Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a great and unmet need for meaningful therapies that will deliver restorative solutions to patients with neurological disorders such as multiple sclerosis (MS), Parkinson's disease and stroke. The emergence of human embryonic stem cells as an experimental and therapeutic resource represents a major opportunity for brain repair. Embryonic stem cells offer the potential to study human cells, model disease, accelerate drug discovery and of themselves act as a cell-based therapy. In contrast to other organs, a "one size fits all" approach is inappropriate for repair of the brain; rather therapies need to be "bespoke". The design and development of embryonic stem-cell based CNS reparative strategies pose many challenges, both conceptual and practical. Using multiple sclerosis as an example, this paper addresses the needs for the translation of embryonic stem cell biology to regenerative neurology.
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PMID:Human embryonic stem cells: an experimental and therapeutic resource for neurological disease. 1792 Jun 31

The analysis of isometric force may provide early detection of certain types of neuropathology such as Parkinson's disease. Our long term goal is to determine if there are detectable differences between model parameters of healthy and unhealthy individuals. In this study we evaluate dynamic system models of isometric force based on fuzzy set theory. The experiments involved subjects exerting isometric force over a range from 5% to 95% of maximal voluntary contraction. The finding suggests that the fuzzy dynamic system model outperforms best fits that were obtained using nonlinear difference equations of higher order.
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PMID:Modeling isometric force response using fuzzy set theory. 1800 87

With functional MRI, we recently identified fronto-cerebellar activations in predicting time to reach a target and basal ganglia activation in velocity estimation, that is, small interval assessment. We now tested these functions in patients with Parkinson's disease (PD) and degenerative cerebellar ataxia. They watched a ball that repeatedly appeared, moved, and disappeared. Velocity, stop locations, and predicted target locations as well as time to reach a target were indicated. Compared with controls, PD patients showed impaired velocity estimation (momentary mode) whereas temporal prediction was selectively impaired in cerebellar ataxia patients. The latter highlights feed-forward processing within fronto-cerebellar circuitry. Impaired velocity estimation in PD fits the concept of a basal ganglia clock function.
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PMID:Time estimation in Parkinson's disease and degenerative cerebellar disease. 1858 May 78

Duplications and triplications of the alpha-synuclein (SNCA) gene have been reported in Parkinson's disease patients belonging to the Southern Swedish "Lister family". Further genealogical research has now shown that these individuals are descended from a large kindred characterized by Herman Lundborg in 1901-1913. In the expanded pedigree, a total of 25 individuals had Parkinson's disease with an autosomal dominant pattern of inheritance. Hereditary dementia, and, historically, dementia praecox have been described in other family members. Furthermore, an autosomal recessively inherited pediatric disease with nocturnal tonic-clonic fits, subsequent progressive myoclonus, startle reactions, tremor and muscle rigidity was described by Lundborg in the same pedigree. The entity was later designated Unverricht-Lundborg disease (ULD) or progressive myoclonus epilepsy type 1 (EPM1). However, Lundborg's clinical description of this disease, based on 17 patients within this kindred, differs from the modern definition of EPM1, which relies on patients with a mutation in the cystatin B (CSTB) gene. We hypothesize that the former pediatric disease, as well as the parkinsonism and dementia phenotypes, are associated with duplications, triplications and possibly higher-order multiplications of the alpha-synuclein (SNCA) gene. This hypothesis is supported by the distribution of afflicted family members within the pedigree and by recently obtained genealogical information.
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PMID:Alpha-synuclein multiplications with parkinsonism, dementia or progressive myoclonus? 1882 90

Extending the 2002 stress-appraisal model of Chappell and Reid, we examined the relationships between caregiver stressors (e.g., cognitive impairment and functional dependency of the recipient), appraisal (informal hours of caregiving), and protective factors (e.g., social support, self-esteem, and quality of the caregiver-recipient relationship) associated with the burden and quality of life of Parkinson's disease caregivers. There were 136 caregivers (M = 64.59 years) who completed an online survey. Using structural equation modeling, we found that the extended stress-appraisal model of Chappell and Reid provided a good fit to the data (chi2 = 67.87, df = 55, p >.05; chi2/df = 1.23, Comparative Fit Index = 0.98, Root Mean Square Error of Approximation = 0.04). This study provides an important contribution to a growing field of research that applies theoretical models to investigate the stressors, appraisals, and protective factors that impact caregiver well-being.
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PMID:Caregiving for Parkinson's disease patients: an exploration of a stress-appraisal model for quality of life and burden. 1909 40

The hospital anxiety and depression scale (HADS) is commonly used to assess mood in Parkinson's disease (PD) patients. Very few studies analyze the scale from the standpoint of item response theory. This article sought to analyze how the HADS fits the Rasch model in PD. The HADS was administered to 387 PD patients. Three sets of Rasch analyses were performed for the HADS total score, and anxiety and depression subscales (HADS-T, -A, and -D, respectively). Although the HADS-T and HADS-A displayed a good fit, with little threshold disordering and no differential item functioning, the HADS-D failed to fit the model. The person separation index, a reliability measure, was 0.87 (HADS-T) and 0.80 (HADS-A). Both HADS-T and HADS-A showed unidimensionality. Our results supported the use of HADS-T as a measure of psychological distress in PD patients. Moreover, the HADS-A was also an adequate anxiety measure. Further research is required to address the use of HADS-D in PD.
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PMID:Rasch analysis of the hospital anxiety and depression scale in Parkinson's disease. 1909 78

