Abstract
Anhedonia is indeed a pathogenetically important clinical phenotype and a promising endophenotype for depressive symptoms with a very high contribution of biological and genetic factors. Neurobiological mechanisms of anhedonia are impaired functioning of the reward system of the brain, which is confirmed by many neuroimaging, genetic and experimental studies. Anhedonia has a trans-diagnoctic character and should be understood as a complex phenomenon, and it is important to correctly evaluate it within the framework of a particular research paradigm. It seems optimal to form several complementary research strategies that evaluate the most important «facets» of anhedonia, regardless of the nosological form of the disease, within the framework of one study using various methods to search for adequate biomarkers of anhedonia severity (genetic, neuroimaging, biochemical). Given the high-quality organization of such comprehensive studies based on the correct methodology of evidence-based medicine, it is likely that significant biomarker systems will be available in the near future, which, if replicated in independent samples, can be used to personalize the diagnosis and treatment of depression.
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