Commentary on “New directions for frontotemporal dementia drug discovery.” Do we know enough to develop meaningful treatments for frontotemporal dementia?

c s a a p o p The recent progress in elucidating both the genetic and europathologic causes of frontotemporal dementia (FTD) as been truly impressive. In light of this recent progress, a orkshop both to assess our current understanding of FTD nd to formulate a plan for development of new drugs to reat this disease was convened. In this issue Trojanowski t al [1] report and summarize their recommendations to direct nd accelerate the identification of meaningful treatments. Treatment of any disease, particularly that involving neuodegeneration, is extraordinarily difficult. Most efforts toay focus on the genetic and/or pathologic basis of the articular disease in question. Superb examples of this aproach to medicine have arisen and been successful in both arkinson’s disease (loss of dopaminergic neurons) and lzheimer’s disease (AD) (loss of cholinergic neurons). On he basis of this general approach and our current state of nderstanding of FTD, the authors review the field and then ake a list of recommendations to speed the process of drug iscovery [1]. Both the clinical and pathologic presentations of FTD are uite diverse. At least three distinct clinical presentations ave been identified, and multiple pathologies and genetic auses are apparently responsible [2]. This makes any genralization about potential treatments for FTD as a whole ifficult. The authors deal with this dilemma by focusing on he therapeutic opportunities for the tau-positive forms of TD. To develop a new drug for a disease, generally there are t least three requirements and needs that must be fulfilled. he first and most important is a valid working hypothesis s to why the new therapeutic approach should work. In the ase of FTD, as the authors point out, the recent genetic and