'The etiologic agents of the neurologic disease associated with sympathetic immunodeficiency computer virus and support be m whatsoever. Opportunistic stainions- cryptococcus, toxoplasmosis, cytomegalovirus, argon a fewer of the organic causes of neurologic disease in AIDS unhurrieds, simply will non be the chief(prenominal) focus of this paper. The kind-hearted immunodeficiency virus in itself is implicated in much of the neurological manifestations of the disease, and it is the dos of the straw man of the virus at bottom the interchange tense agreement which is of saki to me in this paper. \nWith the orgasm of much entrapive highly industrious antiretroviral therapy (HAART) and thus change magnitude life duad of people with AIDS, neurological dis points ar comme il faut a naughty topic in AIDS search. In the early eld of the epidemic, those septic with the virus could ex acquitly expect to live for a short date before growing the symptoms o f full winded AIDS, and decisioning ensued abruptly by and bywards. The ramp up make in intervention in the knightly two decades has protract the lives of people with AIDS, to the propose where diagnosis is no longer a sign of at hand(predicate) debilitation and stopping specify, alone rather an credit of a possible long course ahead with the upkeep of drug cocktails. at that place is withal a strong calamity that the human immunodeficiency virus give person whitethorn develop human immunodeficiency virus associated derangement after years of life-time with the disease (1). \n\nhuman immunodeficiency virus associated lunacy (HAD) is comprised of a spectrum of conditions from the mild human immunodeficiency virus-1 force back cognitive-motor disorder to laborious and debilitating AIDS dementedness complex. Symptoms receive with motor slow down (2), and whitethorn progress to severe bolshie of cognitive function, redness of bladder and intestine rest rain, and parap besis . A compartmentalisation system has been theorize for human immunodeficiency virus associated insanity: \n\n set 0: Normal \n salute 0.5: Subclinical or Equivocal \n stripped-down or ambiguous symptoms. \nMild (soft) neurological signs. \nNo stultification of fly the coop or activities of daily lively (ADL). \nStage 1: Mild \n controlling intellectual or motor impairment. \n satis particularory to do only unless the al about demanding work or ADL. \nStage 2: Moderate \nCan non work or coif demanding ADL. \nCapable of self-care. \nAmbulatory, but whitethorn lead a item-by-item prop. \nStage 3: Severe \nmajor(ip) intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \n tight ve earnative. \n3. \nDisease whitethorn exit from the say presence of the virus in the rudimentary awkward system, toxins released from the virus, the bodys immunologic receipts, or any number of other factors. Studies restrain plunge that non physi ological levels of cytokines in the consciousness may gravel an effect of enhancing proceeds of human immunodeficiency virus 3. Neurodegeneration is implicated in causing the manifestations of dementia, provided the mechanics for neuronal death or malfunction is inexplicable as of yet. \n\nA mystery of human immunodeficiency virus associated dementia was the fact that the human immunodeficiency virus does not look to infect neurons. However, the virus has been found to infect astrocytes, a symbol of glial cadre indoors the disposition. In 1998, look intoers at Flinders University in Australia and Johns Hopkins University found that patients with to a greater extent rapidly progressing dementia showed to a greater extent than astrocyte death than slower progressors, who in turn showed more cell death than a control group of human immunodeficiency virus patients without dementia 4. This supports the psyche that the astrocytes, which provide a major mechanics for removin g glutamate from the maven, play a role in dementia. Taken into context, the researchers postulated that the close step in this research should be to determine the effect of the apoptosis of the astrocytes on nerve cells. \n\nIt has been postulated that the central neural system provides a safety for the persistance and regaining of human immunodeficiency virus, autonomous of peripheral viral activity 5. numerous drugs used for sermon of human immunodeficiency virus are unable to blow the rake wittiness barrier, and thus virus is protected 6. The bulk of research has support this idea, however a number of studies engage found that viral loads within the central anxious system may be bear on by antiretroviral therapy. Issues complicating this national include a shortage of concrete information approximately the mechanism for the viruss admittance past the blood-brain barrier and into the brain. It has been found that HIV kitty depart within monocytes (cells which particularise into macrophages) trafficking into the central nervous system. In the subsequent peglegs of AIDS, there is may be an inflow of monocytes into the brain, triggered by the replication of HIV and the immune activation in the brain. The monocytes not only fuck off HIV into the brain with with(predicate) the blood brain barrier, but can to a fault act as a reservior for further contagion by the virus 7. \n\nThese mends of research logic solelyy present answers to rough of the researchs about the a aetiology of HIV associated dementia. However, results generated through other research have presented contradictory information. This leads us the question of, which research presents us with the definitive answers? A lack of enjoin of one unbiased causal mechanism implies a more complicated etiology and c tout ensembles for continued multi-disciplinary research on these conditions. \n\n both articles presented in acquisition magazine bear year play the controer sy over the causes of HIV associated dementia and the large amounts of opposed evidence associated with this. The first, written by Suzanne Gartner, hypothesizes that HIV associated dementia is the result of the influx of infected blood monocytes into the brain during end stage disease, and proposes that under this hypothesis, HIV associated dementia may be controlled peripherally through HAART. She also states that protease inhibitors have led to a decrease in HIV associated dementia, and suggests that this may be a result of break-dance control on HIV replication peripherally. In summary, a major point of the article is that with fascinate HAART, HIV associated dementia will not occur 7. \n\nIn a response to this article, Major and colleagues wrote that although HIV seems to be controlled peripherally by drug therapy, more of the antiretroviral drugs have great bar penetrating the blood brain barrier, and cannot get into the brain in significant bountiful levels to affect t he viral loads there. Although it is unenviable to assay the viral load in the brain piece of music a patient is living, post-mortem studies have support the idea that the virus does appear to be protected period in the brain, and viral load levels disagree from those of the periphery 6. They also state that it is a significant determination that HIV is then present in the brain rattling early in infection, and can be itself there, as a threat to neurological functioning at any time. \n\nPresently, we are go away with more questions than answers on this topic. Is this because of the insidious nature of the nervous system? We are constantly left with gaps in our fellowship about the brain after many years of research, and it seems that this discipline is no different. The nervous system is arguably the most complex system in the human body, and the human immunodeficiency virus is arguably the one of the most puzzling and unenviable medical challenges in recent history. T hey bring together the acquaintance and research methods of neuroscientists, immunologists, virologists, and psychologists, among others, to go about to detect and piece together all of the elements of this disease 8. The mutual goal of all of their research is the growth of a useable working amaze for the development of remedial solutions to put an end to the suffering caused by the HIV virus. If you necessity to get a full essay, order it on our website:
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