Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disordered immune responses are supposed to alter the function of the central nervous system through the neuroendocrine immunomodulation network. In this paper, we studied the influence of the immune function on learning performances from the angle of pharmacology using aged garlic extract (AGE), an immunomodulator. Splenocyte proliferation, induced by concanavalin A or lipopolysaccharide, and the antibody production response were declined in senescence accelerated mouse-prone 8 (SAMP8) aged 12 months compared with age-matched SAMR1 (SAM-resistant 1). Chronic oral administration of AGE-containing food (2%, w/w) significantly enhanced the immune responses of both SAMP8 and SAMR1. Male ddY mice were thymectomized 4 weeks after birth and fed AGE-containing food after the operation until the experiments were finished. Learning performances, brain monoamine content and choline acetyltransferase (ChAT) activity, as well as the immune response were evaluated 10 months after the operation. Thymectomy resulted in not only immunodeficiency, but also deteriorated learning ability. AGE treatment prevented the reduction of the antibody production response induced by thymectomy and improved the thymectomy-induced deterioration of learning behaviours in passive avoidance performance and in a spatial memory task. The contents of hypothalamic noradrenaline, 3,4-dihydroxyphenylacetic acid and homovanillic acid, and the hypothalamic ChAT activity were increased in thymectomized mice compared to those of sham-operated control, while AGE treatment restored them to the control levels. These results suggest that the improvement of immune function is closely related to the amelioration of age-associated deterioration of learning and memory.
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PMID:Functional relationship between age-related immunodeficiency and learning deterioration. 987 63

HIV infection at late stages is associated with neurological complications including impaired motor and cognitive functions. We used simian immunodeficiency (SIV)-infected rhesus monkeys, an animal model of HIV infection, to investigate changes in choline acetyltransferase (ChAT) activity, a biochemical marker of cognitive function, in post-mortem brains during early, asymptomatic SIV infection and AIDS. ChAT activity was dramatically reduced in putamen and hippocampus already during asymptomatic infection. In animals with AIDS, ChAT activity was further decreased. The reduction of ChAT was not related to brain viral load or CNS pathological lesions. Our results demonstrate deficits in ChAT activity already during the first months of SIV infection and imply that cognitive dysfunction may occur early in immunodeficiency viral infections.
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PMID:Brain choline acetyltransferase reduction in SIV infection. An index of early dementia? 1094 91

Human immunodeficiency virus (HIV) infection is associated with a progressive dementia, in addition to motor and behavioural deficits. Cognitive deterioration and motor impairments have been observed also in simian immunodeficiency virus (SIV)-infected monkeys, an animal model for HIV infection. We found recently that choline acetyltransferase activity is markedly reduced in brains of SIV-infected monkeys. We report now that selegiline, completely restores the reduced choline acetyltransferase activity which encourages for a meaningful anti-dementia therapeutic strategy.
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PMID:Selegiline completely restores choline acetyltransferase activity deficits in simian immunodeficiency infection. 1113 77

The simian immunodeficiency virus (SIV) macaque model resembles human immunodeficiency virus-acquired immunodeficiency syndrome (AIDS) and associated brain dysfunction. Altered expression of synaptic markers and transmitters in neuro-AIDS has been reported, but limited data exist for the cholinergic system and lipid mediators such as prostaglandins. Here, we analyzed cholinergic basal forebrain neurons with their telencephalic projections and the rate-limiting enzymes for prostaglandin synthesis, cyclooxygenase isotypes 1 and 2 (COX1 and COX2) in the brains of SIV-infected macaques with or without encephalitis and antiretroviral therapy and uninfected controls.Cyclooxygenase isotype 1, but not COX2, was coexpressed with markers of cholinergic phenotype, that is, choline acetyltransferase and vesicular acetylcholine transporter (VAChT), in basal forebrain neurons of monkey, as well as human, brain. Cyclooxygenase isotype 1 was decreased in basal forebrain neurons in macaques with AIDS versus uninfected and asymptomatic SIV-infected macaques. The VAChT-positive fiber density was reduced in frontal, parietal, and hippocampal-entorhinal cortex. Although brain SIV burden and associated COX1- and COX2-positive mononuclear and endothelial inflammatory reactions were mostly reversed in AIDS-diseased macaques that received 6-chloro-2',3'-dideoxyguanosine treatment, decreased VAChT-positive terminal density and reduced cholinergic COX1 expression were not. Thus, COX1 expression is a feature of primate cholinergic basal forebrain neurons; it may be functionally important and a critical biomarker of cholinergic dysregulation accompanying lentiviral encephalopathy. These results further imply that insufficiently prompt initiation of antiretroviral therapy in lentiviral infection may lead to neurostructurally unremarkable but neurochemically prominent irreversible brain damage.
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PMID:Lentiviral infection of rhesus macaques causes long-term injury to cortical and hippocampal projections of prostaglandin-expressing cholinergic basal forebrain neurons. 2215 16