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肌肽能否抑制锌介导的蛋白酶体抑制作用和神经退行性变?一种无毒但无专利的二肽的治疗潜力。

Could carnosine suppress zinc-mediated proteasome inhibition and neurodegeneration? Therapeutic potential of a non-toxic but non-patentable dipeptide.

作者信息

Hipkiss Alan R

机构信息

Centre for Experimental Therapeutics, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, UK.

出版信息

Biogerontology. 2005;6(2):147-9. doi: 10.1007/s10522-005-3460-z.

Abstract

Ageing and neurodegenerative conditions are often associated with proteasome dysfunction, possibly mediated by zinc and/or copper ions. Studies have shown that (i) the olfactory lobe is normally enriched in carnosine and zinc, (ii) carnosine can suppress copper and zinc toxicity in olfactory neurones, (iii) olfactory dysfunction is often associated with neurodegenerative conditions and (iv) elevated levels of zinc are found in brains of Alzheimer's patients. It is suggested that nasal administration of carnosine should be explored as a possible way of suppressing zinc/copper-mediated proteasome inhibition and consequent neurodegeneration.

摘要

衰老和神经退行性疾病通常与蛋白酶体功能障碍有关,这可能是由锌离子和/或铜离子介导的。研究表明:(i)嗅叶通常富含肌肽和锌;(ii)肌肽可以抑制嗅神经元中的铜和锌毒性;(iii)嗅觉功能障碍通常与神经退行性疾病有关;(iv)在阿尔茨海默病患者的大脑中发现锌水平升高。有人提出,应探索通过鼻腔给药肌肽,作为抑制锌/铜介导的蛋白酶体抑制及随之而来的神经退行性变的一种可能方法。

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