Millions of Americans suffer from depression. And few find relief even after several months on antidepressants. Research suggests the problem may stem from the way mental illness is diagnosed.
Diseases such as cancer or heart disease can be physically confirmed with objective lab tests, but the problem with diagnosing psychiatric conditions is that they are classified somewhat vaguely as clusters of reported symptoms. A person can be diagnosed as clinically depressed if they say they have low mood and meet at least four additional criteria. Depression can manifest differently from person to person – and symptoms can vary wildly. There really hasn’t been away to differentiate patients who have different kinds of depression. Until now, this has been a
big obstacle in understanding the neurobiology of depression.
Previous studies have shown that stress throws off the flexibility circuits in certain depressed individuals – whereas other people become depressed for different reasons. That is consistent with the view that depression is not just ‘one biological thing.’ In 2008, the National Institute of Mental Health initiated a new set of research priorities which encourages scientists studying mental illness to drill down to core mechanisms rather than placing disorders under blanket labels. This shift in thinking has invigorated the search for a range of biomarkers for depression
—toxic free radicals, the stress hormone cortisol and even epigenetics (environmental triggers that switch genes on and off).
Researchers have previously used functional magnetic resonance imaging (fMRI) to check for differences in brain connectivity between depressed and healthy people. The analysis showed depressed people could be distinguished from healthy ones based on brain connectivity differences measured by fMRI in the limbic and frontostriatal areas. The limbic system controls emotions and frontostriatal networks help coordinate motor and cognitive functions. One brain area, called the subgenual cingulate cortex, has unusually strong connections with other regions of the brain in people who are depressed.
But in the most recent study, researchers used fMRI, to measure the strength of brain connections between neural circuits. Four subtypes of depression were analyzed. These fMRI-based subdivisions could be linked to particular symptoms. Patients falling into the first two subtypes reported more fatigue whereas those in the other two reported more trouble feeling pleasure. This subtyping has implications not just for diagnosis but potentially for non-pharmaceutical treatment.
People with depression subtype 1 were three times as likely to benefit from a newer therapy known as transcranial magnetic stimulation, or TMS. This technology uses a magnet to produce small electric currents in brain areas affected by depression. Another technology being successfully used is trans cranial direct stimulation or alternating current, tDCS/tACS. The brain will mimic or emulate the tDCS/tACS fed into it and the capillary blood flow increases.
These findings and future research could help develop clearer diagnoses and enable doctors to tailor more personalized and new therapies targeting the specific form of depression in each individual patient.