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Evolving theories of the pathophysiology of major depression have implicated overactivation of inflammatory pathways, ill-defined changes in glutamate metabolism, and disconnection of cortical and subcortical components of a neural reward circuit. Two studies provide compelling evidence linking these three phenomena.
In a study of 50 outpatients with untreated depression, researchers used magnetic resonance spectroscopy to measure glutamate in the basal ganglia and anterior cingulate. They also measured C-reactive protein (CRP) levels in plasma and cerebrospinal fluid (CSF), as well as anhedonia and psychomotor slowing (features of depression that can be caused by interferon-alpha treatment). An elevated plasma CRP level was associated with …