Peering into the field of Alzheimer’s disease (AD), the outsider realizes that many of the therapeutic strategies tested (in animal models) have been successful. One also may notice that there is a deficit in translational research, i.e., to take a successful drug in mice and translate it to the patient. Efforts are still focused on novel projects to expand the therapeutic arsenal to “cure mice.” Scientific reasons behind so many successful strategies are not obvious. This article aims to review the current approaches to combat AD and to open a debate on common mechanisms of cognitive enhancement and neuroprotection. In short, either the rodent models are not good and should be discontinued, or we should extract the most useful information from those models. An example of a question that may be debated for the advancement in AD therapy is: In addition to reducing amyloid and tau pathologies, would it be necessary to boost synaptic strength and cognition? The debate could provide clues to turn around the current negative output in generating effective drugs for patients. Furthermore, discovery of biomarkers in human body fluids, and a clear distinction between cognitive enhancers and disease modifying strategies, should be instrumental for advancing in anti-AD drug discovery.
Keywords: adrenergic receptors, lost-in-translation research, resveratrol, transgenic AD models, biomarkers
Citation: Franco R and Cedazo-Minguez A (2014) Successful therapies for Alzheimer’s disease: why so many in animal models and none in humans? Front. Pharmacol. 5:146. doi: 10.3389/fphar.2014.00146
Received: 25 March 2014; Accepted: 03 June 2014;
Published online: 25 June 2014.
Edited by:Marianthi Papakosta, Pfizer, USA
Reviewed by:Muzamil Ahmad, Indian Institute of Integrative Medicine, India
Copyright © 2014 Franco and Cedazo-Minguez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Rafael Franco, Division of Neurosciences, Centro de Investigación Médica Aplicada, Universidad de Navarra, Avenida Pio XII 55, 31008 Pamplona, Spain e-mail: email@example.com