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G. Modinos

3 papers in the library · publishing 2017-2023

Papers

Phenomenology and Social Agent Representation in Psychosis: A Welcome Integration

Clinical psychological science : a journal of the Association for Psychological Science June 20, 2017 Vaughan Bell, K. Mills, G. Modinos et al.

A debate about how to study psychosis in cognitive science is addressed. The authors agree with critics that the subjective experience of psychosis, especially the presence of illusory social agents, cannot be reduced to simple cognitive errors. They argue that current social-cognition models neglect this central phenomenological feature. They propose that research should also examine how social agents are represented and deployed, not just how social information is processed. They suggest that intersubjective instability in psychosis may be reorganized into illusory social agents as a best-fit explanation, a hypothesis for future study. They advocate for a phenomenologically informed cognitive science to better understand psychosis.

Influence of cannabis use on incidence of psychosis in people at clinical high risk

Psychiatry and Clinical Neurosciences April 18, 2023 Lucy Chester, L. Valmaggia, M. Kempton et al.

Cannabis use is associated with an increased risk of developing psychotic disorders among people already at clinical high risk for psychosis. In a prospective study of this population, cannabis use was linked to a higher incidence of psychotic disorders and to more persistent psychotic symptoms, as well as poorer functional outcomes. The findings strengthen evidence that cannabis acts as a risk factor for psychosis, though the direction of causality remains debated.

Neurochemical models of psychosis risk and onset

January 1, 2020 D. Oliver, G. Modinos, P. McGuire

No licensed pharmacological treatments exist to prevent the onset of psychosis in people at clinical high risk. This chapter reviews four preclinical models that inform the development of such treatments: neonatal hippocampal lesion, prenatal immune activation, and administration of PCP or methylazoxymethanol acetate (MAM). The neonatal hippocampal model lacks construct validity, evidence linking prenatal immune activation to psychosis is limited, and the chronic PCP model lacks a neurodevelopmental component. The MAM model best reproduces neural and behavioral changes resembling human psychosis onset. Together, these models have advanced understanding of mechanisms underlying psychotic disorders and provide a rationale for novel preventative interventions.