Som Chaudhury Sutapa, Das Mukhopadhyay Chitrangada
a Centre for Healthcare Science and Technology , Indian Institute of Engineering Science and Technology , Shibpur , West Bengal , India.
Int J Neurosci. 2018 May;128(5):449-463. doi: 10.1080/00207454.2017.1398153. Epub 2017 Nov 16.
Misfolded β-sheet structures of proteins leading to neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) are in the spotlight since long. However, not much was known about the functional amyloids till the last decade. Researchers have become increasingly more concerned with the degree of involvement of these functional amyloids in human physiology. Interestingly, it has been found that the human body is exposed to a tremendous systemic amyloid burden, especially, during aging. Although many findings regarding these functional amyloids come up every day, some questions still remain unanswered like do these functional amyloids directly involve in the fibrillization of amyloid beta (Aβ) 42 peptide or enhance the Aβ42 aggregation rate; whether functional bacterial amyloids (FuBA) co-localize with the senile plaques of AD or not. A detailed review of the latest status regarding the interrelationship between functional amyloids, pathogenic amyloids and misfolded prions and therapeutic assessment of functional amyloids for the treatment of neurodegenerative diseases can help identify an alternative medication for neurodegeneration. A unique mathematical model is proposed here for alteration of Aβ42 aggregation kinetics in AD to carve out the future direction of therapeutic consideration.
导致阿尔茨海默病（AD）和帕金森病（PD）等神经退行性疾病的蛋白质错误折叠β-折叠结构长期以来一直备受关注。然而，直到过去十年，人们对功能性淀粉样蛋白的了解还不多。研究人员越来越关注这些功能性淀粉样蛋白在人体生理中的参与程度。有趣的是，人们发现人体尤其是在衰老过程中会面临巨大的系统性淀粉样蛋白负担。尽管每天都有许多关于这些功能性淀粉样蛋白的发现，但一些问题仍然没有答案，比如这些功能性淀粉样蛋白是否直接参与淀粉样β（Aβ）42肽的纤维化过程或提高Aβ42的聚集速率；功能性细菌淀粉样蛋白（FuBA）是否与AD的老年斑共定位。详细回顾功能性淀粉样蛋白、致病性淀粉样蛋白和错误折叠朊病毒之间相互关系的最新状况以及对功能性淀粉样蛋白治疗神经退行性疾病的治疗评估，有助于确定神经退行性疾病的替代药物。本文提出了一个独特的数学模型，用于改变AD中Aβ42的聚集动力学，以明确治疗考虑的未来方向。
