Reward processing in neurodegenerative disease

Abstract

Representation of reward value involves a distributed network including cortical and subcortical structures. Because neurodegenerative illnesses target specific anatomic networks that partially overlap with the reward circuit they would be predicted to have distinct impairments in reward processing. This review presents the existing evidence of reward processing changes in neurodegenerative diseases including mild cognitive impairment, Alzheimer's disease, frontotemporal dementia, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease, as well as in healthy aging. Carefully distinguishing the different aspects of reward processing (primary rewards, secondary rewards, reward-based learning, and reward-based decision-making) and using tasks that differentiate the stages of processing reward will lead to improved understanding of this fundamental process and clarify a contributing cause of behavioral change in these illnesses.

Deconstructing empathy: Neuroanatomical dissociations between affect sharing and prosocial motivation using a patient lesion model

“…This suggests that being capable of experiencing a reward state may predispose one towards engaging in helping behaviors, while conversely the reduced capacity for reward may decrease the tendency towards prosocial behavior, as has been shown in animal and human models (Heshmati and Russo, 2015; Riga et al, 2015). There is evidence from other NDG lesion studies that some patient groups are less likely to seek out social reward than others (Perry et al, 2014; Perry and Kramer, 2015), and that patients with damage to reward circuitry are more likely to be socially and emotionally detached (Bickart et al, 2014). Taken with our findings, this suggests that reward circuitry may be necessary to experience prosocial motivation.…”

Frontotemporal Dementia: diagnosis, Deficits and Management

“…Given the prominent socioemotional and behavioral symptoms associated with FTD syndromes throughout disease course, there is a great need to further develop clinical tests to operationalize decision-making impairments [165], methods for tracking progression of impairment [84] and ways to prospectively identify patients at greatest risk of harm in the presence of these impairments.…”

Prosocial deficits in behavioral variant frontotemporal dementia relate to reward network atrophy

“…We included age, sex, CDR Total, diagnosis (two variables dummy coded 1 and 0 for the three diagnostic categories), and total intracranial volume (a total of gray matter, white matter, and cerebrospinal fluid volume, to account for individual differences in head size) as nuisance covariates. In order to constrain the scope of the neuroimaging analyses and to offset the loss of power incurred by multiple comparison correction, we masked our analyses to structures in the reward network: thalamus, insula, anterior cingulate cortex, caudate, putamen, pallidum, amygdala, midbrain, and ventromedial prefrontal cortex (Perry & Kramer, 2015; Perry et al., 2014). See Fig S1…”

“…These studies suggest that social relationships have reduced reward value in bvFTD and that patients are less motivated to partake in selfless acts that prioritize the feelings and needs of others. Although alterations in reward‐seeking (e.g., changes in eating, drug and alcohol use, and sexual behavior) are common in bvFTD and are associated with atrophy in reward network structures including the ventral striatum (Ahmed et al., 2015; Bocchetta et al., 2015; Perry & Kramer, 2015; Perry et al., 2014), whether alterations in reward processing also underlie patients’ waning social engagement is not well understood.…”