Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The viral theory of motor neuron disease (MND) has been rejuvenated in the last 5 years for several reasons. First, it is now recognized that enteroviruses and picornaviruses similar to poliovirus can persist and induce immune-mediated diseases. In some picornavirus animal models, the immune-mediated disease can occur and continue long after the infectious virus has been cleared, and in some cases of human MND an immune-mediated disease may occur. Second, the human retroviruses human immunodeficiency virus (HIV) and human T-cell lymphotrophic virus (HTLV) have caused isolated MND syndromes. Neither of these two specific viruses appear to be 'the amyotrophic lateral sclerosis (ALS) retrovirus', because they cause a plethora of neurologic syndromes unrelated to MND. Retroviruses of mice, however, can cause MND and lymphomas, and because there is an increased incidence of lymphomas in ALS patients, it has been suggested that retroviruses are another possible viral agent of human MND.
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PMID:Motor neuron diseases and viruses: poliovirus, retroviruses, and lymphomas. 132 4

Career and treatment attitudes related to potential human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS) exposure are reported based on a survey of 1,228 Maryland career and volunteer prehospital care providers trained to provide basic (BLS) and advanced (ALS) life support. Sixty-five percent stated potential exposure to HIV/AIDS was a major occupational stressor. Ninety-two percent stated they would treat HIV/AIDS patients if protected. Given a choice, 38% would avoid providing treatment to HIV/AIDS patients. Eighteen percent considered resigning from emergency medical services (EMS) work. An attitudinal scale (AIDSTRESS) was developed to evaluate overall treatment and career reactions. Respondents with significantly higher (more negative reactions) AIDSTRESS scores were: BLS providers, men, paid providers, personnel with more than 3 years of field experience, those working in urban areas, personnel with no formal education beyond high school, and those who stated that their HIV/AIDS training was inadequate. Implications of the findings for quality of care, career decision making, and inservice education are discussed.
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PMID:Treatment and career attitudes of prehospital care providers associated with potential exposure to HIV/AIDS. 199 37

Adults with slowly progressive noninherited gait disorders may show no abnormalities on examination other than signs implicating the corticospinal tracts. That is the syndrome of "primary lateral sclerosis" (PLS), a clinical diagnosis that has been avoided because it is a diagnosis of exclusion, proven only at autopsy. Now, modern technology can exclude other disorders that can cause the syndrome with an accuracy of about 95%. That serves to eliminate the following: compressive lesions at the foramen magnum or cervical spinal cord, multiple sclerosis, amyotrophic lateral sclerosis, Chiari malformation, syringomyelia, biochemical abnormality, and persistent infection with human immunodeficiency virus or human T-lymphotrophic virus type I. We studied three autopsy-proved cases of PLS; six living patients in whom PLS was diagnosed clinically after comprehensive evaluations that excluded the alternative diagnoses; and two patients with this syndrome of PLS and antibodies to human immunodeficiency virus seropositivity that clinically resembled PLS. Primary lateral sclerosis is now a respectable and permissible diagnosis.
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PMID:Primary lateral sclerosis. A clinical diagnosis reemerges. 281 50

A man with symptoms of amyotrophic lateral sclerosis and immunodeficiency was treated with intravenous immunoglobulin. After four weekly intravenous injections of 2.5 gm of immunoglobulin, his condition showed progressive improvement when measured by clinical, neurological, and physiological parameters. There was a noticeable increase in general physical well-being, an 80% reduction in fasciculations, and the normalization of sensory and motor nerve conduction velocities.
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PMID:Immunodeficiency associated with motor neuron disease treated with intravenous immunoglobulin. 379 65

Mice with either chemically suppressed immune response or with specifically induced T cell or B cell immunodeficiency were challenged with Aspergillus fumigatus spores. Chemical immunosuppressants used were cortisone, cyclophosphamide or silica. T cell deficiency was produced by thymectomy and ALS administration, whereas, B cell deficiency was produced by administration of anti-mouse IgM antibodies in newborn mice. The susceptibility of such animals to A. fumigatus challenge was monitored by mortality pattern and by demonstration of dissemination of fungus in different organs. The administration of cortisone or silica made mice highly susceptible to A. fumigatus infection, whereas, cyclophosphamide initially lowered host's resistance but later had little effect. Mice with B cell deficiency also did not differ significantly from normal animals. Similarly passive transfer of specific antibodies to A. fumigatus did not enhance the protection of the host to experimental aspergillosis. However, the deficiency of T cells and macrophages either alone or in combination made the animals highly susceptible to experimental aspergillosis. The results provide evidence that T cells and macrophages play essential role in immunity to murine aspergillosis. Whereas, B cell deficiency or even passive transfer of specific antibodies to A. fumigatus does not alter much the host's susceptibility to experimental aspergillosis.
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PMID:Studies on experimental aspergillosis in immunodeficient mice. 632 25

Among Guamanian natives, serum IgA and IgG levels were found to be higher than normal in amyotrophic lateral sclerosis (ALS); serum IgA was higher and IgM lower than normal in parkinsonism-dementia (PD). IgA levels increased with age in ALS, PD, and normal subjects; IgG increased with age in ALS and IgM decreased with age in PD. Serum immunoglobulin (Ig) levels did not correlate with the duration of either disease. Immunodeficient ALS and PD patients had higher IgM and lower IgA levels than the other ALS and PD patients. Neither differences in viral antibody titers nor the presence of autoantibodies or circulating immune complexes could account for the variations in serum Ig levels between patients and controls. We conclude that differences in serum Ig levels in ALS and PD patients are probably due to repeated infections and abnormal immunoregulation accompanying immunodeficiency during the course of ALS and PD, rather than to a specific antiviral or autoimmune response.
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PMID:Humoral immunity in Guamanians with amyotrophic lateral sclerosis and parkinsonism-dementia. 728 4

