Depression - different subtypes and different pathologies

Professor Helen Mayberg discusses evidence that depression may have different subtypes relating to different genes, environments, and neuropathologies.

One of the things that’s become very clear with studies, it’s always been recognized even back to the time of Freud most specifically, that there’s always been sort of reactive kinds of depressions and depressions that seem to melancholic or endogenous, that there doesn’t seem to be a trigger in one’s environment. We got out of categorizing them by trigger related or internally generated, but in fact that kind of classification has always been there even without biology. What’s happening now is that while there may be a continuum of severity, in fact it’s always been recognized by clinicians that there really seem to be different types of depression. We’ve learned very recently that certain genes in combination with the environment really act in a synergistic way to produce a certain kind of depression, but there are patients who don’t have those genes and don’t have bad environments and who still develop depression. So our party line at the present time is not just that it’s a heterogeneous disease, but there are actually emerging ideologies, some that may be genetic-environment interaction in the stress axis, and others that may be actually lesions or interruptions of specific circuits even though those circuits may be where stress and genes interact. We’re actually trying to take at first the very simplistic notion based on the scanning - that in fact the scans can help us to understand subtypes, because in fact what you are trying to do is get the brain back in an equilibrium state. Your brain is a function of the genes, the environment you are in, and so that certain states of the brain being dysfunctional require a different intervention to get them back to an equilibrium state than a brain in a different state. So we’re asking very simply what can the brain tell us about the varying states that it’s in? Depression may be not just the lesion, but what the brain is trying to do about it and that one actually has to work with the brain’s own potential for compensation and that we may be able to define that with the images. So I think there is no doubt that we are learning that there are some patients who really have a genetic predisposition and others it’s as if the network breaks, and how can we characterize that so that our treatments are optimized to match what the brain needs in an individual.