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.