Cognitive Deficits in Transgenic and Knock-in HTT Mice Parallel those in Huntington's Disease

2014 ◽  
Vol 3 (2) ◽  
pp. 145-158 ◽  
Author(s):  
Andrew M. Farrar ◽  
Carol A. Murphy ◽  
Neil E. Paterson ◽  
Stephen Oakeshott ◽  
Dansha He ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cognitive Deficits

Cognitive and Affective Empathy in Huntington’s Disease

2021 ◽  
pp. 1-12
Author(s):  
Arnau Puig-Davi ◽  
Saul Martinez-Horta ◽  
Frederic Sampedro ◽  
Andrea Horta-Barba ◽  
Jesus Perez-Perez ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cognitive Deficits ◽  
Perspective Taking ◽  
Neural Correlates ◽  
Affective Empathy ◽  
Grey Matter Volume ◽  
Empathy Deficits ◽  
Almost All

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.

Early cognitive deficits in Swedish gene carriers of Huntington's disease.

2007 ◽  
Vol 21 (1) ◽  
pp. 31-44 ◽  
Author(s):  
Tarja-Brita Robins Wahlin ◽  
Anders Lundin ◽  
Keith Dear
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cognitive Deficits ◽  
Gene Carriers

Reversal learning reveals cognitive deficits and altered prediction error encoding in the ventral striatum in Huntington’s disease

2016 ◽  
Vol 11 (6) ◽  
pp. 1862-1872 ◽  
Author(s):  
Katharina Nickchen ◽  
Rebecca Boehme ◽  
Maria del Mar Amador ◽  
Thomas D. Hälbig ◽  
Katharina Dehnicke ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Reversal Learning ◽  
Cognitive Deficits ◽  
Prediction Error ◽  
Ventral Striatum

Huntington's Disease: Update and Review of Neuropsychiatric Aspects

1994 ◽  
Vol 24 (3) ◽  
pp. 189-208 ◽  
Author(s):  
Mario F. Mendez
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cognitive Deficits ◽  
Neuropsychological Testing ◽  
Genetically Engineered ◽  
Caudate Nuclei ◽  
Neuropsychological Profile ◽  
Personality Changes ◽  
Testing Management ◽  
Brain Behavior

Objective: This article presents a general update on Huntington's disease (HD) and reviews the psychiatric and cognitive features of this disorder. Method: HD is discussed in five sections: an introduction and update, the psychiatric aspects, the cognitive aspects, brain-behavior relationships, and the differential diagnosis and management. Results: Recent advancements in HD include the identification of presymptomatic testing methods and HD gene defect, structural and metabolic neuroimaging findings, and a neuropsychological profile. HD is associated with mood disorders, personality changes, irritable and explosive behavior, a schizophrenia-like illness, suicidal behavior, sexuality changes, and specific cognitive deficits. Conclusions: HD results in organic mental disorders from dysfunction of prefrontal-subcortical circuits coursing through the caudate nuclei. The diagnosis of HD is aided by genetic testing, neuroimaging, and neuropsychological testing. Management involves education, genetic counseling, and psychotropic medications. Finally, the future of HD holds promise for the development of rational, neurobiologically-based treatments and genetically engineered therapies.

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