1) If stress vulnerability can be thought of as reduced capacity to handle events, why does NA emerge when this capacity is exceeded? Are there are other signs that a limited capacity has been exceeded, besides NA? What are the neurocircuits which carry this load? |
Animal models, neuroimaging studies, stress and emotion challenges, experience sampling methodologies, computational modeling |
2) What are the developmentally sensitive periods for the emergence of NA associated with the development of psychosis? |
Longitudinal studies including critical developmental periods, animal models |
3) What is the relationship between vulnerability and cognition? Between vulnerability and negative symptoms? |
Clinical phenotyping and analytics, eg, network analysis, structural equation modeling, causal modeling, etc. |
4) If cognitive function is improved, can NA be properly regulated? |
Cognitive behavior therapy for psychosis, cognitive training, pharmacologic cognitive enhancers |
5) How can we separate NA related to a GABAergic (PVI) deficit from other causes of NA? |
Multimodal neuroimaging and EEG with pharmacologic challenge; animal models |
6) How much of the vulnerability in schizophrenia is shared across other disorders? |
Transdiagnostic studies (including postmortem samples), genetic markers (polygenic risk scores) |