Abstract

GENERAL COMMENTARY article Front. Neurol., 29 September 2014Sec. Neuropharmacology https://doi.org/10.3389/fneur.2014.00182

Highlights

  • In their article, Franco and CedazoMinguez open the debate on why it is difficult to translate successful preclinical research in Alzheimer’s disease (AD) mouse models into clinical practice [1]

  • Many of the therapies assayed on the AD models that are ineffective in people with the already established pathology might possibly be effective in preventing or delaying disease progression toward dementia

  • None of the animal models may represent the best option for evaluating novel therapeutic approaches for mild to moderate AD cases, they might be the first step in evaluating drugs that could reverse the synapse loss that underlies the “silent” phase of the disease

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Summary

Introduction

Franco and CedazoMinguez open the debate on why it is difficult to translate successful preclinical research in Alzheimer’s disease (AD) mouse models into clinical practice [1]. Despite a full preclinical and clinical trial package, the large majority of drugs with initial phases based on translational-laboratory-based discoveries fail to complete the development process.

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