当前位置: X-MOL 学术Mol. Ther. Nucl. Acids › 论文详情
MiRNA-31 improves cognition and abolishes amyloid-β pathology by targeting APP and BACE1 in an animal model of Alzheimer’s disease
Molecular Therapy - Nucleic Acids ( IF 5.919 ) Pub Date : 2020-01-17 , DOI: 10.1016/j.omtn.2020.01.010
Ana Teresa Barros-Viegas; Vítor Carmona; Elisabete Ferreiro; Joana Guedes; Pedro Cunha; Luís Pereira de Almeida; Catarina Resende de Oliveira; João Pedro de Magalhães; João Peça; Ana Luísa Cardoso

Alzheimer’s disease (AD) is the most common form of dementia worldwide, characterized by progressive memory impairment, behavioral changes and, ultimately, loss of consciousness and death. Recently, miRNA dysfunction has been associated with increased production and impaired clearance of Aβ peptides, whose accumulation is one of the most well-known pathophysiological markers of this disease. In this study, we identified several miRNAs capable of targeting key proteins of the amylodoigenic pathway. The expression of one of these miRNAs, miR-31, previously found to be decreased in AD patients, was able to simultaneously reduce the levels of APP and Bace1 mRNA in the hippocampus of 17-months old 3xTg-AD female mice, leading to a significant improvement of memory deficits and a reduction in anxiety and cognitive inflexibility. In addition, lentiviral-mediated miR-31 expression significantly ameliorated AD neuropathology in this model, drastically reducing Aβ deposition in both the hippocampus and subiculum. Furthermore, the increase of miR-31 levels was enough to reduce the accumulation of glutamate vesicles in the hippocampus to levels found in non-transgenic age-matched animals. Overall, our results suggest that miR-31-mediated modulation of APP and BACE1 can become a therapeutic option in the treatment of AD.
更新日期:2020-01-21

 

全部期刊列表>>
化学/材料学中国作者研究精选
ACS材料视界
南京大学
自然科研论文编辑服务
剑桥大学-
中国科学院大学化学科学学院
南开大学化学院周其林
课题组网站
X-MOL
北京大学分子工程苏南研究院
华东师范大学分子机器及功能材料
中山大学化学工程与技术学院
试剂库存
天合科研
down
wechat
bug