People with untreated depression have lower levels of mitochondrial proteins. For those who responded to the SSRI antidepressants, the proteins returned to a normal level, but showed no increase in those who did not respond to medication.
A comparison of medical records reveals people who took SSRI antidepressants, specifically fluoxetine (Prozac), were less likely to die of COVID-19 than a matched control group. The findings add to a growing body of evidence that SSRIs may have beneficial effects against the worst symptoms of coronavirus.
Ketamine's rapid antidepressant action is due to specific synaptic effects, researchers report.
Combining neuroimaging and artificial intelligence, researchers identified novel brain signatures unique to the response of each antidepressant.
The placebo effect combined with dopamine levels can determine whether symptoms of depression and social anxiety will improve in patients prescribed SSRI antidepressants. Researchers found the positive effect of the medications was four times higher in patients with high expectations the treatment would work compared to those with lower expectations.
Mirtazapine, an antidepressant commonly prescribed to treat dementia-associated agitation, is no more effective than a placebo and may increase mortality risks, researchers report.
Psilocybin, a natural psychoactive compound currently being considered for the treatment of depression, alters people's emotional states while listening to music. While listening to music, those who used psilocybin reported enhanced emotional processing. Researchers say combining music with psychedelic therapy may have positive benefits for those suffering from depression.
In the absence of neural activity, BDNF expression can still be activated. The findings shed light on how therapeutic ketamine used has an antidepressant effect and how it works in both the long and short term.
Prozac reduced polyunsaturated fatty acid lipid concentrations in the brains of juvenile macaque monkeys.
Allopregnanolone, a neuroactive steroid used in the treatment of postpartum depression, alters neural communication in the basolateral amygdala, an area of the brain associated with emotion and mood regulation. The drug may alter the network associated with chronic stress, which may explain its persistent antidepressant effect.
A new study adds to the growing body of research linking inflammation to depression. Researchers found the molecule histamine directly inhibits the release of serotonin in the brain by attaching to inhibitory receptors on serotonin neurons in mice.
The MeCP2 gene influences ketamine's behavioral effect and strengthens synapses, leading to an improvement in the drug's antidepressant effect over time.
