[The intestinal microbiota: A new player in depression?] / Le microbiote intestinal : un nouvel acteur de la dépression ?

Depression is the leading cause of disability in the world according to the World Health Organization. The effectiveness of the available antidepressant therapies is limited. Data from the literature suggest that some subtypes of depression may be associated with chronic low grade inflammation. The uncovering of the role of intestinal microbiota in the development of the immune system and its bidirectional communication with the brain have led to growing interest on reciprocal interactions between inflammation, microbiota and depression. Our purpose is to review the state of knowledge on these interactions. METHODS: We carried out a literature search on Pubmed, Go pubmed, psyC info, Elsevier, Embase until August 13, 2016 using the keywords "depression", "microbiota" and "inflammation". RESULTS: Dysbiosis reported in patients suffering from depression seems to contribute to low grade systemic inflammation which in turn feeds back depression. The hypothetical mechanisms behind these interactions are multiple: leaky gut, hyperreactivity of the corticotropic axis, disturbed neurotransmission. Abnormal microbial exposure during childhood and perinatal stress are reported to influence both the maturation of the immune system and the microbiota hence contributing to the ethiopathogeny of depression. There is no evidence in the literature to support a role for diet. CONCLUSION: The evidence supporting a causal relationship between dysbiosis and depression through low grade inflammation is limited and precludes us from drawing firm conclusions. Further studies are needed to improve our knowledge.

Telomere length and mitochondrial DNA copy number in bipolar disorder: identification of a subgroup of young individuals with accelerated cellular aging.

The 10-15-years decrease in life expectancy observed in individuals with bipolar disorder (BD) has been linked to the concept of accelerated cellular aging. Telomere length (TL) and mitochondrial DNA copy number (mtDNAcn) have been proposed as markers of cellular aging and comparisons between individuals with BD and healthy controls (HC) sometimes led to conflicting results. Previous studies had moderate sample sizes and studies combining these two markers into a single analysis are scarce. Using quantitative polymerase chain reaction, we measured both TL and mtDNAcn in DNA (peripheral blood) in a sample of 130 individuals with BD and 78 HC. Regression analyses, receiver operating characteristic (ROC), and clustering analyses were performed. We observed significantly lower TL and mtDNAcn in individuals with BD as compared to HC (respective decrease of 26.5 and 35.8%). ROC analyses showed that TL and mtDNAcn highly discriminated groups (AUC = 0.904 for TL and AUC = 0.931 for mtDNAcn). In the whole population, clustering analyses identified a group of young individuals (age around 36 years), with accelerated cellular aging (both shorter TL and lower mtDNAcn), which consisted mostly of individuals with BD (85.5%). The subgroup of patients with young age but accelerated aging was not characterized by specific clinical variables related to the course of BD or childhood maltreatment. However, patients in this subgroup were more frequently treated with anticonvulsants. Further characterization of this subgroup is required to better understand the molecular mechanisms and the risk factors of accelerated cellular aging in BD.