Cognitive deficits precede motor deficits in a slowly progressing model of parkinsonism in the monkey

Schneider, Jay S.; Pope-Coleman, A.

doi:10.1016/1055-8330(95)90014-4

Cited by 95 publications

(45 citation statements)

References 31 publications

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“…Primates given chronic low doses of MPTP (to mimic Parkinson's disease) or 3-NP (to mimic Huntington's disease) display profound cognitive and visual deficits prior to the development of gross motor impairments (see Schneider & Roeltgen, 1993;Roeltgen & Schneider, 1994;Schneider & Pope-Coleman, 1995;Palfi et al, 1996). These results, along with those from selective lesions of the sensorimotor and associative portions of the primate striatum (e.g., Divac et al, 1967;Miyachi et al, 1997), support the concept that basal ganglia systems contain separate motor and cognitive circuits.…”

Section: Clinical and Pathological Studiessupporting

confidence: 69%

Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies

Middleton

Strick

2000

Brain and Cognition

603

392

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The traditional view that the basal ganglia are simply involved in the control of movement has been challenged in recent years. Three lines of evidence indicate that the basal ganglia also are involved in nonmotor operations. First, the results of anatomical studies clearly indicate that the basal ganglia participate in multiple circuits or 'loops' with cognitive areas of the cerebral cortex. Second, the activity of neurons within selected portions of the basal ganglia is more related to cognitive or sensory operations than to motor functions. Finally, in some instances basal ganglia lesions cause primarily cognitive or sensory disturbances without gross motor impairments. In this report, we briefly review some of these data and present a new anatomical framework for understanding the basal ganglia contributions to nonmotor function.

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Section: Clinical and Pathological Studiessupporting

confidence: 69%

Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies

Middleton

Strick

2000

Brain and Cognition

603

392

View full text Add to dashboard Cite

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“…Neuropsychological examination conducted in PD patients demonstrates specific impairment of executive functions in early stages [3] , thus these results suggest that this deficit may also occur in the premotor phase of the disease, a notion supported by observations in nonhuman primates that show executive dysfunction before the clinical presentation of motor symptoms [8] and by investigations in relatives of PD patients [9] .…”

Section: Discussionsupporting

confidence: 52%

Olfactory Deficits and Cognitive Dysfunction in Parkinson’s Disease

et al. 2012

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Background: Olfactory deficits and executive dysfunction have been reported in Parkinson’s disease (PD). However, the association between these deficits has not been thoroughly examined. Methods: We studied 44 PD subjects and 17 age-matched controls. In PD subjects, symptoms were assessed with the Unified Parkinson’s Disease Rating Scale and the Hoehn and Yahr scale. Cognition in both groups was assessed by a neuropsychological battery. Olfactory identification and sensitivity was evaluated with the Sniffin’ Sticks® test and olfactory detection threshold, respectively. Results: PD subjects showed significant deficits in olfactory function and working memory, executive function, speed of information processing, visuospatial skills and phonological verbal fluency tests when compared with the control group. Moreover, there was a significant correlation between olfactory sensory deficits and executive dysfunction. In PD patients with up to 12 months of motor symptoms, results were equivalent. Conclusion: Our preliminary results suggest a significant association between olfactory deficits and impairments of executive functions in PD.

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“…In addition, behavioral alterations precede the onset of motor symptoms. In this pre-motor phase, monkeys suffer from frontal signs such as attention deficit, deficit in short-term memory processes, increased irritability, restlessness when sitting in a chair and increased hesitation to respond (Schneider and Pope-Coleman, 1995). In rodents, contradictory results have been reported (for review, see Sedelis et aI., 2001).…”

Section: Mptp Model Of Parkinson's Diseasementioning

confidence: 95%

Animal models of Parkinson’s disease in rodents induced by toxins: an update

Hirsch

Höglinger

Rousselet

et al. 2003

Advances in Research on Neurodegeneration

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Summary. The development of animal models of Parkinson's disease is of great importance in order to test substitutive or neuroprotective strategies for Parkinson's disease. Such models should reproduce the main characteristics of the disease, such as a selective lesion of dopaminergic neurons that evolves over time and the presence of neuronal inclusions known as Lewy bodies. Optimally, such models should also reproduce the lesion of non-dopaminergic neurons observed in a great majority of patients with Parkinson's disease. From a behavioral point of view, a parkinsonian syndrome should be observed, ideally with akinesia, rigidity and rest tremor. These symptoms should be alleviated by dopamine replacement therapy, which may in turn lead to side effects such as dyskinesia. In this review, we analyze the main characteristics of experimental models of Parkinson's disease induced by neurotoxic compounds such as 6-hydroxydopamine, MPTP and rotenone. We show that, whereas MPTP and 6-hydroxydopamine induce a selective loss of catecholaminergic neurons that in most cases evolves over a short period of time, rotenone infusion by osmotic pumps can induce a chronically progressive degeneration of dopaminergic neurons and also of non-dopaminergic neurons in both the basal ganglia and the brainstem.

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Cognitive deficits precede motor deficits in a slowly progressing model of parkinsonism in the monkey

Cited by 95 publications

References 31 publications

Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies

Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies

Olfactory Deficits and Cognitive Dysfunction in Parkinson’s Disease

Animal models of Parkinson’s disease in rodents induced by toxins: an update

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