Relationship between functional connectivity and weight-gain risk of antipsychotics in schizophrenia.

Schizophr Res

Department of Psychiatry, University of Colorado School of Medicine, Anschutz Medical Campus, Anschutz Health Sciences Building, 1890 N Revere Ct, Aurora, CO 80045, USA; Research Service, Rocky Mountain Regional VA Medical Center, 1700 N Wheeling St, Aurora, CO 80045, USA. Electronic address:

Published: May 2024

AI Article Synopsis

  • The study explores the link between antipsychotic medications and obesity in individuals with schizophrenia by examining how these medications affect brain connectivity.
  • When participants were in a fasted state, higher weight-gain risk from antipsychotics correlated with increased connectivity between brain areas involved in sensory processing and body movement.
  • In a fed state, higher weight-gain risk was associated with stronger connectivity among regions related to reward and visual processing, suggesting that these effects may contribute to eating behaviors and anticipation of food consumption.

Article Abstract

Background: The mechanisms by which antipsychotic medications (APs) contribute to obesity in schizophrenia are not well understood. Because AP effects on functional brain connectivity may contribute to weight effects, the current study investigated how AP-associated weight-gain risk relates to functional connectivity in schizophrenia.

Methods: Fifty-five individuals with schizophrenia (final N = 54) were divided into groups based on previously reported AP weight-gain risk (no APs/low risk [N = 19]; moderate risk [N = 17]; high risk [N = 18]). Resting-state functional magnetic resonance imaging (fMRI) was completed after an overnight fast ("fasted") and post-meal ("fed"). Correlations between AP weight-gain risk and functional connectivity were assessed at the whole-brain level and in reward- and eating-related brain regions (anterior insula, caudate, nucleus accumbens).

Results: When fasted, greater AP weight-gain risk was associated with increased connectivity between thalamus and sensorimotor cortex (pFDR = 0.021). When fed, greater AP weight-gain risk was associated with increased connectivity between left caudate and left precentral/postcentral gyri (pFDR = 0.048) and between right caudate and multiple regions, including the left precentral/postcentral gyri (pFDR = 0.001), intracalcarine/precuneal/cuneal cortices (pFDR < 0.001), and fusiform gyrus (pFDR = 0.008). When fed, greater AP weight-gain risk was also associated with decreased connectivity between right anterior insula and ventromedial prefrontal cortex (pFDR = 0.002).

Conclusions: APs with higher weight-gain risk were associated with greater connectivity between reward-related regions and sensorimotor regions when fasted, perhaps relating to motor anticipation for consumption. Higher weight-gain risk APs were also associated with increased connectivity between reward, salience, and visual regions when fed, potentially reflecting greater desire for consumption following satiety.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332974PMC
http://dx.doi.org/10.1016/j.schres.2024.03.033DOI Listing

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