We also touch on potential neural substrates of illness-related cortical thinning in psychosis, and find alignment with normative levels of specific receptor systems, while certain highly differentiated and early maturing sensory/koniocortical areas appeared relatively protected. 2/3

🧠💊New preprint differentiating antipsychotic medication vs. illness effects on cortical thickness in people w/ psychosis.

Finding: People receiving placebo show prominent cortical thinning over 1st year of illness, whereas those receiving antipsychotics do not. 1/3

www.medrxiv.org/content/10.1...

Finally, to model the dynamic process that led to observed synaptic deficit patterns, we use network diffusion models to simulate movement of pathology starting at each region, allowing spread via axons to areas with similar receptor profiles—finding left inferior frontal regions as initial sources

We then test many different competing network models to understand whether connectivity, regional molecular/cellular features, or a combination, constrain synaptic deficits. We find that a model constrained by axonal connectivity + receptor similarity between regions fits best.

While we find some canonical functions networks preferentially house synaptic deficits, there is a stronger association between regional synaptic deficits and chemoarchitecture, esp. normative concentrations of 5HT1b, 2a, 1a, GABA-A/BZ and CB1 receptors.

🧩New study: "Network Constraints on 𝘪𝘯 𝘷𝘪𝘷𝘰 Synaptic Alterations in Schizophrenia"

medrxiv.org/content/10.1...

We map a prominent brain-wide pattern of synaptic defects in people with Schizophrenia using PET, then model the molecular, cellular & connectomic features shaping this pattern 🧵1/3👇