DRUG TREATMENT OF BRAIN INFLAMMATION IN ALZHEIMER'S DISEASE

阿尔茨海默病脑部炎症的药物治疗

• 批准号: 7375030
• 负责人: Dana Giulian
• 金额: $ 1.71万
• 依托单位: BAYLOR COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7375030
• 关键词: DRUG; TREATMENT; BRAIN; INFLAMMATION; ALZHEIMER

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Alzheimer's Disease (AD) is a degenerative disorder associated with senile plaques and marked reactive microgliosis. Dementia is thought to arise from loss of neurons and decreased synaptic connections. A number of studies have implicated neurotoxins released by microglia activated by A (Beta)1-42 as one casue of neuronal and synaptic damage in AD brain. Moreover, it is now widely believed that anti-inflammatory drugs might reduce immune-mediated neuron injury occurring in AD. Based upon extensive pre-clinical testing from in vitro and in vivo models, we have selected 3 candidate drugs as immuno-suppressants for AD. Here, we will examine the ability of immuno-suppressing drugs to reduce production of microglia-derived neurotoxins detected within cerebrospinal fluid and to inhibit microglia responses to A (Beta)1-42. In Aim 1, candidate anti-inflammatory agents will be examined for the ability to suppress immune responses in AD subjects. If successful, this proposed research will spur the development of new strategies to treat AD dementia.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。阿尔茨海默氏病（AD）是一种与老年斑块有关的退化性疾病，并明显反应性小胶质细胞增多。痴呆症被认为是由于神经元的丧失和突触连接减少而引起的。许多研究暗示了由A（beta）1-42激活的小胶质细胞释放的神经毒素，是AD脑中神经元和突触损伤的一个壳体。此外，现在人们普遍认为，抗炎药可能会减少AD中发生的免疫介导的神经元损伤。基于体外和体内模型的广泛临床前测试，我们选择了3种候选药物作为AD的免疫抑制剂。在这里，我们将研究免疫抑制药物减少脑脊液中检测到的小胶质细胞衍生神经毒素的产生的能力，并抑制对A（beta）1-42的小胶质细胞反应。在AIM 1中，将检查候选抗炎药的抗炎药，以抑制AD受试者的免疫反应的能力。如果成功的话，这项拟议的研究将刺激治疗痴呆症的新策略的发展。