Altered Dopamine-Linked Striatal Hemodynamic Latency in Early Psychosis
- 1Temple University
Abstract
Key Points Question: Is striatal hemodynamic latency, a novel indirect correlate of dopamine physiology, altered in individuals with early psychosis? Findings: In this cross-sectional study of 105 individuals with early psychosis and 55 healthy comparison participants, early psychosis was associated with significantly lower striatal hemodynamic latency. Differences were observed in the dorsal striatum (caudate and putamen), whereas ventral striatal (nucleus accumbens) latency did not significantly differ between groups. Meaning: These findings support further evaluation of striatal hemodynamic latency as a noninvasive, indirect marker of dopamine-linked physiology in early psychosis. Abstract Importance: Psychosis is strongly associated with striatal dopamine dysfunction, but noninvasive measures that capture variation in dopamine remain limited. Hemodynamic latency, which quantifies the timing of low-frequency blood oxygen level-dependent (BOLD) fluctuations, may provide a way to indirectly probe dopamine dysfunction in psychosis. Objective: To determine whether striatal hemodynamic latency differs between individuals with early psychosis (EP) and healthy control (HC) participants and whether latency is associated with positive or negative symptom severity. Design: Cross-sectional analysis of resting-state functional magnetic resonance imaging (fMRI) data from the Human Connectome Project (HCP)-EP dataset. Setting: Multisite study at 4 sites using 3T Siemens Prisma MRI scanners. Participants: 105 individuals with EP and 55 HC participants with usable resting-state fMRI and hemodynamic latency data. Exposure: EP status. Main Outcomes and Measures: Voxel-wise hemodynamic latency was estimated using RapidTide and summarized within 6 striatal regions: nucleus accumbens core and shell, anterior and posterior caudate and putamen. Group differences were evaluated using linear mixed-effects models accounting for region and subject-level random effects and controlling for age, sex, and mean framewise displacement. Positive symptoms were measured using the Positive and Negative Syndrome Scale positive subscale; negative symptoms using the Clinical Assessment Interview for Negative Symptoms. Associations with symptoms were assessed using nested linear regressions within the EP group. Results: Latency was significantly lower in the dorsal than ventral striatum in HC and EP, with a greater difference in EP (b=-119.46 ms, SE=52.16, p=.022). Follow-up six-subregion models found significant main effects of group F(1,156.55)=7.79, p=.006, and region F(5,2760)=187.99; p< .001, but no group-by-region interaction F(5,2760)=1.74; p=.121. Region-specific contrasts showed lower latency in EP in the anterior caudate (p=.014), posterior caudate (p<.001), anterior putamen (p=.007), and posterior putamen (p=.029), but not NAc core or shell. Striatal latency was not significantly associated with positive or negative symptom severity among participants with EP. Conclusions and Relevance: EP was associated with broadly reduced striatal hemodynamic latency, with the strongest differences in the caudate and putamen. Altered striatal latency in psychosis warrants further evaluation as a noninvasive indirect marker of striatal pathophysiology linked to dopamine.
Related
- Nicotinic control of dopamine release shapes striatal output and engages adaptive action selection.
- TPH2 knockout impairs skilled motor performance and alters striatal dopamine metabolism in female rats
- Lateral hypothalamic control of the striatal dopamine landscape during consummatory behavior
- Increased slow oscillatory activity in substantia nigra pars reticulata triggers abnormal involuntary movements in the 6-OHDA-lesioned rat in the presence of excessive extracelullar striatal dopamine
- Dopamine release-associated striatal blood oxygenation and whole-brain dynamics during associative learning
BibTeX
@misc{mopuru2026altered,
title = {{Altered Dopamine-Linked Striatal Hemodynamic Latency in Early Psychosis}},
author = {R. Mopuru and B. L. Elliott and L. J. Hoffman and L. M. Ellman and I. R. Olson and I. Ballard},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.23.753620},
url = {https://www.biorxiv.org/content/10.64898/2026.09.23.753620v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Altered Dopamine-Linked Striatal Hemodynamic Latency in Early Psychosis
AU - R. Mopuru
AU - B. L. Elliott
AU - L. J. Hoffman
AU - L. M. Ellman
AU - I. R. Olson
AU - I. Ballard
PY - 2026
DA - 2026/09/23
PB - bioRxiv
DO - 10.64898/2026.09.23.753620
UR - https://www.biorxiv.org/content/10.64898/2026.09.23.753620v1
AB - Key Points Question: Is striatal hemodynamic latency, a novel indirect correlate of dopamine physiology, altered in individuals with early psychosis? Findings: In this cross-sectional study of 105 individuals with early psychosis and 55 healthy comparison participants, early psychosis was associated with significantly lower striatal hemodynamic latency. Differences were observed in the dorsal striatum (caudate and putamen), whereas ventral striatal (nucleus accumbens) latency did not significantly differ between groups. Meaning: These findings support further evaluation of striatal hemodynamic latency as a noninvasive, indirect marker of dopamine-linked physiology in early psychosis. