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.
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