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DESIGN AND SYNTHESIS OF SHORT PEPTD3ES FOR THE TREATMENT OF ALZHEIMER'S AND PARKINSON'S DISEASES

机译:用于治疗阿尔茨海默氏菌和帕金森疾病的短PEPTD3ES的设计与合成

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Alzheimer's disease (AD) and Parkinson's disease (PD) are progressive neurodegenerative disorders which are marked by neuronal accumulation of toxic misfolded proteins which form amyloid plaques. The main components of the plaques are β-amyloid peptides (Aβ[1-40] and Aβ[1-42]) and α-synuclein. The key process in the pathology of AD and PD is the formation of fibrils and aggregates of Aβ peptides and α-synuclein. We have previously shown that small peptides structurally related to the sequence of Aβ[1-42] protect against the neurotoxicity of Aβ peptides. Recent studies by other groups have shown that β-synuclein can counteract the aggregation of α-synuclein in the neurodegenerative process of PD, hereby might protect the central nervous system from the neurotoxic effects of alpha-synuclein.
机译:阿尔茨海默病(AD)和帕金森病(PD)是进一步的神经变性障碍,其由形成淀粉样斑块的毒性错配蛋白的神经元积累标记。斑块的主要成分是β-淀粉样肽(Aβ[1-40]和Aβ[1-42])和α-突触核苷酸。 AD和Pd病理学中的关键过程是形成Aβ肽和α-突触核苷酸的原纤维和聚集体。我们之前已经表明,与Aβ[1-42]序列的序列是否有关的小肽保护免受Aβ肽的神经毒性。其他组的最近的研究表明,β-突触核蛋白可以抵消Pd的神经变性过程中α-突触核蛋白的聚集,从而可以保护中枢神经系统免受α-突触核蛋白的神经毒性作用。

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