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New therapeutic target identified for Alzheimer's disease

机译:确定了阿尔茨海默氏病的新治疗靶标

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A team of scientists has reported that cathepsin B (CatB) gene knockout, or its reduction by an enzyme inhibitor, blocks the creation of key neurotoxic pGlu-Ap peptides, which are linked to Alzheimer's disease (AD).pGlu-Ap peptides are N-terminally truncated forms of full-length Ap peptides (flAP(140/42)), in which the N-terminal glutamate is cyclized to pyrogluta-mate to generate pGlu-AP 0 . P-secretase cleavage of amyloid-P precursor protein (APPP) produces flAP(1 _40/42), but it was not yet known whether the p-secretase BACE1 or the alternative P-secretase CatB participate in the production of pGlu-Ap.
机译:一组科学家报告说,组织蛋白酶B(CatB)基因敲除或被酶抑制剂还原可阻止关键的神经毒性pGlu-Ap肽的产生,该肽与阿尔茨海默氏病(AD)相关.pGlu-Ap肽为N -末端截短形式的全长Ap肽(flAP(140/42)),其中N末端谷氨酸被环化为焦谷氨酸以生成pGlu-AP 0。淀粉样蛋白-P前体蛋白(APPP)的P-分泌酶裂解产生flAP(1 _40 / 42),但尚不清楚p-分泌酶BACE1或替代P-分泌酶CatB是否参与pGlu-Ap的生产。

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