Studies that used conflict paradigms such as the Eriksen Flanker task show that many individuals with Parkinson's disease (PD) have pronounced difficulty resolving the conflict that arises from the simultaneous activation of mutually exclusive responses. This finding fits well with contemporary views that postulate a key role for the basal ganglia in action selection. The present experiment aims to specify the cognitive processes that underlie action selection deficits among PD patients in the context of variations in speed-accuracy strategy. PD patients (n=28) and healthy controls (n=17) performed an arrow version of the flanker task under task instructions that either emphasized speed or accuracy of responses. Reaction time (RT) and accuracy rates decreased with speed compared to accuracy instructions, although to a lesser extent for the PD group. Differences in flanker interference effects among PD and healthy controls depended on speed-accuracy strategy. Compared to the healthy controls, PD patients showed larger flanker interference effects under speed stress. RT distribution analyses suggested that PD patients have greater difficulty suppressing incorrect response activation when pressing for speed. These initial findings point to an important interaction between strategic and computational aspects of interference control in accounting for cognitive impairments of PD. The results are also compatible with recent brain imaging studies that demonstrate basal ganglia activity to co-vary with speed-accuracy adjustments.
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PMID:The effect of speed-accuracy strategy on response interference control in Parkinson's disease. 1942 16

Neuromelanin is a complex molecule accumulating in the catecholaminergic neurons that undergo a degenerative process in Parkinson's disease. It has been shown to play either a protective or a toxic role depending on whether it is present in the intraneuronal or extraneuronal milieu. Understanding its structure and synthesis mechanisms is mandatory to clarify the reason for this remarkable dual behavior. In the present study, X-ray absorption spectroscopy is employed to investigate the sulfur binding mode in natural human neuromelanin, synthetic neuromelanins, and in certain structurally known model compounds, namely cysteine and decarboxytrichochrome C. Based on comparative fits of human and synthetic neuromelanin spectra in terms of those of model compounds, the occurrence of both cysteine- and trichochrome-like sulfur coordination modes is recognized, and the relative abundance of these two types of structural arrangement is determined. Data on the amount of cysteine- and trichochrome-like sulfur measured in this way indicate that among the synthetic neuromelanins those produced by enzymatic oxidation are the most similar ones to natural neuromelanin. The interest of the method described here lies in the fact that it allows the identification of different sulfur coordination environments in a physically nondestructive way.
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PMID:An XAS study of the sulfur environment in human neuromelanin and its synthetic analogs. 1947 20

This study focused on the relationship between the asymmetry of initial motor symptoms of Parkinson's disease (PD) and premorbid handedness of patients. Structural equation modeling has been used for this purpose. The survey consisting of validated items measuring handedness and questions related to side of occurrence of initial symptoms was administered to 472 patients with PD [277 men, 195 women, mean age 66.5 (9.3), mean duration of the disease 10 (6.1) years]. The unidimensional model of handedness fits the data well (chi(2) = 37.86, df = 20, P = 0.009, Root Mean Square Error of Approximation = 0.044, Comparative Fit Index = 1.00, Standardized Root Mean Square Residual = 0.042) and side of initial motor symptoms is not significantly related to the factor of handedness (r =0.11, SE = 0.07, P = 0.14). In contrast to several other studies, the results indicate that the side of first occurrence of PD signs cannot be predicted from premorbid handedness of patients.
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PMID:Handedness does not predict side of onset of motor symptoms in Parkinson's disease. 1951 74

Orphenadrine is an anticholinergic drug used in the treatment of Parkinson's disease, and is also known to exert nonspecific antagonistic activity at the phencyclidine binding site of the N-methyl-D-aspartate (NMDA) receptor. The aim of this study was to assess the anticonvulsant properties of orphenadrine and to evaluate its effect on the anticonvulsant activity of antiepileptic drugs against maximal electroshock-induced seizures in mice. Orphenadrine given at a dose of 5.65 mg/kg elevated the electrical seizure threshold from 5.7 (5.4-6.1) to 6.8 (6.3-7.3) mA, while a dose of 2.8 mg/kg was ineffective. The ED(50) values of orphenadrine administered 10, 30 and 120 min before maximal electroshock-induced convulsions were 16.8 (11.3-25.1), 17.8 (15.7-20.0) and 25.6 (23.3-28.3) mg/kg, respectively. Orphenadrine at a sub-threshold dose of 2.8 mg/kg significantly enhanced the anticonvulsant activity of valproate by reducing its ED(50) value from 315.8 (270.0-369.4) to 245.9 (207.1-292.0) mg/kg without affecting the free plasma levels of valproate. However, orphenadrine failed to enhance the protective activity of carbamazepine, phenytoin, phenobarbital, lamotrigine, topiramate, or oxcarbazepine against maximal electroshock-induced seizures.
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PMID:Influence of orphenadrine upon the protective activity of various antiepileptics in the maximal electroshock-induced convulsions in mice. 1981 57


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