHtt-associated impairments in HD patients. However, how mHtt interferes with insulin signaling in neurons is still unknown. In the present study, we used a HD cell model to demonstrate that the miR-302 cluster, an embryonic stem cell-specific polycistronic miRNA, is significantly downregulated in mHtt-Q74-overexpressing neuronal cells. On the contrary, restoration of miR-302 cluster was shown to attenuate mHtt-induced cytotoxicity by improving insulin sensitivity, leading to a reduction of mHtt aggregates through the enhancement of autophagy. In addition, miR-302 also promoted mitophagy and stimulated Sirt1/AMPK-PGC1α pathway thereby preserving mitochondrial function. Taken together, these results highlight the potential role of miR-302 cluster in neuronal cells, and provide a novel mechanism for mHtt-impaired insulin signaling in the pathogenesis of HD.