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Sure, we know insufficient serotonin levels get a bad rap when it comes to depression, but that's like blaming one person in a full-scale riot. Depression isn't caused by only one factor. In fact, study co-author Elyse Aurbach says we're probably not getting to the core of why people are depressed because "the brain is immensely complex." In this study, the research team conducted eight experiments (four on animal brains, four on brains of the deceased human kind) of varying sample sizes - from 20 to 90 brains in each - and found that the brains of deceased humans who'd been depressed had increased levels of hippocampal FGF9 and that live animals with increased FGF9 levels demonstrated depressive, anxious behavior. "This is not just a correlation," study leader Huda Akil of the University of Michigan says. Less really may be more, at least when it comes to FGF9.

By early 2014, Flint, Kendler and a team of collaborators had analysed DNA sequences from 5,303 Chinese women with depression, and another 5,337 controls. As Flint expected, 85% of the depressed women had a severe form of the disorder called melancholia, which robs people of the ability to feel joy. "You can be a doting grandparent and your favourite grandchildren can show up at your door," says Douglas Levinson, a psychiatrist at Stanford University in California, "and you can't feel anything." The analysis yielded two genetic sequences that seemed to be linked to depression: one in a stretch of DNA that codes for an enzyme whose function is not fully understood, and the other next to the gene SIRT1, which is important for energy-producing cell structures called mitochondria. The correlations were confirmed in another set of more than 3,000 depressed men and women and over 3,000 controls.

Researchers have for the first time used electrical pulses delivered from a cochlear implant to deliver gene therapy, thereby successfully regrowing auditory nerves. The research also heralds a possible new way of treating a range of neurological disorders, including Parkinson's disease, and psychiatric conditions such as depression through this novel way of delivering gene therapy.

Adverse life experiences, particularly those in childhood, contribute to disease morbidity and mortality [1, 2, 3, 4, 5, 6, 7]. There is considerable interest in understanding the mechanisms through which they do so, as it remains unclear how illness becomes apparent decades after the presumed initiating event. Long-standing hypotheses include chronic activation of the hypothalamic-pituitary-adrenal axis [8, 9, 10] and alterations of neuroimmune function [11]. Molecular signatures of stressful life experiences and their relation to disease are therefore of special interest to clarify the causal relationship between signature, disease, and stress.

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