首页> 美国卫生研究院文献>Drug Design Development and Therapy >Neuroprotective Effect of S-trans Trans-farnesylthiosalicylic Acid via Inhibition of RAS/ERK Pathway for the Treatment of Alzheimer’s Disease
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Neuroprotective Effect of S-trans Trans-farnesylthiosalicylic Acid via Inhibition of RAS/ERK Pathway for the Treatment of Alzheimer’s Disease

机译:S-反式反式-法呢基硫代水杨酸通过抑制RAS / ERK途径对阿尔茨海默氏病的神经保护作用

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摘要

Alzheimer’s disease (AD), a leading cause of dementia, becomes a serious health issue for individuals and society around the world. AD is a neurodegenerative disease characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFT) and the loss of large numbers of neurons. To date, there is no effective treatment for AD, and thus, to enhance neurogenesis in the AD brain may be a therapeutic strategy. RAS signaling pathway involves in synaptic plasticity and memory formation, which is overexpressed in brains with AD. This study used Aβ -injected mice (Aβ -mice) as the AD model to investigate the effects of S-trans, trans-farnesylthiosalicylic acid (FTS), a synthetic Ras inhibitor, on the impairment of neurogenesis and the spatial cognitive deficits.
机译:阿尔茨海默氏病(AD)是痴呆症的主要原因,已成为世界各地个人和社会面临的严重健康问题。 AD是一种神经退行性疾病,其特征在于淀粉样β(Aβ)肽和神经原纤维缠结(NFT)的沉积以及大量神经元的丢失。迄今为止,尚无针对AD的有效疗法,因此,增强AD大脑中的神经发生可能是一种治疗策略。 RAS信号通路涉及突触可塑性和记忆形成,这在患有AD的大脑中过表达。这项研究使用注射Aβ的小鼠(Aβ-小鼠)作为AD模型,研究了合成的Ras抑制剂S-反式,反式法呢基硫代水杨酸(FTS)对神经发生损害和空间认知缺陷的影响。

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