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)

Micrographia (MG), an acquired impairment of writing characterized by diminution of letter size, coupled with slowing and loss of accuracy, is most frequently observed in the course of degenerative disease of basal ganglia, such as Parkinson's Disease. Only a few cases of MG without concomitant extrapyramidal signs have been described, mostly following vascular lesion of the left basal ganglia. In this article we report an isolated pattern of MG following an extensive traumatic cerebral lesion centered in the left basal ganglia. The nature of this impairment is analyzed according to a cognitive model of writing and interpreted as a specific example of peripheral dysgraphia.
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PMID:Post graphemic impairments of writing: the case of micrographia. 1600 45

The effects of HSV-1 amplicon and polyethyleneimine (PEI)-mediated transfection of dominant negative FGF receptor-1 mutant FGFR1(TK-) into the rat brain substantia nigra (SN) were examined in vivo to model the reduced FGF signaling documented to occur in Parkinson's disease. The number of SN neurons that expressed tyrosine hydroxylase (TH) was significantly reduced following HSV-1 FGFR1(TK-) intranigral delivery and similar changes were observed after PEI-mediated FGFR1(TK-) transfections. Further, we also observed a significantly lower striatal dopamine content following the PEI transfection of FGFR1(TK-). Thus, we conclude that reduced FGF signaling in the SN of Parkinsonian patients could play a role in the impaired dopaminergic transmission associated with the degenerative disease.
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PMID:Transfection of tyrosine kinase deleted FGF receptor-1 into rat brain substantia nigra reduces the number of tyrosine hydroxylase expressing neurons and decreases concentration levels of striatal dopamine. 1603 6

Multiple system atrophy (MSA) is a degenerative disease manifesting a combination of parkinsonism, cerebellar, pyramidal, and autonomic (including urinary, sexual and anorectal) dysfunction. It is pathomorphologically defined, but lacks a definitive clinical diagnostic test. In patients with probable MSA, abnormal sphincter EMG, as compared to control subjects, has been found in the majority of patients in all the different forms of the disease in most studies, including patients who, as yet, have no urological or anorectal problems. Patients with Parkinson's disease (PD) as a rule do not show marked sphincter EMG abnormalities in the first five years of the disease. Thus, abnormal spontaneous activity or marked motor unit potential changes in sphincter muscles are helpful in distinguishing MSA from PD in the first five years after the onset of symptoms and signs, and from pure autonomic failure, as well as from cerebellar ataxias, if other causes for sphincter denervation have been ruled out. EMG does not distinguish MSA from progressive supranuclear palsy. How early in the course of MSA these abnormalities become significant enough to support diagnosis remains to be established by prospective studies.
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PMID:How to diagnose MSA early: the role of sphincter EMG. 1628 9

Parkinson' disease (PD) is a most common and debilitating degenerative disease resulted from massive loss of dopamine neurons in the substantia nigra pars compacta, which is characterized by severe motor symptoms of tremor, bradykinesia, rigidity and postural instability. Protection of nigral dopamine neurons from progressive degenerative death and cell replacement of novel dopamine neurons are hopeful strategies against PD in humans. The reactive astrocytes or functional activation of astrocytes abundantly occurred in brain insults including trauma, ischemia, and 6-OHDA or MPTP-treated PD animal models. Although they were traditionally assumed to impede neuronal regeneration by forming glial scars, growing evidence has indicated that reactive astrocytes do offer crucial benefits in functional recovery of brain injuries. The reactive astrocytes can produce various neurotrophic factors for neuron survival, synthesize extracellular substrates for axonal outgrowth and synaptogenesis, act as scavengers for free radical and excess glutamate, and promote neurogenesis of neural progenitor cells in the adult brains. We thereafter hypothesize that reactive astrocytes may also play important roles in the protection of nigral dopamine neurons or transplanted dopamine cells through their neurotrophic functions and active interaction with dopamine neurons or neural progenitor cells. Future approaches deserve to target on neurotrophic functions of reactive astrocytes in the basal ganglia and interventions to facilitate survival and axonal regeneration of dopamine neurons or differentiation of dopamine progenitor cells. Novel pharmaceutical and cell replacement strategies will hopefully be developed by potential manipulation of reactive astrocytes in the basal ganglia in prevention and treatment of Parkinson's disease.
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PMID:Reactive astrocytes as potential manipulation targets in novel cell replacement therapy of Parkinson's disease. 1630 61

