DYRK1A型
神经退行性变
痴呆
疾病
阿尔茨海默病
21号染色体
医学
生物信息学
唐氏综合症
生物
生物信息学
基因
遗传学
病理
精神科
染色体
作者
Márcia María de Souza,Arthur Ribeiro Cenci,Kerolain Faoro Teixeira,Valkiria Machado,Majory Christina Garcia Mendes Schuler,Ana Elisa Gonçalves,Ana Paula Dalmagro,Camila André Cazarin,Leonardo L. G. Ferreira,Aldo Sena de Oliveira,Adriano D. Andricopulo
标识
DOI:10.2174/0929867329666220620162018
摘要
Alzheimer's disease (AD) is a chronic neurodegenerative disease and the most common form of dementia, especially in the elderly. Due to the increase in life expectancy, in recent years, there has been an excessive growth in the number of people affected by this disease, causing serious problems for health systems. In recent years, research has been intensified to find new therapeutic approaches that prevent the progression of the disease. In this sense, recent studies indicate that the dual-specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) gene, which is located on chromosome 21q22.2 and overexpressed in Down syndrome (DS), may play a significant role in developmental brain disorders and early onset neurodegeneration, neuronal loss and dementia in DS and AD. Inhibiting DYRK1A may serve to stop the phenotypic effects of its overexpression and, therefore, is a potential treatment strategy for the prevention of ageassociated neurodegeneration, including Alzheimer-type pathology.In this review, we investigate the contribution of DYRK1A inhibitors as potential anti-AD agents.A search in the literature to compile an in vitro dataset including IC50 values involving DYRK1A was performed from 2014 to the present day. In addition, we carried out structure-activity relationship studies based on in vitro and in silico data.molecular modeling and enzyme kinetics studies indicate that DYRK1A may contribute to AD pathology through its proteolytic process, reducing its kinase specificity.further evaluation of DYRK1A inhibitors may contribute to new therapeutic approaches for AD.
科研通智能强力驱动
Strongly Powered by AbleSci AI