There is evidence that there may be neurological indicators of early onset<unk> . There are several brain structures (corpus callosum and frontal lobe) that are different in women with<unk>  than in those without<unk> . This may indicate that there is a developmental difference between these two groups. Another study, which used fMRI techniques to assess the differences between individuals with<unk>  and other people, found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing emotions such as fear) was more activated in<unk>  patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion). A study comparing healthy individuals to people with<unk>  indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas people with<unk>  expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with<unk> . This provides neurological evidence of the dulling of emotion that individuals with<unk>  have learned to use to protect themselves from overly strong negative feelings, compared to healthy people. There is some evidence of a genetic basis for all types of depression, including<unk> . A study using identical and fraternal twins indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that<unk>  is caused in part by heredity. A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress) and its involvement with<unk>  (e.g. phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal functioning) as well as forebrain serotonergic mechanisms. Since this model is highly provisional, further research is still needed.
Dysthymia
Euthymia 
Cyclothymia
Myokymia
Congenital athymia
Minor depressive disorder
Atypical depression
Panic disorder