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“Y ou may delay, but time will not.” Truer words were never said. For patients diagnosed with Alzheimer’s disease (AD), this represents a cruel truth. Most AD patients are left with a few good years before neurodegeneration strips them away of their daily competence and, ultimately, their identity. Since its discovery more than 100 years ago, significant advancements have been made in understanding the pathology underlying AD. However, in terms of therapeutic strategies, we are no closer to curing it than we were decades ago. Even today, only five drugs are approved by the Food and Drug Administration (FDA) for the treatment of AD. These drugs treat AD only symptomatically and do not target the underlying neurodegenerative pathology. Currently approved therapeutics are successful in slowing the progression of AD but not in reversing or preventing the symptoms of AD. Although numerous promising novel drugs remain in the pipeline, the time taken to establish safety profiles, approve these novel drug candidates, and get them out into the market runs nearly a decade. Unfortunately, time is not a luxury that patients with AD have. A promising approach is to revisit and screen FDAapproved drugs for a different disease. A very good example of such a candidate drug is bexarotene. Bexarotene has been approved by the FDA for treatment of cutaneous T-cell lymphoma. However recent work by Cramer et al. showed that bexarotene is quite effective in ameliorating symptoms of AD in a rodent model (1). Studies further characterizing the mechanism of action of bexarotene in AD are underway. But, because this drug is already FDA approved, its safety and toxicity profiles are already known. Repurposing of such drugs allows us to bypass cost and time hurdles in bringing the drug to the market. Today at least 5 million people in the United States alone are diagnosed with AD. This number is projected to explode to 16 million by the year 2050, as the aging population continues to increase (2). This warrants a hard look at current drug discovery paradigms as well as therapeutic targets for AD. Most research groups in search of a cure for AD have mostly focused on the amyloid beta hypothesis (3). However, an equal if not more critical suspect in AD as well as other neurodegenerative disorders is aggregation of the microtubule-associated protein tau. Tauopathies and their hallmark neurofibrillary tangles, are found in a wide variety of neurodegenerative diseases such as frontotemporal dementia with Parkinsonism, Pick’s disease, etc. (4). Yet they are relatively understudied as a target for therapeutic intervention in neurodegenerative disorders. One reason for this is the lack of robust, physiologically relevant in vivo models of tauopathies.