Therapeutic Perspectives of Drugs Targeting Toll-Like Receptors Based on Immune Physiopathology Theory of Alzheimer's Disease
Therapeutic Perspectives of Drugs Targeting Toll-Like Receptors Based on Immune Physiopathology Theory of Alzheimer's Disease
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DOI：
10.2174/1871527313666140711093858
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发表时间：
2014-01-01
影响因子：
3
通讯作者：
Sari, Youssef
中科院分区：
文献类型：
--
作者：
Schneider, Andrew R.;Sari, Youssef
阿尔茨海默病(AD)是一种与痴呆症发展相关的神经退行性疾病。已经证实，神经原纤维tau蛋白缠结和老年性β淀粉样蛋白斑块的病理特征通过炎症途径导致神经元退化。神经元的渐进性死亡，主要是胆碱能，导致认知能力和记忆的逐渐和致命的下降。通过针对这些病理特征及其相关途径，AD药物治疗可能会缓解疾病状态。在这篇综述文章中，我们重点介绍新提出的和实验性的AD药物治疗。我们讨论了AD治疗的三个特点：防止神经毒性β-淀粉样蛋白斑块的形成，神经元tau蛋白的稳定性，以及增加神经元的生长和功能。讨论的主要药物治疗方法和专利包括使用神经营养因子和靶向淀粉样前体蛋白裂解途径以防止β-淀粉样蛋白形成和tau聚集。
Alzheimer's disease (AD) is a neurodegenerative disease associated with the development of dementia. It has been established that the pathological hallmarks of neurofibrillary tau protein tangles and senile beta-amyloid protein plaques lead to degeneration of neurons via inflammatory pathways. The progressive death of neurons, primarily cholinergic, results in a gradual and fatal decline of cognitive abilities and memory. By targeting these pathological hallmarks and their associated pathways, AD drug therapy can potentially attenuate the disease state. In this review article, we focus on newly proposed and experimental AD drug treatment. We discuss three characteristic areas of AD treatment: prevention of neurotoxic beta-amyloid protein plaque formation, stability of neuronal tau proteins, and increase in neuronal growth and function. The primary drug therapy methods and patents discussed include the use of neurotrophic factors and targeting of the amyloid precursor protein cleavage pathway as prevention of beta-amyloid formation and tau aggregation.