Reconsidering anhedonia in depression: Lessons from translational neuroscience

In the citing paper

“Anhedonia and impaired reward circuit pathways are associated with a poorer prognosis and suboptimal treatment response (Buckner et al., 2008;Uher et al., 2012;Treadway and Zald, 2011).”

In the citing paper

“studies of the neurobiology of reward processing have highlighted the variety of distinct pathways involved in its different aspects resulting in the recognition of separate subtypes of anhedonia, including consummatory, anticipatory, motivational and decisional [20,21].”

In the citing paper

“Anhedonia is a broad construct that includes deficits in anticipation of, motivation toward, and responsiveness to reward, as well as deficits in reward learning (ability to recall and make decisions based on past rewarding experiences) (Treadway and Zald, 2011) and is estimated to be 46% heritable in studies of monozygotic twins (Bogdan and Pizzagalli, 2009).”

In the citing paper

“hyposensitivity to reward and hypersensitivity to punishment have been a consistent finding in depression”

In the citing paper

“Dysregulation of dopamine release in motivating responses to rewarding and aversive stimuli, as well as cognitive demand, is a plausible mechanistic cause that can explain a range of depression symptoms [24][25][26][27][28][29].”

In the citing paper

“Particularly relevant in the present context are previous reports [290,296,297] that although both DA and non-DA agents can be used to effectively treat mood disorders, DA agents generally have superior effects on symptoms of anhedonia, specifically when compared with non-DA agents [19,298-300].”

In the citing paper

“The mesolimbic DA system represents only one component of a very complex and integrated set of circuits, and although DA is clearly a crucial neurotransmitter in the reward-processing system, non-DA systems clearly also modulate reward responsibility [19,735].”

In the citing paper

“Additionally, multiple non-DA compounds have shown efficacy in improving reward responses, such as agents that affect glutamate circuits involved in regulating monoamine systems [19].”

In the citing paper

“However, recent studies suggest that many patients with schizophrenia or Parkinson’s, and possibly some with major depression, are not actually anhedonic after all: they report normal sensory pleasure ratings of ice cream or other sensory reward in the moment, even though they attach little value to any sensory, social or other pleasant reward in life.”

In the citing paper

“Some investigators therefore have suggested their deficit really reflects a selective loss of incentive motivation or ‘wanting,’ rather than loss of pleasure ‘liking’ (Sienkiewicz-Jarosz et al., 2005; Dowd and Barch, 2010; Treadway and Zald, 2011; Barch et al., 2014).”

In the citing paper

“Anhedonia typically does not respond to first-line pharmacotherapies [5, 7, 8]”

In the citing paper

“co-morbid traits, such as depression, anxiety, or inattention/hyperactivity, are often associated with ASD [212], and are known to affect general reward processing [213,214] and intervention response [215].”