Repurposing Licensed Drugs for Use Against Alzheimer's Disease.

Leslie C Norins

doi:10.3233/jad-210080

Abstract

Substantial evidence, composed of drug mechanisms of action, in vivo testing, and epidemiological data, exists to support clinical testing of FDA-approved drugs for repurposing to the treatment of Alzheimer’s disease (AD). Licensed compound investigation can often proceed at a faster and more cost-effective manner than un-approved compounds moving through the drug pipeline. As the prevalence of AD increases with life expectancy, the current rise in life expectancy amalgamated with the lack of an effective drug for the treatment of AD unnecessarily burdens our medical system and is an urgent public health concern. The unfounded reluctance to examine repurposing existing drugs for possible AD therapy further impedes the possibility of improving the quality of patient lives with a terminal disease. This review summarizes some evidence which exists to suggest certain already-approved drugs may be considered for the treatment of AD and will perhaps encourage physicians to off-label prescribe these safe therapeutics.

Highlights

Many therapeutic areas including cancer, erectile dysfunction, irritable bowel syndrome, and attention deficit disorder have benefited from repositioning existing drugs
The heavy burden Alzheimer’s disease (AD) presents on our medical system is only increasing as life expectancy grows and the world’s population exponentially multiplies
This review has identified FDA-approved therapeutics, commonly cited in literature and systematic reviews, for repurposing as some evidence exists to suggest that they may be useful in the treatment of AD

Summary

Introduction

Many therapeutic areas including cancer, erectile dysfunction, irritable bowel syndrome, and attention deficit disorder have benefited from repositioning existing drugs. L.C. Norins / Repurposing Licensed Drugs often, this preclinical evidence does not translate to the bedside, this review delves into some of the in vitro and in vivo data that exist to support certain therapeutic candidates on the basis of improving ADassociated pathologies, functional disturbances and biomarkers, such as neuronal cell death, neuronal plasticity, A␤ deposition, and tau protein hyperphosphorylation.

Results

Conclusion