| The study used a mouse model where amphetamine is used to simulate schizophrenia. Obviously, it's not guaranteed to map to real humans having real schizophrenia. That doesn't mean it's a useless result, but everyone should remember that research is an accumulation of decades of many little pieces of information. This is another clue, not a "nail in the coffin" of old theories. The ultimate evaluation of medication is how well it actually performs in studies. If someone can develop a new medication that is more selective for D1 and show that it performs better and/or has fewer side effects then this would be a great result. However, don't get too excited. The pharmaceutical industry is often 10 steps ahead of public findings like this. A selective D1/D5 antagonist with negligible D2 affinity has already been trialed for schizophrenia without good results: https://en.wikipedia.org/wiki/Ecopipam Many of the most prescribed schizophrenia medications already have significant D1 affinity, too, so it's not really correct to say that we're "off target" These findings tend to be very aggravating to computer scientists who are familiar with systems that (mostly) obey clear-cut rules and can examined in extremely fine detail with enough equipment and motivation. Neuroscience is not so simple, but that doesn't mean it's all wrong. Each finding is one more piece of the puzzle. |