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

A 61-year-old man with Parkinson's disease (PD) developed sudden-onset visual impairment after initiation of amantadine treatment. Ophthalmologic examination revealed corneal endothelial edema. Discontinuation of amantadine resulted in rapid improvement of visual acuity. A review of the literature indicated only a few reports of amantadine-associated corneal dysfunction in patients with neurological disorders as well as influenza syndrome, but none with PD. Amantadine-associated visual impairment in PD could be possibly overlooked, since PD mainly affects elderly people who often develop aging-related ocular changes. The present report alerts neurologists and physicians in general to the peculiar ophthalmologic side effect of amantadine.
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PMID:Visual impairment in Parkinson's disease treated with amantadine: case report and review of the literature. 1750 24

Some clinical reports and epidemiological data suggest that a virus may play a role in the etiology of Parkinson's disease (PD). Following intracerebral injection of a neurovirululent strain of influenza A virus into mice, the virus was found to be particularly localized in neurons of the substantia nigra and hippocampus. Although efforts to detect virus particles in the brains, or antibodies in the serum or CSF of patients with PD have been generally unsuccessful, recent immunohistochemical work has revealed the presence of complement proteins and the interferon-induced MxA in association with Lewy bodies and swollen neuronal processes. Although a viral etiology for PD is not now widely accepted, we proposed such an hypothesis. Neurovirulent influenza A virus is a candidate, but some other viruses or complex infection of these viruses may be responsible for the formation of Lewy bodies and the later death of nigral neurons.
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PMID:Viral etiology of Parkinson's disease: Focus on influenza A virus. 1859 Oct 27

One of the clinical features in the patients with Parkinson's disease (PD) is an apparent low incidence of colds. MxA protein is an interferon-induced protein which inhibits influenza A viral infection. MxA protein has been found in association with Lewy bodies in neurons in PD patients' brains. We performed a semiquantitative mRNA analysis by reverse transcription-polymerase chain reaction using specific primers for MxA protein. When the peripheral blood mononuclear cells (PBMC) were incubated with alpha-interferon (alpha-IFN), the relative levels of mRNA from the PD patients increased equally to those of the normal controls. However, when PBMC were incubated without alpha-IFN, the relative levels of mRNA in the PBMC from PD patients showed marked lower levels overall compared with those of the normal controls. These results may mean that the induction of MxA mRNA by alpha-IFN in the PD patients is higher than in the controls and suggest that a remarkable increase of MxA mRNA may be linked to the clinical tendency to rarely catch a cold among the PD patients.
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PMID:Expression of MxA mRNA in peripheral blood mononuclear cells in Parkinson's disease. 1859 Nov 18

Parkinson's disease is a debilitating neurological disorder that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a genetic susceptibility to any number of environmental agents. One such agent may be viruses. It has been shown that numerous viruses can enter the nervous system, i.e. they are neurotropic, and induce a number of encephalopathies. One of the secondary consequences of these encephalopathies can be parkinsonism, that is both transient as well as permanent. One of the most highlighted and controversial cases of viral parkinsonism is that which followed the 1918 influenza outbreak and the subsequent induction of von Economo's encephalopathy. In this review, we discuss the neurological sequelae of infection by influenza virus as well as that of other viruses known to induce parkinsonism including Coxsackie, Japanese encephalitis B, St. Louis, West Nile and HIV viruses.
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PMID:Viral parkinsonism. 1876 Mar 50

The adamantanes are a class of compounds that have found use in the treatment of influenza A and Parkinson's disease, among others. The mode of action for influenza A is based on the adamantanes' interaction with the transmembrane M2 channel, whereas the treatment of Parkinson's disease is thought to relate to a channel block of N-methyl-D-aspartate receptors. An understanding of how these compounds interact with the lipid bilayer is thus of great interest. We used molecular-dynamics simulations to calculate the potential of mean force of adamantanes in a lipid bilayer. Our results demonstrate a preference for the interfacial region of the lipid bilayer for both protonated and deprotonated species, with the protonated species proving significantly more favorable. However, the protonated species have a large free-energy barrier in the center of the membrane. In contrast, there is no barrier (compared with aqueous solution) at the center of the bilayer for deprotonated species, suggesting that the permeant species is indeed the neutral form, as commonly assumed. We discuss the results with respect to proposed mechanisms of action and implications for drug-delivery in general.
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PMID:Distribution and dynamics of adamantanes in a lipid bilayer. 1883 6

Parkinson's disease (PD) is characterised by degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Inflammation may be associated with the neuropathology of PD due to the following accumulating evidence: excessive microglial activation and increased levels of the pro-inflammatory cytokines tumour necrosis factor-alpha and interleukin-1beta in the SNpc of patients with PD; the emergence of PD-like symptoms following influenza infection; the increased susceptibility to PD associated with bacterial vaginosis; the presence of inflammatory mediators and activators in animal models of PD; the ability of anti-inflammatory drugs to decrease susceptibility to PD; and the emerging possibility of the use of microglial activation inhibitors as a therapy in PD. In this review, we will discuss the role of inflammation in PD. We will focus on the influence of microglia in the pathogenesis of PD and discuss potential therapeutic interventions for PD, that target microglia.
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PMID:The influence of microglia on the pathogenesis of Parkinson's disease. 1968 99

