Introduction
Alzheimer’s disease is the most common cause of dementia, whose global frequency ranges from 60-70%. Despite the tremendous increase in AD prevalence and severity, only a few licensed medicines are available to treat the symptoms of the disease. Aducanumab is a disease-modifying human monoclonal antibody approved by the United States Food and Drug Administration, and is the first Alzheimer’s disease medication to be licensed. It explicitly targets Aβ aggregates like insoluble fibrils and soluble oligomers.
Objective
This systematic review aims to explore available clinical trials on the effectiveness and safety of aducanumab for the treatment of AD.
Methods
- This systematic review was performed following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) guidelines.
- A comprehensive literature search was conducted for suitable studies on Aducanumab using the electronic database MEDLINE through PubMed, EMBASE, Web of Science, and Scopus.
- Studies evaluating the benefit and adverse effects of aducanumab for the treatment of AD were included.
- Studies not evaluating aducanumab, not focusing on AD, animal studies, laboratory experiments, case reports, and case series were excluded.
Results
- The comprehensive search from five databases retrieved 2622 articles. After removing 215 duplicates, a total of 2407 articles were listed for screening the title and abstract. 2381 articles were excluded due to not meeting the inclusion criteria.
- Studies reported that aducanumab reduces brain amyloid-beta plaques in a time and dose-dependent manner (dose-response, P<0.05) and a slow decline in cognition in the high-dose treated group.
- Amyloid-related imaging abnormality was reported as a serious adverse event and was profound in the high-dose treated group.
Conclusion
The results of this systematic review suggest that aducanumab has been the first drug targeting the AD pathophysiologic hallmarks (Aβ and Tau) and has effectively reduced the clinical progression of the disease. However, it was only effective in the mild or early stages of AD.