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NEUROPROTECTION WITH SELENIUM THERAPY IN HIV+ IDUS

NEUROPROTECTION WITH SELENIUM THERAPY IN HIV+ IDUS
硒治疗对 HIV 感染者的神经保护
批准号:
6017658
负责人:
Gail Shor-Posner
金额:
$14.68万
依托单位国家:
美国
项目类别:
财政年份:
1999
资助国家:
美国
项目状态:
已结题
起止时间:
1999-08-05 至 2003-07-31

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中文摘要
翻译
HIV疾病的主要神经精神并发症是认知运动障碍,据报道,HIV-1血清阳性吸毒者患HIV相关痴呆的风险更高,神经功能障碍的进展更快。氧化应激可导致神经元退化,在HIV-1疾病中会增加,而且滥用药物似乎会加剧氧化应激。这项辅助研究的主要目的是确定补充硒是否可以为HIV-L血清阳性慢性吸毒者提供神经保护和帮助维持认知功能。硒是一种生物抗氧化剂,用于保护细胞免受氧化损伤。补充硒已被证明可以改善HIV/AIDS患者的氧化防御系统,并抑制神经病患者的精神退化。我们对感染HIV-L的吸毒者的初步调查表明,低水平的硒与精神表现下降有关,短期补硒对精神功能和情绪状态有很大的改善潜力。这些数据表明,补硒可能是预防认知能力丧失的有效策略。我们建议扩大我们目前由NIDA资助的临床试验,“硒疗法减缓HIV注射人群的疾病进展”,以比较硒和安慰剂对神经心理功能的影响。同意的艾滋病毒-L感染的吸毒者(n=120)将在父母研究的基线访问中登记,在补充之前,每6个月进行一次心理社会和认知成套检查,为期30个月。药物使用、营养、免疫、氧化应激和健康状况数据将由父母研究在认知和心理社会小组访问的同一时间收集,并提供给拟议的项目。这两项研究之间没有直接的科学重叠。拟议的合作和成本效益研究提供了一个独特的机会,以进一步了解艾滋病毒-L血清阳性的滥用药物的男性和女性的神经心理功能,并为艾滋病毒-1疾病的认知障碍的管理提供必要的重要信息。
英文摘要
The major neuropsychiatric complication in HIV-disease is cognitive-motor impairment, with HIV-1 seropositive drug users reported to be at higher risk for the development of HIV-associated dementia and more rapid progression in neurologic disability. Oxidative stress, which can lead to neuronal degeneration, is increased in HIV-1 disease and appears to be potentiated by drugs of abuse. The primary objective of this ancillary study is to determine whether supplementation with selenium, a biologic antioxidant that is required for protecting cells from oxidative damage, can provide neuroprotection and help maintain cognitive function in HIV-l seropositive chronic drug users. Supplementation with selenium has been shown to improve oxidative defense systems in HIV/AIDS patients, and inhibit mental deterioration in neurologic patients. Our preliminary investigations in HIV- l infected drug users indicate that low levels of selenium are associated with decreased mental performance, and that short-term selenium supplementation results in a strong potential for improvement in mental function and mood state. These data suggest that administration of selenium may be an effective strategy to prevent loss of cognitive ability. We propose to extend our currently NIDA-funded, clinical trial, "Selenium Therapy to Slow Disease Progression in HIV+ IDUs", to compare the effects of selenium or placebo on neuropsychological function. Consented HIV-l infected drug users (n=120) will be enrolled at the baseline visit of the parent study, prior to supplementation, and administered a psychosocial and cognitive battery every 6 months for 30 months. Drug use, nutritional, immunologic, oxidative stress, and health status data will be collected by the parent study at the same visit as the cognitive and psychosocial battery, and made available for the proposed project. There is no direct scientific overlap between the two studies. The proposed collaborative and cost-effective research provides a unique opportunity to further our understanding of neuropsychological function in HIV-l seropositive men and women who abuse drugs, as well as provide important information necessary for the management of cognitive impairment in HIV-1 disease.
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