Twenty years ago, circumstantial evidence was compiled to link the 1918 pandemic influenza virus to a CNS disorder called epidemic encephalitis or encephalitis lethargica. A challenge was issued to naysayers. During the past two decades, the knowledge about the influenza virus and the 1918 pandemic virus in particular has had dramatic advancement. The 1918 virus has been resurrected and reconstructed. Experimental studies of mice inoculated with a neurovirulent avian virus have delineated the neuropathology of influenza encephalitis. Review of autopsy cases of encephalitis lethargica revealed that the neuropathology during and shortly after the pandemic was unique. Surprisingly two different viruses were involved with the great pandemic. A single amino acid difference in the hemagglutinin of the two viruses changed the preferred receptor of the virus in the host cell. One virus has qualities that suggest that it is neurovirulent. Circumstantial evidence suggests that the cause of death in some influenza patients was neurogenic congestive heart failure with pulmonary edema. Theories about the pathophysiology of encephalitis lethargica and postencephalitic Parkinson's disease are offered.
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PMID:Influenza caused epidemic encephalitis (encephalitis lethargica): the circumstantial evidence and a challenge to the nonbelievers. 2006 Feb 30

Amantadine (AMA) is an uncompetitive antagonist of the N-methyl-d-aspartate receptor, with clinical application, acting on treatment of influenza A virus and Parkinson's disease. It has been proposed that AMA can indirectly modulate dopaminergic transmission. In high doses, the central nervous system is its primary site of toxicity. To examine deleterious effects on CNS induced by AMA, this study evaluated possible neurobehavioral alterations induced by AMA such as stereotyped behavior, the effects on locomotion and memory and its possible genotoxic/mutagenic activities. Adult male CF-1 mice were treated with a systemic injection of AMA (15, 30 or 60 mg kg(-1) ) 20 min before behavioral tasks on open field and inhibitory avoidance. Higher AMA doses increased the latency to step-down inhibitory avoidance test in the training session in the inhibitory avoidance task. At 60 mg kg(-1) AMA induced impairing effects on locomotion and exploration and hence impaired habituation to a novel environment. Stereotyped behavior after each administration in a 3-day trial was observed, suggesting effects on dopaminergic system. Amantadine was not able to induce chromosomal mutagenesis or toxicity on bone marrow, as evaluated by the micronucleus assay. At the lowest dose tested, AMA did not induce DNA damage and it was unable to impair memory, locomotion, exploration or motivation in mice. However, higher AMA doses increased DNA damage in brain tissue, produced locomotor disturbances severe enough to preclude testing for learning and memory effects, and induced stereotypy, suggesting neurotoxicity.
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PMID:DNA damage in brain cells and behavioral deficits in mice after treatment with high doses of amantadine. 2057 81

Although much is known regarding the molecular mechanisms leading to neuronal cell loss in Parkinson's disease (PD), the initiating event has not been identified. Prevailing theories including a chemical insult or infectious agent have been postulated as possible triggers, leading to neuroinflammation. We present immunohistochemical data indicating the presence of influenza A virus within the substantia nigra pars compacta (SNpc) from postmortem PD brain sections. Influenza A virus labeling was identified within neuromelanin granules as well as on tissue macrophages in the SNpc. Further supporting a role for neuroinflammation in PD was the identification of T-lymphocytes that colocalized with an antibody to caspase-cleaved Beclin-1 within the SNpc. The presence of influenza A virus together with macrophages and T-lymphocytes may contribute to the neuroinflammation associated with this disease.
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PMID:Immunolocalization of influenza A virus and markers of inflammation in the human Parkinson's disease brain. 2165 65

Distributed systems and grid computing systems are used to connect several computers to obtain a higher level of performance, in order to solve a problem. During the last decade, projects use the World Wide Web to aggregate individuals' CPU power for research purposes. This paper presents the existing active large scale distributed and grid computing projects with research focus in human health. There have been found and presented 11 active projects with more than 2000 Processing Units (PUs) each. The research focus for most of them is molecular biology and, specifically on understanding or predicting protein structure through simulation, comparing proteins, genomic analysis for disease provoking genes and drug design. Though not in all cases explicitly stated, common target diseases include research to find cure against HIV, dengue, Duchene dystrophy, Parkinson's disease, various types of cancer and influenza. Other diseases include malaria, anthrax, Alzheimer's disease. The need for national initiatives and European Collaboration for larger scale projects is stressed, to raise the awareness of citizens to participate in order to create a culture of internet volunteering altruism.
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PMID:Distributed and grid computing projects with research focus in human health. 2249 Nov 23


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