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At the recent Psych Congress 2023opens in a new tab or window, a session titled “State of the Science: Focus on Schizophrenia” was presented by Peter J. Weiden, MD, a clinical professor of psychiatry at the Renaissance School of Medicine at Stony Brook University in New York. His talk provided an overview of the latest research findings and emerging treatments in psychiatry.
In this exclusive MedPage Today video, Weiden highlights why clinicians need to be prepared for new options expected to hit the field over the next few years.
Following is a transcript of his remarks:
My career has been on new treatments for schizophrenia, and I’ve worked on new treatments, both medication and psychosocial. But in the last 6 or 7 years, I’ve been working with the pharmaceutical industry as an employee of the pharmaceutical industry and developing new drugs for schizophrenia. And what I’ve learned is that when we show a new treatment or a new mechanism, it’s really hard for doctors or clinicians to wrap their heads around that. And since leaving industry and now going back into academics, I wondered why. Why is that?
And here’s my thought on this, is that we – and I’m including myself – have been trained on the receptor theory of medication. You have a receptor, you have something in the brain that’s making the receptor too active or too little. You have a drug that then affects that receptor, and that’s all outside the cell. And that’s been such a good explanation over the years. Like the dopamine hypothesis of schizophrenia and how our meds work for psychosis. It’s worked so well that we haven’t had to look at what’s under the cell, what happens after that receptor has bound.
So we in psychiatry are behind the times relative to other clinicians and other disease areas that have drugs that have more nuanced or fancier mechanisms. These mechanisms go underneath the cell membrane. These mechanisms take advantage of how receptors grow and show up on the membrane or get taken in, or these new drugs take advantage of new receptors that no one ever knew about having new ligands. This just blows everyone’s mind.
So my advice is, don’t worry about the specific medicine and the advances in the sense that you have to know it all right away. But I would say you’re going to need, we as a field, need to be prepared for the very good news that these advances in drug development are going to hit psychiatry, and they’re going to hit psychiatry in the next few years.
I really think it’s different this time with antipsychotics for the treatment of schizophrenia. I really think we’re going to have antipsychotics in the next few years that do not directly antagonize dopamine. And patients will benefit from that in ways that we don’t understand. But what we’re going to learn is that blocking dopamine is a Band-Aid. Blocking dopamine is almost like treating heart failure with diuretics. Yes, you can treat heart failure with diuretics, but it doesn’t cause – it is not the fundamental cause of heart failure. You don’t have diuretic deficiency in heart failure.
Well, we’re going to learn that you don’t need dopamine antagonism to treat schizophrenia, and that this was in many ways a late treatment. So stay tuned; be open-minded.
He doesn’t get specific unfortunately.
At least its hopeful. May we all live to experience this new style of approach to meds
BE OPENMINDED. I have been saying it is not the dopamine. If dopamine were the cause, there would be very little side effects of medications.
That’s really interesting, i didn’t need an account to read that and watch the video,
I really hope these new drugs are really good, i was worried that my dopamine was being blocked too much recently like a rev limiter in my brain. I think i have some med related brain damaged though.
This seems hopeful
great to hear this.i m so sick of this anhedonia.i want to be normal again
Dopamine is the solution and problem at the same time. My pdoc told me positive symptoms are caused by high dopamine in one brain region and negative symptoms are cause by low dopamine in another region. I read in medical books and studies that positive symptoms are caused by high dorsal striatum dopamine and that negative symptoms are caused by low dopamine in frontal lobes. This means that all newer meds will have effect on dopamine, either directly or indirectly via other receptors. Remember the brain is a network of receptors, for example increasing NMDA in a brain region decreases striatal dopamine, same for GABA. I think thats the reason Clozapine is strongest, it acts on all these receptors.
Of course part of negative symptoms is also from meds and possibly brain damage. Sz is an imbalance of dopamine, not only high or only low. Maybe in the future they can modify dopamine through genetic engineering, that would be optimal.