Approximately a third of adults and half of children with acquired immunodeficiency syndrome (AIDS) eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. Among the various pathologies reported in the brain of patients with AIDS is neuronal injury and loss. A paradox arises, however, because neurons themselves are for all intents and purposes not infected by human immunodeficiency virus type 1 (HIV-1). This paper reviews evidence suggesting that at least part of the neuronal injury observed in the brain of AIDS patients is related to excessive influx of Ca2+. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or death of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes, and neurons. Human immunodeficiency virus-infected monocytoid cells (macrophages, microglia, or monocytes), especially after interacting with astrocytes, secrete substances that potentially contribute to neurotoxicity. Not all of these substances are yet known, but they may include eicosanoids, that is, arachidonic acid and its metabolites, as well as platelet-activating factor. Macrophages activated by HIV-1 envelope protein gp120 also appear to release arachidonic acid and its metabolites. These factors can lead to increased glutamate release or decreased glutamate reuptake. In addition, gamma interferon (IFN-gamma) stimulation of macrophages induce release of the glutamate-like agonist quinolinate. Human immunodeficiency virus-infected or gp120-stimulated macrophages also produce cytokines, including tumor necrosis factor-alpha and interleukin-1 beta, which contribute to astrogliosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, neuropathic pain, and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca2+ channels and N-methyl-D-aspartate (NMDA) receptor-operated channels, and therefore offers hope for future pharmacological intervention. This review focuses on clinically tolerated calcium channel antagonists and NMDA antagonists with the potential for trials in humans with AIDS dementia in the near future.
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PMID:AIDS-related dementia and calcium homeostasis. 784 72

Perhaps as many as 25-50% of adult patients and children with acquired immunodeficiency syndrome (AIDS) eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. How can human immunodeficiency virus type 1 (HIV-1) result in neuronal damage if neurons themselves are for all intents and purposes not infected by the virus? This article reviews a series of experiments leading to a hypothesis that accounts at least in part for the neurotoxicity observed in the brains of AIDS patients. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions among macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells (macrophages, microglia, or monocytes), after interacting with astrocytes, secrete eicosanoids, i.e., arachidonic acid and its metabolites, including platelet-activating factor. Macrophages activated by HIV-1 envelope protein gp120 also appear to release arachidonic acid and its metabolites. In addition, interferon-gamma (IFN-gamma) stimulation of macrophages induces release of the glutamate-like agonist, quinolinate. Furthermore, HIV-infected macrophage production of cytokines, including TNF-alpha and IL1-beta, contributes to astrogliosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, neuropathic pain, and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca2+ channels and N-methyl-D-aspartate (NMDA) receptor-operated channels, and, therefore, offers hope for future pharmacological intervention. This article focuses on clinically tolerated calcium channel antagonists and NMDA antagonists with the potential for trials in humans with AIDS dementia in the near future.
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PMID:HIV-related neuronal injury. Potential therapeutic intervention with calcium channel antagonists and NMDA antagonists. 799 15

Neuromuscular diseases occur in as many as 50% of patients infected with human immunodeficiency virus type 1 (HIV-1). All forms of neuromuscular disease have been reported, including axonal neuropathy, demyelinating neuropathy, mononeuropathy multiplex, polyradiculitis, ALS-like syndromes, disorders of neuromuscular transmission, myopathy, and toxic neuropathies due to medication side effects. Neuromuscular disease is often the presenting manifestation of HIV-1 infection. Infection with cytomegalovirus (CMV) is associated with different types of neuropathy including mononeuritis multiplex and polyradiculopathy. There is effective treatment for many of the associated disorders including chronic inflammatory demyelinating neuropathy, CMV-mediated neuropathies, and myopathy. Treatment of CMV-mediated mononeuropathy multiplex may be life saving. The different neuromuscular syndromes associated with different stages of HIV-1 infection may be due, in part, to different levels of immunocompetence.
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PMID:AAEM minimonograph #41: neuromuscular diseases associated with HIV-1 infection. 826 98

Foamy viruses share complex genome organization with lentiviruses and certain oncoviruses. The open reading frame 3' of env encodes a transcriptional transactivator. Distinct responsive sequences were identified in the long terminal repeats (LTRs) of simian (SFV-1 and SFV-3) and human foamy viruses (HFV). Transactivation of heterologous LTRs was described including those of simian and human immunodeficiency viruses. Foamy viruses persist for the whole lifetime in infected hosts (primates, cats, hamsters, cattle, and probably other mammals). The virus may be orally shed and transmitted, while being latent in various internal organs. Selective viral gene expression in the brains of mice transgenic for HFV has suggested a particular relationship to neural tissue. In latently SFV-3-infected cultured cells, methylation of proviral DNA is apparently involved in the control of latency. Demethylation as well as transfection with the transactivator were shown to be instrumental in viral reactivation. Natural infections with foamy viruses are common, elicit strong immune responses, and seem to be asymptomatic in nonhuman primates. Detection of such infections, however, may not be a triviality in man. While accidental transmission of foamy viruses to man is well documented, reported seroprevalence in human populations and the association of HFV with specific pathology (e.g. thyroiditis de Quervain, amyotrophic lateral sclerosis, and Graves' disease) are controversial and remain to be proven.
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PMID:Foamy viruses. 840 46


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