会员体验
专利管家(专利管理)
工作空间(专利管理)
风险监控(情报监控)
数据分析(专利分析)
侵权分析(诉讼无效)
联系我们
交流群
官方交流:
QQ群: 891211   
微信请扫码    >>>
现在联系顾问~
热词
    • 1. 发明申请
    • TREATMENT OF ALZHEIMER DISEASE BY MODULATION OF SYNAPSINS
    • 通过调节SYNPSINS治疗阿尔茨海默病
    • WO1996035446A1
    • 1996-11-14
    • PCT/US1996006835
    • 1996-05-13
    • THE ROCKEFELLER UNIVERSITYBRIGHAM AND WOMEN'S HOSPITAL
    • THE ROCKEFELLER UNIVERSITYBRIGHAM AND WOMEN'S HOSPITALHAN, Hui-QuanGREENGARD, PaulKOSIK, Kenneth, S.FERREIRA, Adriana
    • A61K38/18
    • A61K31/7076A61K38/185A61K38/1883
    • The role of synapsin II in both the reformation and the maintenance of synaptic connections in cultured hippocampal neurons can be the basis of therapy for neurodegenerative disorder, particularly Alzheimer disease, which involve the disruption of synapses. When synapsin II expression in neurons is blocked by antisense synapsin II oligonucleotides, the ability of hippocampal neurons to reform as well as to maintain synapses is severely disrupted. Antisense suppression of synapsin II after axon formation but immediately before synaptogenesis prevents synapse formation. Suppression of synapsin II after synaptogenesis disrupts the majority of existing synapses. Re-expression of synapsin II in synapsin deficient neurons achieved after removing the antisense oligonucleotides leads to the re-establishment of synaptic connections, providing direct evidence that synapsin II is required for the maintenance and/or restoration of synapses. Thus, therapeutic methods based on the reformation and the maintenance of synapses, including delivery of the synapsin cDNAS or proteins into the patient's nervous system, use of the synapsin cDNAS to promote the synapse forming ability of cells for grafting, and use of agents that increase the expression of, enhancing the activity of, or mimic the activity of, the endogenous synapsins, can provide treatment of neurodegenerative disorders.
    • 突触素II在培养的海马神经元的突触连接的重建和维持中的作用可以作为神经变性疾病,特别是涉及突触中断的阿尔茨海默氏病的治疗的基础。 当突触素II在神经元中的表达被反义突触蛋白II寡核苷酸阻断时,海马神经元改变的能力以及维持突触的能力被严重地破坏。 在突触形成之后但紧接在突触发生之前的突触体II的反义抑制阻止突触形成。 突触后突触素II的抑制破坏了大多数现有的突触。 在去除反义寡核苷酸后实现的突触素缺陷型神经元中突触素II的重新表达导致突触连接的重新建立,提供突触间质II用于维持和/或恢复突触所需的直接证据。 因此,基于重建和维持突触的治疗方法,包括将突触素cDNAS或蛋白质递送到患者神经系统中,使用突触素cDNAS来促进细胞用于移植的突触形成能力,并且使用增加的试剂 增强内源性突触素的活性或模拟活性的表达可提供治疗神经变性疾病。