Increasing evidence indicates that the dysfunction of ubiquitin-proteasome system (UPS) is associated with Alzheimer's disease (AD). In the ubiquitin-proteasome pathway, Ubiquitin Carboxy-terminal Hydrolase-L1 (UCH-L1) plays an important role for the cellular clearance of abnormal proteins. Since a substitution of serine by tyrosine at codon 18, exon 3 (S18Y polymorphism) of the UCH-L1 gene exhibits a protective effect against the development of degenerative disease such as sporadic Parkinson's disease (PD) in several different ethnic groups, we hypothesized that UCH-L1 gene S18Y polymorphism may have that same effect on the pathologic process of AD. We examined UCH-L1 S18Y polymorphism genotypes of 116 sporadic AD patients and 123 healthy subjects in Chinese Han population using PCR-restriction fragment length polymorphism (RFLP) analysis. The allele and genotype data as well as data after stratification by age of onset failed to demonstrate any association between AD and S18Y polymorphism. However, after stratification by gender, female AD patients showed significantly less frequencies of Y allele and YY genotype in S18Y polymorphism than female controls (P = 0.003 and P = 0.015 respectively). We conclude that Y allele and YY genotype of S18Y in the UCH-L1 gene may have a protective effect against sporadic AD in female subjects, probably due to altering the function of UCH-L1 and the interactions among different risk factors.
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PMID:Genetic association between Ubiquitin Carboxy-terminal Hydrolase-L1 gene S18Y polymorphism and sporadic Alzheimer's disease in a Chinese Han population. 1662 67

The concept of gliodegenerative diseases has not been widely established although there is accumulating evidence that glial cells may represent a primary target of degenerative disease processes. In the central nervous system (CNS), examples that provide a "proof of concept" include at least one alpha-synucleinopathy, multiple system atrophy (MSA), but this disease is conventionally discussed under the heading of "neurodegeneration". Additional evidence in support of primary glial affection has been reported in neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease and transmissible spongiform encephalopathies. Based on biochemical, genetic and transcriptomic studies it is also becoming increasingly clear that the molecular changes measured in whole tissue extracts, e.g. obtained from Parkinson's disease brain, are not based on a purely neuronal contribution. This important evidence has been missed in cell culture or laser capture work focusing on the neuronal cell population. Studies of animal and in vitro models of disease pathogenesis additionally suggest glial accountability for some CNS degenerative processes. This review provides a critical analysis of the evidence available to date in support of the concept of gliodegeneration, which we propose to represent an essential although largely disregarded component of the spectrum of classical "neurodegeneration". Examples from the spectrum of alpha-synucleinopathies are presented.
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PMID:Glial degeneration and reactive gliosis in alpha-synucleinopathies: the emerging concept of primary gliodegeneration. 1689 5

Parkinson's disease is primarily considered a motor disease characterized by rest tremor, rigidity, bradykinesia and postural disturbances. However, neuropsychiatric complications, including mood and anxiety disorders, fatigue, apathy, psychosis, cognitive impairment, dementia, sleep disorders and addictions, frequently complicate the course of the illness. The pathophysiologic features of these complications are multifaceted and include neuropathophysiologic changes of a degenerative disease, exposure to antiparkinsonian treatments and emotional reactions to having a disabling chronic illness. Changes in mental status have profound implications for the well-being of patients with Parkinson's disease and of their caregivers. Treatment is often efficacious but becomes a challenge in advanced stages of Parkinson's disease. In this article, we review the key clinical features of neuropsychiatric complications in Parkinson's disease as well as what is known about their epidemiologic characteristics, risk factors, pathophysiologic features and management.
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PMID:Recognition and management of neuropsychiatric complications in Parkinson's disease. 1714 92

