The annual 2025 Southern California Psychiatry Conference (So Cal Psych), held July 11-12 in Huntington Beach, California, brings together regional clinical experts to deliver evidence-based insights. Sessions will not only cover novel therapeutic agents, including the newly approved xanomeline‑trospium for schizophrenia, but also explore mood disorders, digital therapeutics, long‑acting injectables, and neuromodulation.
As psychiatry continues to evolve mechanistically and technologically—with muscarinic receptor modulators, glutamatergic and GABAergic agents, neuromodulation, and metabolic-focused treatments, So Cal Psych offers the most up-to-date, hands-on education and insights. Attendees will engage in practical learning through case-based presentations, device demonstrations, and expert panels aimed at facilitating real-world clinical implementation.
Gus Alva, MD, DFAPA, is the medical director of ATP Clinical Research in Orange, CA, and serves as chair of the upcoming 2025 Southern California Psychiatry Conference for his second year. HCPLive’s sister site, Psychiatry Times, caught up with Alva during the meeting to learn more about what attendees have to look forward to, including a deep dive into cutting-edge neuropsychiatric care, strategically bookended by sessions on muscarinic agonism’s role in schizophrenia and advances in treating Alzheimer’s disease.
HCPLive: What is the significance of muscarinic agonism in schizophrenia and Alzheimer’s, and how will this be addressed in the meeting?
Alva: The reason that this is so important is that as we commence with our sessions on schizophrenia, we need to recall it’s a chronic, disabling brain disorder that affects maybe about 1% of the population. It’s got multiple symptoms where individuals can’t trust what they think or feel, and as a consequence of that, we definitely know there’s an overlap with Alzheimer’s disease. In fact, the term schizophrenia comes from the Greek for “splitting up the mind,” and that very first session is going to entail some interesting themes, specifically tied in with an M1/M4 agonist called xenomeline, just to give everybody a good historical backdrop. Xenomeline was found to improve psychosis and behavioral disturbances in those suffering from Alzheimer’s disease. As a consequence, the thought was, hey, this might actually be something useful for individuals with schizophrenia.
Unfortunately, the early points of xenomeline exploration were met with a lot of side effects, including salivation, sweating, and GI distress, all of which were likely attributed to the non-selective stimulation of muscarinic receptors beyond the M1/M4 agonism, predominantly M2 and M3 in the periphery. So, although xenomeline was not statistically significant in showing improvement in cognition, it did show a reduction in vocal outbursts, suspiciousness, delusions, agitation, and hallucinations—themes we’ll be touching on in the last session of our meeting.
HCPLive: What can attendees expect to learn from sessions on mood disorders and digital therapeutics?
Alva: After the first session, we speak about bipolar disorder and characteristics associated with the condition, preceded by a non-CE talk led by Dr. Jerry Maguire. It’s important that people remember acetylcholine is important for mood. Quite a while ago, we figured out that there are overriding factors that tie back to acetylcholine in depression. Contrary to M1/M4 agonism, M1 antagonism may provide a nice avenue for correcting mood in unipolar and bipolar depression.
Then we’ll discuss digital therapeutics—a new modality in medicine. We’ve known about remote physiological monitoring and remote therapeutic monitoring, but now we’re looking at smart applications on phones and tools like watches that might help our patients benefit more with the challenges they face. We’ll speak about major depressive disorder and the advances within the glutamatergic system. Acetylcholine is deeply involved here too. The M1 receptor is coupled to the NMDA receptor, and antagonizing it might evoke a rapid response in individuals with depression.
We’ll review those mechanisms and discuss newer agents coming out soon. We’ll also touch on manipulating potassium channels, the opioid system, and incretins—which Dr. Roger McIntyre will address in his keynote speech, tying metabolic and neuropsychiatric states.
HCPLive: What other clinical challenges will the meeting address on day two?
Alva: Day two will begin with difficult-to-treat depression. It’s important to distinguish that from treatment-resistant depression. We’ll look beyond pharmacological modalities to include augmentation strategies, quicker-acting agents, and neuromodulation. We’ll have a great discussion on vagal nerve stimulation through a non-CE product theater, followed by a session on long-acting injectables to improve adherence in schizophrenia.
We’ll also address postpartum depression and the use of neurosteroids, tying into the GABAergic pathway, glutamate, and acetylcholine. Finally, we’ll talk about the continuum of Alzheimer’s disease and advances with monoclonal antibodies, as well as how to manage agitated or psychotic symptoms in later stages.
HCPLive: What are some key takeaways you hope clinicians walk away with?
Alva:The overall takeaway points that we hope get threaded through every participant are that it’s not difficult to stay up to date with the latest findings. Session 1 is a great refresher on why it makes sense to adopt new tools for treating schizophrenia. We now have an M1/M4 agonist for adults with schizophrenia that is not an antipsychotic. This helps de-stigmatize schizophrenia and move away from black box warnings, metabolic issues, and extrapyramidal symptoms.
Session 2 will offer a comprehensive look at bipolar disorder, including diagnostic and treatment updates from DSM-IV to DSM-5. Session three will explore digital therapeutics, including smartphone tools for schizophrenia and depression. Session 4 will dive into advanced treatment options for unipolar depression, from glutamate and GABA to potassium channels and GLP-1 agonists. Session five will focus on tardive dyskinesia and how to properly manage it. We’ll close with more about long-acting injectables and cognition in the aging brain, rounding out 2 full days of highly applicable, up-to-date information for clinicians.
Our faculty—Dr. Jonathan Meyer, Chelsea Monroe, Melanie Barrett, Deb York, Yvette Elpedio, Saeed Jacob, Jacob Hene, Dr. Alex Alba, Dr. Jason Kellogg, Dr. Elon Melnick, Dr. Roger McIntyre, Dr. Gerald McGuire, and myself—are all thrilled to be part of this effort. I’m so happy to be here. Thank you for joining us.
This transcript has been edited for clarity. Relevant disclosures for Alva include Teva Pharmaceuticals, Otsuka America Pharmaceuticals, AbbVie Inc., Axsome Therapeutics, Janssen Pharmaceuticals, and more.
