That depends on the study.
In order to find a cure (through scientific means), we need to first precisely identify the root cause. Ablating androgens with finasteride (or sp, accutane, ssri’s, etc.) has changed something in our bodies, to put it high level. This change is very likely some epigenetic effect in our cells. Environmental factors (chemicals, medication) have been shown to induce epigenetic changes in countless publications, this is undisputed. Epigenetic changes can persistently alter the way our cells work, and thereby the function of our organs (which are obviously made of cells).
Given the above, the big question is which genes exactly are deregulated, and which genes predispose us to this mess in the first place, given than most guys can take these meds without any negative effects (which still amazes me). Studies which are looking into these questions are by their nature paving the road on the way to finding a cure, or at least some half way effective treatment.
Where I unfortunately have to agree with you, is that Melcangi’s studies do not fit the above criteria. His studies so far have been designed to demonstrate the effects of finasteride and pfs in patients. Such included demonstrating altered neurosteroid levels, methylation of 5ar and altered gut microbiota. This undoubtedly is valuable at a scientific level, makes for some cool publications, and is important for keeping the conversation going in the scientific community. Such information can also be useful for potential future law suits, but it doesn’t pay in well to our “cure” objective. Therefore I feel that we need to keep our expectations regarding Melcangi’s work at a realistic level.
Brigham and Women’s Hospital, Baylor and our own community GWAS project on the other hand, theoretically fit the bill. Needless to say, Brigham was a total flop. Baylor, on the other hand is looking into full genome gene expression, and is therefore 100% on mark with regard to what I wrote above. The problem of course with Baylor is that the study has been going on forever, and is frankly way overdue. I am still hopeful though, that they will end up publishing the goods in the near future. If the publication will not be muddled by political factors (as seems to have been the case with Brigham), the Baylor study could be the scientific equivalent of a Tsunami. Let’s keep our fingers crossed.
Last but not least comes our very own community GWAS project. With some more genomes, and collaboration of the right specialists, we could have a chance of finding some underlying genetic drivers to our predisposition. This would be key to developing an animal model. Melcangi has been feeding finasteride to a bunch of rats, and has shown that they show some depressive symptoms. However, it would not be reasonable to call this PFS. One could only start talking about PFS if the effect (along with other typical PFS symptoms) would persist for many months after discontinuing the drug. This not have being demonstrated to be the case, we cannot be talking about an animal model here. An animal model would need to be genetically engineered to mimic our predisposition, and then “get” “real” persistent PFS once being administrated these drugs.
At the end of the day, we cannot put all of our egs in one basked. We need different baskets: Bespoke ones, scientific ones, community made ones and also some luck. With all those ingredients, in the right mix, I believe that we have the best chance to advance.