Mohamad El Haj1, Marie Caillaud2, Luciano Fasotti3, Christophe Verny4, Philippe Allain5. 1. LUNAM Université, Laboratoire de Psychologie des Pays de la Loire, Université de Nantes et Angers, France Neuropsychology and Auditory Cognition, Department of Psychology, University of Lille, France Laboratoire Epsylon, EA 4556, Université Paul-Valery, Montpellier III, France. 2. LUNAM Université, Laboratoire de Psychologie des Pays de la Loire, Université de Nantes et Angers, France Neuropsychology and Auditory Cognition, Department of Psychology, University of Lille, France. 3. Radboud University Nijmegen, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands Rehabilitation Medical Centre Groot Klimmendaal, SIZA Support and Rehabilitation, Arnhem, The Netherlands. 4. Centre Mémoire de Ressources et de Recherches, CHU Angers, France. 5. LUNAM Université, Laboratoire de Psychologie des Pays de la Loire, Université de Nantes et Angers, France Centre Mémoire de Ressources et de Recherches, CHU Angers, France.
Abstract
BACKGROUND: Huntington's disease (HD) is characterized by episodic memory deterioration. OBJECTIVE: Our paper investigates the cognitive mechanisms that might underlie this decline. To this aim, we tested two executive hypotheses, the binding and the inhibition hypotheses. METHODS: Fifteen HD patients (Mean Cytosine-Adenine-Guanine repeats = 44.93, SD = 2.82), and eighteen controls matched for age, gender and education were assessed with a neuropsychological battery tapping episodic memory and several executive functions, including binding and inhibition. RESULTS: Episodic decline in patients with HD was only related to binding performance. CONCLUSIONS: Our study shows that HD patients suffer from a perturbation of the associative or integrative mechanisms responsible for the combination of different memory features into complex episodic representations. Damage to frontal-hippocampal circuitry in HD is likely to be responsible for this impairment.
BACKGROUND:Huntington's disease (HD) is characterized by episodic memory deterioration. OBJECTIVE: Our paper investigates the cognitive mechanisms that might underlie this decline. To this aim, we tested two executive hypotheses, the binding and the inhibition hypotheses. METHODS: Fifteen HDpatients (Mean Cytosine-Adenine-Guanine repeats = 44.93, SD = 2.82), and eighteen controls matched for age, gender and education were assessed with a neuropsychological battery tapping episodic memory and several executive functions, including binding and inhibition. RESULTS:Episodic decline in patients with HD was only related to binding performance. CONCLUSIONS: Our study shows that HDpatients suffer from a perturbation of the associative or integrative mechanisms responsible for the combination of different memory features into complex episodic representations. Damage to frontal-hippocampal circuitry in HD is likely to be responsible for this impairment.
Entities:
Keywords:
Binding; Huntington's disease; episodic memory; executive function
Authors: Jason Geyer; Philip Insel; Faraz Farzin; Daniel Sternberg; Joseph L Hardy; Michael Scanlon; Dan Mungas; Joel Kramer; R Scott Mackin; Michael W Weiner Journal: Alzheimers Dement (Amst) Date: 2015-06-03