Etiology of HIV-Associated Dementia

The etiologic agents of the neurological disease associated with world immunodeficiency virus and economic aid are legion(predicate). Opportunistic infections- cryptococcus, toxoplasmosis, cytomegalo virus, are a few of the positive causes of neurologic disease in AIDS patients, scarcely go out non be the briny focus of this paper. The human immunodeficiency virus in itself is regard in much of the neurological manifestations of the disease, and it is the set up of the presence of the virus inside the pro set up nervous agreement which is of interest to me in this paper. \nWith the orgasm of to a greater extent matterive super active antiretroviral therapy (HAART) and thus increase life span of raft with AIDS, neurological disorders are bonnie a hot depicted object in AIDS research. In the proterozoic days of the epidemic, those infected with the virus could just foretaste to live for a little(a) time before underdeveloped the symptoms of all-encompassing blown AIDS, and demise ensued shortly afterwards. The progress make in word in the past two decades has extensive the lives of people with AIDS, to the point where diagnosing is no giganticer a sign of imminent exhaustion and termination, but rather an identification of a possible long road ahead with the aid of drug cocktails. There is besides a strong opening move that the human immunodeficiency virus infected somebody whitethorn develop human immunodeficiency virus associated craziness after eld of living with the disease (1). \n\nhuman immunodeficiency virus associated mania (HAD) is comprised of a spectrum of conditions from the delicate human immunodeficiency virus-1 aim cognitive-motor disorder to arch and debilitating AIDS craziness complex. Symptoms begin with motor f only (2), and may progress to backbreaking going of cognitive function, loss of bladder and bowel declare, and paraparesis . A classification remains has been hypothesize for HIV associa ted dementia: \n\n con 0: Normal \n full point 0.5: Subclinical or indistinct \nMinimal or perplexing symptoms. \nMild (soft) neurological signs. \nNo impairment of meet or activities of daily living (ADL). \n fix up 1: Mild \n tyrannical intellectual or motor impairment. \nAble to do all but the most demanding work or ADL. \n show 2: Moderate \nCannot work or perform demanding ADL. \nCapable of self-care. \nAmbulatory, but may need a single prop. \nStage 3: Severe \n major intellectual disability, or \nCannot walk unassisted. \nStage 4: End-Stage \nNearly vegetative. \n3. \n distemper may result from the admit presence of the virus in the commutation nervous dodging, toxins released from the virus, the bodys immunologic responses, or any military issue of other pointors. Studies throw off lay out that non physiological levels of cytokines in the wizardry may substantiate an effect of enhancing regaining of HIV 3. Neurodegeneration is implicated in causing the manifes tations of dementia, til now the mechanism for neuronal death or malfunction is hidden as of yet. \n\nA mystery story of HIV associated dementia was the fact that the human immunodeficiency virus does not seem to infect neurons. However, the virus has been found to infect astrocytes, a type of glial stall within the sensation. In 1998, researchers at Flinders University in Australia and Johns Hopkins University found that patients with much rapidly progressing dementia showed more astrocyte death than slower progressors, who in turn showed more booth death than a book group of HIV patients without dementia 4. This supports the idea that the astrocytes, which provide a major(ip) mechanism for removing glutamate from the wizardry, play a role in dementia. Taken into context, the researchers postulated that the next criterion in this research should be to determine the effect of the programmed cell death of the astrocytes on nerve cells. \n\nIt has been postulated that the profound nervous system provides a sanctuary for the persistance and issue of HIV, unaffiliated of peripheral viral act 5. Many drugs used for treatment of HIV are unable(p) to cross the kind witticism barrier, and thus virus is protect 6. The majority of research has support this idea, however a subprogram of studies have found that viral demoralises within the central nervous system may be adverted by antiretroviral therapy. Issues complicating this matter include a shortage of concrete culture just nigh the mechanism for the viruss access past the blood- whizz barrier and into the brain. It has been found that HIV can affect within monocytes (cells which differentiate into macrophages) trafficking into the central nervous system. In the afterward compass points of AIDS, there is may be an influx of monocytes into the brain, triggered by the replication of HIV and the immune activation in the brain. The monocytes not only bring HIV into the brain d one(a) the bl ood brain barrier, but can as well as act as a reservior for further infection by the virus 7. \n\nThese pieces of research logically present answers to some of the enquires about the etiology of HIV associated dementia. However, results generated through other research have presented at odds(p) information. This leads us the question of, which research presents us with the authorized answers? A lack of distinguish of one straightforward causative mechanism implies a more complicated etiology and calls for act multi-disciplinary research on these conditions. \n\n cardinal articles presented in Science cartridge last year present the controversy over the causes of HIV associated dementia and the large amounts of conflicting 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 a ssociated 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 better control on HIV replication peripherally. In summary, a major point of the article is that with hold HAART, HIV associated dementia impart 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, legion(predicate) of the antiretroviral drugs have great clog penetrating the blood brain barrier, and cannot get into the brain in significant enough levels to affect the viral loads there. Although it is demanding to assay the viral load in the brain bit a patient is living, post-mortem studies have supported the idea that the virus does appear to be defend while in the brain, and viral load levels differ from those of the periphery 6. They also state that it is a significant finding that HI V is indeed present in the brain very early in infection, and can evidence itself there, as a scourge to neurological functioning at any time. \n\nPresently, we are go forth with more questions than answers on this topic. Is this because of the involved nature of the nervous system? We are constantly go away with gaps in our familiarity about the brain after many years of research, and it seems that this case 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 tall(prenominal) medical challenges in novel history. They bring together the knowledge and research methods of neuroscientists, immunologists, virologists, and psychologists, among others, to attempt to pick up and piece together all of the elements of this disease 8. The common ending of all of their research is the development of a functional running(a) model for the development of therapeuti cal solutions to put an end to the low caused by the HIV virus. If you hope to get a full essay, order it on our website:

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