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)

To evaluate the relationship between cytokines and cerebrospinal fluid (CSF) cells, we detected interferon (IFN)-gamma and interleukin (IL)-6 producing cells in CSF from the patients with central nervous system (CNS) infectious diseases by immunocytochemistry. Five CSF cell smears from three herpes encephalitis patients, three from a patient with EB virus radiculoneuritis, four from the three patients with purulent meningitis, five from five patients with viral meningitis were obtained during early or subacute stages of diseases. Control CSF cell smears were taken from twenty seven patients with motor neuron disease, Parkinson's disease and spinocerebellar degeneration. Immunocytochemistry using specific polyclonal anti-IFN-gamma and IL-6 sera were used to detect each producing cell. Simultaneously, individual positively immuno-reactive cells were morphologically classified macrophage or lymphocyte. The IFN-gamma positive cells immunostained with specific antibody showed brown-colored deposits within the cytoplasm whereas no deposit was in the nucleus (Fig. 1). These phenotype of IFN-gamma positive cells were considered to be lymphocytes or macrophages. However, IFN-gamma-positive macrophages were predominantly seen at the early stages of herpes simplex encephalitis and purulent meningitis. The percent of IFN-gamma positive cells in total CSF cells obtained from the patients with the CNS infectious diseases was 2.3-38.7 as shown in Table 1. The IL-6 positive cells (Fig. 2) were also found early in the course and in subacute stages in the CNS infectious diseases and ranged from 2.5-50 percent in total CSF cells (Table 1). In contrast neither IFN-gamma- nor IL-6-positive cells were detected in non-inflammatory diseases (Table 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Detection of interferon-gamma and IL-6 producing cells in cerebrospinal fluid cells in the central nervous system infectious diseases using immunocytochemistry]. 149 Mar 21

Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of hereditary to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful.
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PMID:Epidemiology of Parkinson's disease--an overview. 726 26

Amyloid deposits of the CNS caused clinical symptoms in four members of a Hungarian family. Histological investigations revealed a systemic disease, immunohistologically the deposited material was a transthyretin variant, DNA analysis showed a new transthyretin mutation (TTRAsp 18Gly). The disease--named meningocerebrovascular amyloidosis, Hungarian type--is inherited dominantly like other already known familial amyloidoses caused by transthyretin variants, however it does not cause the usual familial polyneuropathy but symptoms similar to those of the rare oculoleptomeningeal amyloidosis. The aim of the present study is to point to differential diagnosis. Its complaints, neurological signs and clinical findings which may be suspect of atypical migraine, brain tumour, chronic leptomeningitis or herpes encephalitis, multiple sclerosis and Parkinson disease are analysed and compared with those of other known types of familial amyloidoses. Attention is drawn to symmetrical calcification on CT scans. Skin biopsy may help the diagnosis. At present, therapy is only symptomatic.
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PMID:[Clinical characteristics of Hungarian-type familial meningo-cerebrovascular amyloidosis]. 899 35

Several cases encountered in psychiatric practice are described in which herpetic involvement of the trigeminal nerve appeared to be crucial to the pathophysiology of the patient's illness. A brief history of herpes is discussed in terms of the anatomy and physiology of the trigeminal nerve. Particular attention is given to the effects of intraneuronal herpes on gasserian ganglion and spinal nuclei discharge thresholds, as well as viral pathways directly impacting the substantia nigra. Evidence characterizing Parkinson's disease as one of several important manifestations of CNS herpes is covered.
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PMID:Tic douloureux, Parkinson's disease and the herpes connection. 932 15

The replication-incompetent HSV-1-based vectors are herpesviruses in which genes that are 'essential' for viral replication have been either mutated or deleted. These deletions have substantially reduced their cytotoxicity by preventing early and late viral gene expression and, together with other deletions involving 'nonessential' genes, have also created space to introduce distinct and independently regulated expression cassettes for different transgenes. Therapeutic effects in gene therapy applications requiring simultaneous and synergic expression of multiple gene products are easily achievable with these vectors. A number of different HSV-1-based nonreplicative vectors for specific gene therapy applications have been developed so far. They have been tested in different gene therapy animal models of neuropathies (Parkinson's disease, chronic pain, spinal cord injury pain) and lysosomal storage disorders. Many replication-incompetent HSV-1-based vectors have also been used either as potential anti-herpes vaccines, as well as vaccine vectors for other pathogens in murine and simian models. Anticancer gene therapy approaches have also been successfully set up; gene therapy to other targets by using these vectors is feasible.
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PMID:Development and application of replication-incompetent HSV-1-based vectors. 1623 Oct 61

Castleman disease is a quite uncommon lymphoproliferative disorder usually occurring in the lymph nodes. Rarely, Castleman disease develops in an extranodal anatomic location. We report on the first biopsy-proven case of multicentric plasma cell type of Castleman disease involving the orbital areas in a human herpes virus 8 (HHV-8)-unassociated/ human immunodeficiency virus (HIV)-seronegative 70-year-old man suffering from Parkinson disease. The diagnosis was established on the basis of morphologic, immunophenotypic, and molecular findings of a lymph node and orbital soft tissue biopsy. We additionally provide a review of all previously published cases of Castleman disease with an orbital involvement, discussing the distinctive characteristics and potential associations with regard to their counterparts at other sites. Although Castleman disease involving the orbit is an exceptionally rare occurrence that may present initially with ocular signs and symptoms, this should be included in the complete differential diagnosis of orbital mass lesion.
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PMID:Orbital involvement in Castleman disease. 2007 Sep 98

Growing evidence suggests that peripheral factors to the brain driving neuro-inflammation could affect Alzheimer's Disease (AD) and Parkinson's Disease (PD) severity. Herpes simplex virus type 1 (HSV1) infection has been associated with AD while other related viruses, including cytomegalovirus (CMV), Epstein-Bar virus and human herpesvirus 6 (HHV6), are known to infect neurons. Here we compare gene expression profiles between AD or PD patients to those afflicted with herpes viral infections as to discover novel potential neuro-inflammation pathways. We found multiple significant differentially expressed genes (DEGs) shared between AD/PD and viral infections including SESN3 which has a genetic association for increased AD risk. Pathway enrichment analysis revealed viruses shared Oxidative Stress Defense System and LRRK2 pathways with AD and PD, respectively. We further processed our data to identify novel target and drug-repurposing opportunities including anti-inflammatory therapy, immune-modulators and cholinesterase inhibitors which could lead to new therapeutics paradigms for these neurodegenerative diseases.
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PMID:Shared Molecular Signatures Across Neurodegenerative Diseases and Herpes Virus Infections Highlights Potential Mechanisms for Maladaptive Innate Immune Responses. 3121 89