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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Australian statistics have shown that 10.9% of AIDS cases have occurred in the 50 years and over age group. To date little attention has been given to the many issues surrounding HIV infection in the older population, for example, the failure to consider HIV as an aetiological factor in the older person presenting with neuropsychiatric disorder and the potential for misdiagnosis of AIDS dementia complex as dementia of the Alzheimer type. This paper includes a discussion of the clinical features of the AIDS dementia complex, its resemblance to the syndrome of "subcortical dementia", and review of the literature reporting dementia as the presenting feature of HIV infection in older individuals.
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PMID:Human immunodeficiency virus infection, dementia and the older patient. 848 Nov 75

The number of AIDS patients over age 60 has risen steadily in the past decade. The number of transfusion-acquired AIDS cases probably has peaked--or will soon peak. Homosexual (or bisexual) behavior remains the predominant risk factor for AIDS until the seventh decade. Disease progression appears to be more rapid in the elderly, although the observed shorter survival time may result from a delay in diagnosis. Symptoms of HIV infection are often nonspecific, such as fatigue, anorexia, weight loss, and decreased physical and cognitive function. The five most common opportunistic infections in older HIV-infected patients are Pneumocystis carinii pneumonia, tuberculosis, Mycobacterium avium complex, herpes zoster, and cytomegalovirus. A number of features of HIV-related dementia may help to distinguish it from Alzheimer's disease.
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PMID:HIV infection in older patients: when to suspect the unexpected. 850 Jul 75

To better understand the role the human amyloid precursor protein (hAPP) plays in Alzheimer's disease (AD), it is essential to define its primary function(s). Here we expressed different hAPPs in neurons of transgenic (tg) mice to characterize their effects on the intact central nervous system (CNS). Immunolabeled brain sections of tg and non-tg mice were compared quantitatively by microdensitometry and computer-aided analysis of laser scanning confocal digitized images. Compared with non-tg mice, tg mice overexpressing hAPPs showed an increase in the number of synaptophysin immunoreactive presynaptic terminals as well as in the expression of the growth-associated marker GAP-43. While non-tg controls and tg mice expressing hAPP751 at moderate levels displayed a normal pattern of reinnervation of the dentate gyrus following perforant pathway transection, tg mice expressing hAPP695 at severalfold higher levels showed an accentuation of the synaptic loss and no sprouting reaction. In addition, expression of hAPP751 at moderate levels effectively protected neurons against excitotoxic injury induced either acutely by systemic injection of kainic acid or chronically by transgene-driven glial production of the soluble HIV-1 protein gp120. Neuronal expression of hAPP695 at higher levels provided less excitoprotection. Our findings are consistent with the postulate that APP plays a role in the formation/maintenance of synapses and that processes which affect this function could contribute to the synaptic pathology seen in AD. Our study also revealed that hAPPs can exert important excitoprotective functions in vivo and that the efficiency of this protection may depend on the hAPP isoform expressed as well as on the level of neuronal hAPP expression. Neuronal overexpression of hAPP beyond a certain level may have detrimental effects on the CNS, particularly in the context of secondary neural injuries.
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PMID:Neurotrophic and neuroprotective effects of hAPP in transgenic mice. 862 31

A novel 14-amino acid peptide, with stress-protein-like sequences, exhibiting neuroprotection at unprecedented concentrations, is revealed. This peptide prevented neuronal cell death associated with the envelope protein (GP 120) from HIV, with excitotoxicity (N-methyl d-aspartate), with the beta amyloid peptide (putative cytotoxin in Alzheimer's disease), and with tetrodotoxin (electrical blockade). The peptide was designed to contain a sequence derived from a new neuroprotective protein secreted by astroglial cells in the presence of vasoactive intestinal peptide. The neurotrophic protein was isolated by sequential chromatographic methods combining ion exchange, size separation, and hydrophobic interaction. The protein (mol mass, 14 kD and pI, 8.3 +/- 0.25) was named activity-dependent neurotrophic factor, as it protected neurons from death associated with electrical blockade. Peptide sequencing led to the synthesis of the novel 14-amino acid peptide that was homologous, but not identical, to an intracellular stress protein, heat shock protein 60. Neutralizing antiserum to heat shock protein 60 produced neuronal cell death that could be prevented by cotreatment with the novel protein, suggesting the existence of extracellular stress-like proteins with neuroprotective properties. These studies identify a potent neuroprotective glial protein and an active peptide that provide a basis for developing treatments of currently intractable neurodegenerative diseases.
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PMID:A femtomolar-acting neuroprotective peptide. 863 93

The mechanism for the pathological increase in cell death in various disease states e.g. HIV immunodefficiency or even ageing or Alzheimer's disease, occurs by complex and as yet undefined mechanism(s) related to immunological, virological or biochemical disturbances (i.e. energy depletion, oxidative stress, increased protein degradation). We have studied mitochondrial uncoupling or inhibitor toxicity on neurones at the cellular level and at the mitochondrial level using rhodamine (Rh123) and 10-nonylacridine orange (NAO) fluorescence with confocal microscopy. Blockade of the mitochondrial chain complexes at various points was studied. The possible protective effects of the compound L-carnitine, which plays a central role in mitochondrial function, was tested in this form of neurotoxicity. It appears that L-carnitine and its acetylated form, acetyl-L-carnitine, can attenuate the cell damage, as assessed by lactate dehydrogenase (LDH) release, evoked by the uncoupler, p-(trifluoromethoxy)phenylhdyrazone (FCCP), or by the inhibitors, 3-nitropropionic acid (3-NPA) or rotenone. Further, the FCCP-induced inhibition of Rh123 uptake was antagonized by the preincubation of cells with L-carnitine. Since such neurotoxic mechanisms may be operating in the various pathological forms of myotoxicity and neurotoxicity, these observations suggest potential for a therapeutic approach.
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PMID:Protective actions of L-carnitine and acetyl-L-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors. 873 90

