Aspects of procedural memory are differentially impaired in huntington's disease

Abstract

Procedural memory encompasses several phenomena, including motor and perceptual learning, cognitive rule learning and priming. These subclasses are differentially affected by differing neuropathologies, suggesting their functional independence and reliance upon different neural substrates. To test this hypothesis, performance on a maze learning task was compared in 15 Huntington's disease (HD) patients and 15 normal controls (NC) to assess specific route learning, cognitive skill learning and the effects of route predictability on performance. Results revealed that the HD group: (1) showed normal learning curves for a specific maze route; (2) are deficient in generalizing the cognitive skills across mazes; and, (3) fail to improve performance on a maze with a predictable route relative to mazes with unpredictable routes. These results are interpreted as supporting the independence of procedural memory subclasses. The basal ganglia are suggested as important structures in mediating the ability to generalize skills and appreciate patterned organization in to-be-acted-upon stimuli.

The operant serial implicit learning task reveals early onset motor learning deficits in the HdhQ92 knock‐in mouse model of Huntington's disease

“…The Hdh Q92 ⁄ Q92 mice were unimpaired on the implicit learning component of the task as has been previously reported in mice with striatal lesions (Trueman et al, 2005). Several studies have reported that implicit learning is deficient in HD patients (Heindel et al, 1989;Bylsma et al, 1990;Knopman & Nissen, 1991;Gabrieli et al, 1997). By contrast, the Hdh Q92 ⁄ Q92 mice failed to show any detectable deficit in their ability to utilize implicit information on the predictable trials, notwithstanding their overall impairments in both speed and accuracy in responding on both predictable and unpredictable trials alike.…”

“…Several studies have reported that implicit learning is deficient in HD patients (Heindel et al. , 1989; Bylsma et al. , 1990; Knopman & Nissen, 1991; Gabrieli et al.…”

Procedural and declarative memory in obsessive-compulsive disorder

“…It should be noted that procedural memory likely involves several processes, as demonstrated by dissociations in performance on different procedural memory tasks within the same group of patients (Gabrieli et al, 1997). Nonetheless, numerous studies using a variety of tasks have shown that aspects of procedural memory are abnormal in patients with basal ganglia dysfunction such as those with Tourette's syndrome, Parkinson's and Huntington's disease, as well as animals with damage to frontostriatal circuitry (Bylsma et al, 1990;Gomez Beldarrain et al, 1999;Heindel et al, 1988;Miyachi et al, 2002;Packard & Knowlton, 2002;Pascual-Leone et al, 1995;Sarazin et al, 2002;Stebbins et al, 1995).…”

Huntington's Disease: Pathological Mechanisms and Therapeutic Strategies

“…This cognitive deficit is characterhuntingtin can also cause cell death (93). These results indicate that some inherent properties of mutant huntingized by disruptions in executive functions, procedural memory, and psychomotor skills (20,46,60). HD patin, irrespective of its ability to remain soluble or form aggregates, cause death to neurons.…”