Reward sensitivity deficits modulated by dopamine are associated with apathy in Parkinson’s disease

Muhammed, Kinan; Manohar, Sanjay; Yehuda, Michael Ben; Chong, Trevor T.‐J.; Tofaris, George K.; Lennox, Graham; Bogdanovič, Marko; Hu, Michèle; Husain, Masud

doi:10.1093/brain/aww188

Cited by 115 publications

(153 citation statements)

References 110 publications

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“…However, because we did not include a condition in which no reward was given, we cannot exclude motivational differences between groups as a potential contributor. In fact, based on recent findings (Muhammed et al, 2016), it is possible that Fig. 8 Correlations between composite awareness and the effect of reward on learning scores for HCs (black) and PD patients (gray).…”

Section: Comparison To Previous Studies Of Reward and Parkinson's Dismentioning

confidence: 99%

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Freedberg

Schacherer

Chen

et al. 2017

Cogn Affect Behav Neurosci

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Parkinson's disease (PD) is associated with procedural learning deficits. Nonetheless, studies have demonstrated that reward-related learning is comparable between patients with PD and controls (Bódi et al., Brain, 132(9), 2385-2395 Frank, Seeberger, & O'Reilly, Science, 306(5703), 1940-1943, 2004; Palminteri et al., Proceedings of the National Academy of Sciences of the United States of America, 106(45), 19179-19184, 2009). However, because these studies do not separate the effect of reward from the effect of practice, it is difficult to determine whether the effect of reward on learning is distinct from the effect of corrective feedback on learning. Thus, it is unknown whether these group differences in learning are due to reward processing or learning in general. Here, we compared the performance of medicated PD patients to demographically matched healthy controls (HCs) on a task where the effect of reward can be examined separately from the effect of practice. We found that patients with PD showed significantly less reward-related learning improvements compared to HCs. In addition, stronger learning of rewarded associations over unrewarded associations was significantly correlated with smaller skin-conductance responses for HCs but not PD patients. These results demonstrate that when separating the effect of reward from the effect of corrective feedback, PD patients do not benefit from reward.

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Section: Comparison To Previous Studies Of Reward and Parkinson's Dismentioning

confidence: 99%

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Freedberg

Schacherer

Chen

et al. 2017

Cogn Affect Behav Neurosci

View full text Add to dashboard Cite

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“…In contrast with lesion-related markers, generalized markers of vascular brain pathology like white matter hyperintensities (WMH), cerebral microbleeds, (silent) old infarcts, as well as degenerative pathology like cerebral atrophy are less frequently studied in association with PSD, though there are suggestions that they play a role in the development of PSD as well. [46][47][48][49] Furthermore, there are hypotheses that PSD may be related to an increased inflammatory response 50 and also genetic polymorphisms in the serotonin system might be involved. 51 In addition to abovementioned biological factors, psychosocial mechanisms are suggested to be involved in the development of PSD.…”

Section: Etiology and Predictors Of Psdmentioning

confidence: 99%

“…47 It was traditionally seen as a symptom of other syndromes (e.g. depression and dementia), but mounting evidence suggests that it might be an independent syndrome with a different etiology.…”

Section: Post-stroke Apathymentioning

confidence: 99%

“…Therefore, apathy can also be measured with a behavioural task, like a reward sensitivity task. Studies using this task showed that stroke patients 46 and patients with Parkinson's disease 47 with apathy showed impaired reward sensitivity. This reward insensitivity appeared to be related to reduced pupillary dilation, 47 and may therefore provide a novel and useful objective clinical marker of apathy.…”

Section: Conceptual and Clinical Implicationsmentioning

confidence: 99%

“…This is important for treatment and rehabilitation, as focusing on early detection of PSD and PSA might result in a better clinical outcome after stroke. 47 Strengths of this study are the longitudinal design and the low dropout rates at follow-up. In addition, validated instruments were used to evaluate the presence and level of depression, apathy, and personality traits.…”

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Depression and apathy after stroke

Douven¹

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Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: A potential candidate vulnerability mechanism for neurodegeneration in PTSD

Olivé

Makris

Densmore

et al. 2021

Human Brain Mapping

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Individuals with posttraumatic stress disorder (PTSD) are at increased risk for the development of various forms of dementia. Nevertheless, the neuropathological link between PTSD and neurodegeneration remains unclear. Degeneration of the human basal forebrain constitutes a pathological hallmark of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. In this seed-based resting-state (rs-)fMRI study identifying as outcome measure the temporal BOLD signal fluctuation magnitude, a seed-to-voxel analyses assessed temporal correlations between the average BOLD signal within a bilateral whole basal forebrain region-of-interest and each whole-brain voxel among individuals with PTSD (n = 65), its dissociative subtype (PTSD+DS) (n = 38) and healthy controls (n = 46). We found that compared both with the PTSD and healthy controls groups, the PTSD+DS group exhibited increased BOLD signal variability within two nuclei of the seed region, specifically in its extended amygdaloid region: the nucleus accumbens and the sublenticular extended amygdala. This finding is provocative, because it mimics staging models of neurodegenerative diseases reporting allocation of neuropathology in early disease stages circumscribed to the basal forebrain. Here, underlying candidate etiopathogenetic mechanisms are neurovascular uncoupling, decreased connectivity in local-and large-scale neural networks, or disrupted mesolimbic dopaminergic circuitry, acting indirectly upon the basal forebrain cholinergic pathways. These abnormalities may underpin reward-related deficits representing a putative link between persistent traumatic memory in PTSD and anterograde memory deficits in neurodegeneration.Observed alterations of the basal forebrain in the dissociative subtype of PTSD point towards the urgent need for further exploration of this region as a potential candidate vulnerability mechanism for neurodegeneration in PTSD.

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Reward sensitivity deficits modulated by dopamine are associated with apathy in Parkinson’s disease

Cited by 115 publications

References 110 publications

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Depression and apathy after stroke

Altered basal forebrain BOLD signal variability at rest in posttraumatic stress disorder: A potential candidate vulnerability mechanism for neurodegeneration in PTSD

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