Astrocytes are glial cells able to release nitric oxide (NO) under basal conditions as well as following different neurochemical stimuli including cytokines, endotoxins and soluble antigens, thereby participating in neuroimmune responses. In particular, the inducible isoform of NO synthase seems to be activated during co-incubation of this cell type with cytokines as well as in the presence of the HIV coating gp120 glycoprotein, an effect which is associated with an enhancement of prostanoid release. This seems also to occur via activation of cyclooxygenase by NO. Thus, the L-arginine-NO pathway found in astrocytes may represent a novel approach in the treatment of neuroimmune disorders such as multiple sclerosis, Alzheimer's disease and AIDS.
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PMID:Release of nitric oxide from astroglial cells: a key mechanism in neuroimmune disorders. 874 14

Differential diagnosis of dementing diseases is very important to rule in the so-called treatable dementia. The new DSM-IV criteria for dementia include memory disturbances and one or more of aphasia, apraxia, or frontal lobe dysfunctions as essentials. Alzheimer disease requires, in addition, slowly progressive course and ruling out other brain or systemic diseases. Vascular dementia requires focal neurological or neuroimaging signs. Other diseases which cause dementia include chronic subdural hematoma, infection and brain tumor. CT or MRI can readily diagnose them if suspected and they may be treated. Systemic diseases associated with treatable dementia include electrolyte disturbances, hypothyroidism, vitamin deficiency, alcohol or drug intoxication, syphilis and HIV infection. Prevention of dementia seems to be the future problem as we could prevent cerebrovascular diseases by treating hypertension.
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PMID:[Clinical aspects of dementia]. 875 26

The CANTAB battery was developed for the assessment of cognitive deficits in humans with neurodegenerative diseases or brain damage. It consists of a series of interrelated computerized tests of memory, attention, and executive function, administered via a touch sensitive screen. It allows a decomposition of complex tasks commonly used in clinical assessment into their cognitive components and enables the extrapolation of findings from the animal literature. Tests include versions of the Wisconsin Card-Sorting Test and the Tower and London and also the Delayed Matching-to-Sample test, widely used in monkeys for visual recognition memory. The tests are constructed in such a way that they may be given to animals (monkeys) with minimal change. The nonverbal nature of the CANTAB tests makes them largely language independent and culture free. CANTAB has been standardized on a large, predominantly elderly, population and validated in neurosurgical patients as well as in patients with basal ganglia disorders, Alzheimer's disease, depression, and schizophrenia. In addition, CANTAB has been used to evaluate: a) the therapeutic effects of dopaminergic and cholinergic medication in neurodegenerative disease; b) cognition in 5-11-year-old normal, learning-disabled, and autistic children; c) deficits in patients with HIV infection; and d) early, asymptomatic Huntington's disease. The latter illustrate its usefulness in early identification of progressive disorders. It is suggested that the battery should have particular utility across a wide range of age and intelligence in longitudinal assessment after exposure to toxicants, and allow meaningful comparison with experimental studies of toxic effects in other species.
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PMID:CANTAB battery: proposed utility in neurotoxicology. 886 44

Apoptosis plays a role in AIDS pathogenesis in the immune system, but its role in HIV-1-induced neurological disease is unknown. In this study, we examine apoptosis induced by HIV-1 infection of the central nervous system (CNS) in an in vitro model and in brain tissue from AIDS patients. HIV-1 infection of primary brain cultures induced apoptosis in neurons and astrocytes in vitro as determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and propidium iodide staining and by electron microscopy. Apoptosis was not significantly induced until 1-2 wk after the time of peak virus production, suggesting induction by soluble factors rather than by direct viral infection. Apoptosis of neurons and astrocytes was also detected in brain tissue from 10/11 AIDS patients, including 5/5 patients with HIV-1 dementia and 4/5 nondemented patients. In addition, endothelial cell apoptosis was frequently detected in the brain of AIDS patients and was confirmed by electron microscopy. Most of the apoptotic cells were not localized adjacent to HIV-1-infected cells, providing further evidence for induction by soluble factors. In six non-AIDS control patients with normal brain, apoptotic cells were absent or limited to rare astrocytes. However, TUNEL-positive neurons and astrocytes were frequently detected in seven patients with Alzheimer's disease or abundant senile plaques. These studies suggest that apoptosis is a mechanism of CNS injury in AIDS which is likely to be induced by soluble factors. The apoptosis of endothelial cells in the CNS raises the possibility that some of these factors may be blood-derived.
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PMID:Apoptosis induced by HIV-1 infection of the central nervous system. 890 16

The caregiving literature has focused on European-American caregivers who are providing care to spouses or parents with Alzheimer's disease. The article reports ethnographic research exploring aspects of caregiving by rural African-American mothers for adult children with human immunodeficiency virus (HIV) disease. Eight African-American mothers were interviewed to elicit cultural domains of caregiving. Two major domains were a personal relationship with God and God's will. Taken together, these domains framed the context in which African-American mothers understood HIV disease, provided care, and resolved the death of their adult child.
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PMID:Going home: African-American caregiving for adult children with human immunodeficiency virus disease. 903 19


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