Parkinson's disease (PD) is a common and debilitating degenerative disease resulting from massive degenerative loss of dopamine neurons, particularly in the substantia nigra. The most classic therapy for PD is levodopa administration, but the efficacy of levodopa treatment declines as the disease progresses. The neuroprotective strategies to rescue nigral dopamine neurons from progressive death are currently being explored, and among them, the Chinese herbs and herbal extracts have shown potential clinical benefit in attenuating the progression of PD in human beings. Growing studies have indicated that a range of Chinese herbs or herbal extracts such as green tea polyphenols or catechins, panax ginseng and ginsenoside, ginkgo biloba and EGb 761, polygonum, triptolide from tripterygium wilfordii hook, polysaccharides from the flowers of nerium indicum, oil from ganoderma lucidum spores, huperzine and stepholidine are able to attenuate degeneration of dopamine neurons and sympotoms caused by the neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) in vitro and in vivo conditions. In addition, accumulating data have suggested that Chinese herbs or herbal extracts may promote neuronal survival and neurite growth, and facilitate functional recovery of brain injures by invoking distinct mechanisms that are related to their neuroprotective roles as the antioxidants, dopamine transporter inhibitor, monoamine oxidase inhibitor, free radical scavengers, chelators of harmful metal ions, modulating cell survival genes and signaling, anti-apoptosis activity, and even improving brain blood circulation. New pharmaceutical strategies against PD will hopefully be discovered by understanding the various active entities and valuable combinations that contribute to the biological effects of Chinese herbs and herbal extracts.
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PMID:Chinese herbs and herbal extracts for neuroprotection of dopaminergic neurons and potential therapeutic treatment of Parkinson's disease. 1769 84

Neuroprotective properties of cannabinoids have been extensively studied in the last years in different neurodegenerative pathologies. This potential is based on the antioxidant, anti-inflammatory and anti-excitotoxic properties exhibited by these compounds that allow them to afford neuroprotection in different neurodegenerative disorders like Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS) and others. PD and HD are chronic pathologies that are caused by the degeneration of specific structures within the basal ganglia. In both disorders, the key mechanisms involved in the neuroprotection provided by cannabinoids include cannabinoid receptor-independent effects aimed at reducing the oxidative injury, and also cannabinoid 2 receptors (CB2)-mediated effects exerted by regulating the influence of reactive microglia on neuronal homeostasis. MS is an inflammatory demyelinating disorder primarily affecting spinal neurons and secondarily producing a malfunctioning and/or degeneration of other neuronal subpopulations located in supraspinal brain structures. There is evidence that both cannabinoid 1 receptors (CB1) and CB2 may afford a protective effect in this disease due to their immunomodulatory, anti-inflammatory and anti-excitotoxic properties. Lastly, neuroprotective effects of cannabinoids exerted by the activation of CB1 but also CB2 receptors have been also identified in amyotrophic lateral sclerosis (ALS), another degenerative disease characterized by the selective death of spinal motoneurons. In the present review, we will collect the latest advances in the knowledge of the cellular and molecular mechanisms through which cannabinoids might arrest/delay the degeneration of specific neuronal subpopulations in these motor-related disorders. This should serve to encourage that the present promising evidence obtained mainly at the preclinical level might progress to a real exploitation of neuroprotective benefits of potential cannabinoid-based medicines.
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PMID:Cannabinoids and neuroprotection in motor-related disorders. 1822 Jul 77

Parkinson's disease is a degenerative disease of the central nervous system. One of the most effective treatments is deep brain stimulation. This technique requires the localization of an objective structure: the subthalamic nucleus. Unfortunately this structure is difficult to locate. In this work the creation of a deformable brain atlas that enables the identification of the subthalamic nucleus in T1-weighted magnetic resonance imaging (MRI) in an automatic, precise and fast way is presented. The system has been validated using data from 10 patients (20 nucleus) operated on for Parkinson's. Our system offers better results using a Wendland function with an error of 1.8853+/-0.9959mm.
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PMID:Deformable brain atlas validation of the location of subthalamic nucleus using T1-weighted MR images of patients operated on for Parkinson's. 1840 78


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