Through your eyes or mine? The neural correlates of mental state recognition in Huntington's disease

Background: Empathy is a multidimensional construct and a key component of social cognition. In Huntington’s disease (HD), little is known regarding the phenomenology and the neural correlates of cognitive and affective empathy, and regarding how empathic deficits interact with other behavioral and cognitive manifestations. Objective: To explore the cognitive and affective empathy disturbances and related behavioral and neural correlates in HD. Methods: Clinical and sociodemographic data were obtained from 36 healthy controls (HC) and 54 gene-mutation carriers (17 premanifest and 37 early-manifest HD). The Test of Cognitive and Affective Empathy (TECA) was used to characterize cognitive (CE) and affective empathy (AE), and to explore their associations with grey matter volume (GMV) and cortical thickness (Cth). Results: Compared to HC, premanifest participants performed significantly worse in perspective taking (CE) and empathic distress (AE). In symptomatic participants, scores were significantly lower in almost all the TECA subscales. Several empathy subscales were associated with the severity of apathy, irritability, and cognitive deficits. CE was associated with GMV in thalamic, temporal, and occipital regions, and with Cth in parietal and temporal areas. AE was associated with GMV in the basal ganglia, limbic, occipital, and medial orbitofrontal regions, and with Cth in parieto-occipital areas. Conclusion: Cognitive and affective empathy deficits are detectable early, are more severe in symptomatic participants, and involve the disruption of several fronto-temporal, parieto-occipital, basal ganglia, and limbic regions. These deficits are associated with disease severity and contribute to several behavioral symptoms, facilitating the presentation of maladaptive patterns of social interaction.

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G01 Neural correlates of empathy and context evaluation in Huntington's disease patients

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp.2010.222646.1 ◽

2010 ◽

Vol 81 (Suppl 1) ◽

pp. A31.1-A31

Author(s):

E Lepron ◽

H Gros ◽

F Calvas ◽

G Viallard ◽

J-F Démonet

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Neural Correlates

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Confirming a Drosophila Melanogaster Model of Huntingtin Aggregation

Innovation in Aging ◽

10.1093/geroni/igab046.3673 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. 1036-1037

Author(s):

Akosua Biritwum ◽

Simon Levy ◽

Bess Frost ◽

Atanu Duttaroy

Keyword(s):

At Risk ◽

Drosophila Melanogaster ◽

Huntington's Disease ◽

Huntington’S Disease ◽

Mental State ◽

Research Study ◽

Autosomal Dominant ◽

Robust Approach ◽

The Future ◽

Experimental Process

Abstract For decades, doctors, psychologists, and psychiatrists alike have struggled to treat the symptomatic effects of Huntington’s disease. Huntington’s disease is an autosomal dominant brain disease that results in the deterioration of a person’s physical and mental state. Once a person inherits the disease, they end up dying from it more often than not. At present, there are 41,000 Americans with symptomatic Huntington’s disease, and 200,000 more are currently at-risk of inheriting the disease. Given its 50/50 chance of inheritance, there seems to be no end in sight to this degenerative ailment. My research study, however, will show that with a more robust approach, finding a cure for this disease is possible. Ultimately, the aim of this project was to test an already established model in Drosophila melanogaster regarding the “huntingtin” protein responsible for Huntington’s disease. This was achieved by first demonstrating that the flies which were modified to produce huntingtin could, in fact, produce the protein. Secondly, an experimental process was created to configure a system through which the amount of protein produced by each fly could be quantified. This quantification was vital in creating a baseline that would allow for the identification of potential therapeutic treatments in the future. In short, by establishing a quantifiable model for huntingtin, this study will pave the way to new insights on huntingtin aggregation and the identification of possible treatments for Huntington’s disease in the future.

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Neural correlates associated with impaired disgust processing in pre-symptomatic Huntington's disease

Brain ◽

10.1093/brain/awh165 ◽

2004 ◽

Vol 127 (6) ◽

pp. 1446-1453 ◽

Cited By ~ 114

Author(s):

A. Hennenlotter

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Neural Correlates

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H01 How Do Mental State Inferences Shape The Social World In Huntington's Disease?

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2014-309032.146 ◽

2014 ◽

Vol 85 (Suppl 1) ◽

pp. A51-A52

Author(s):

C. Eddy ◽

H. Rickards

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Mental State ◽

Social World ◽

The Social

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Corticostriatal signatures of schadenfreude: evidence from Huntington’s disease

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2017-316055 ◽

2017 ◽

Vol 89 (1) ◽

pp. 112-116 ◽

Cited By ~ 14

Author(s):

Sandra Baez ◽

Mariana Pino ◽

Mildred Berrío ◽

Hernando Santamaría-García ◽

Lucas Sedeño ◽

...

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Neural Correlates ◽

Brain Regions ◽

Reward Processing ◽

Social Emotion ◽

The Relationship ◽

Regional Brain Atrophy ◽

Shed Light

Schadenfreude—pleasure at others’ misfortunes—is a multidetermined social emotion which involves reward processing, mentalising and perspective-taking abilities. Patients with Huntington’s disease (HD) exhibit reductions of this experience, suggesting a role of striatal degeneration in such impairment. However, no study has directly assessed the relationship between regional brain atrophy in HD and reduced schadenfreude. Here, we assessed whether grey matter (GM) atrophy in patients with HD correlates with ratings of schadenfreude. First, we compared the performance of 20 patients with HD and 23 controls on an experimental task designed to trigger schadenfreude and envy (another social emotion acting as a control condition). Second, we compared GM volume between groups. Third, we examined brain regions where atrophy might be associated with specific impairments in the patients. While both groups showed similar ratings of envy, patients with HD reported lower schadenfreude. The latter pattern was related to atrophy in regions of the reward system (ventral striatum) and the mentalising network (precuneus and superior parietal lobule). Our results shed light on the intertwining of reward and socioemotional processes in schadenfreude, while offering novel evidence about their neural correlates.

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