Aducanumab: advancing Alzheimer’s treatment through regulation of excessive β-amyloid accumulation Clotilde Nsimire Katana Kachungunu [1] , Subhash Namdeo Mashal [1] , Priyadarshi Soumyaranjan Sahu* [1]

https://www.academia.edu/academia-immunity-and-disease/1/1/10.20935/AcadImmunoDis8055 Abstract Objective: Several drugs have been studied in past decades, with the main purpose of primarily being used for the symptomatic relief of Alzheimer’s Disease (AD). As of today, there are hundreds of ongoing studies to find a pharmacological treatment that will not only lessen the neurological symptoms of AD but will also slow down the progression or find a definite cure for the disease. We hypothesized that the emerging treatments for AD, such as Aducanumab, should primarily target the excessive brain accumulation of either β-amyloid peptides or tau proteins, thus delay the progression of illness when compared to the standard pharmacological treatment. The present systematic review explored and addressed Aducanumab therapy as an emerging treatment to cure, prevent, or slow down AD progression. Methods: A comprehensive literature search was conducted on PubMed using predefined search terms; the identified studies were then screened. Finally, 47 of the 210 articles were included for data extraction and analysis. Results: This study analyzed the validity and efficacy of Aducanumab. Aducanumab is a pharmacotherapy that targets excessive β-amyloid peptides in the brain; however, it does not have any role in reducing aggregated hyperphosphorylated tau proteins. Aducanumab has been analyzed and juxtaposed with the standard treatment, acetylcholinesterase inhibitors. Aducanumab is an effective pharmacotherapy that lowers β-amyloid peptides in the brain, and therefore, it helps treat AD. The side effects of Aducanumab are not deemed significant enough to justify FDA disapproval, and they can easily be monitored and prevented. Conclusions: Aducanumab has been proven to be a very effective and promising pharmacotherapy in treating AD. It is also the first disease-modifying pharmacotherapy for AD, and compared to the standard treatment, it is preferable in all aspects for slowing down or stopping the progression of AD.