Cognitive deficits in Parkinson’s disease

Abstract

Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.

Periodic Limb Movements in Sleep are Associated with Greater Cognitive Decline in Older Men without Dementia

“…[21][22][23] Moreover, dopamine deficit, as a frequently suggested cause of PLMS, 4 also plays a key role in neurodegeneration and affects particularly the prefrontal cortex area, which regulates executive function. 24,25 Previous research suggests that executive function is a better predictor of functional decline and mortality in older women 26 ; thus, the current finding on PLMS and decline in executive function might have important clinical implications. Finally, PLMS could be a marker of sleep fragmentation, 2 and there is increasing recognition on the role of sleep disturbances in cognitive impairment.…”

Distinct Contribution of the Striatum and Cerebellum to Motor Learning

“…One possible interpretation of these results, is that this deficit might be attributed to difficulties in ancillary cognitive processes and not to a learning impairment per se. Given that the SRT task requires both attentional and visuospatial processing abilities and that deficits in each of these functions have been reported in patients with a striatal dysfunction (Boller, Passafiume, Keefe, Rogers, Morrow, & Kim, 1984;Doyon, Bourgeois, & Bédard, 1996a;see Brown & Marsden, 1990;Dubois, Boller, Pillon, & Agid, 1991;Ogden, 1990, for reviews), one could argue that the impairment is due to a deficit in these processes. However, the results of the present study suggest that this is not the case because if a problem in attentional and/or visuospatial functions was the source of the impairment, group differences should have been readily observed on the first session of training.…”

A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice

“…Cognitive decline afflicts virtually all aging animals and in humans is also associated with neuropathologies such as Alzheimer's (AD) and Parkinson's (PD) diseases (Kausler 1994;Dubois and Pillon 1997;Chen et al 2001). Modern industrialized societies face rapidly aging cohorts at high risk for cognitive deterioration and pathology.…”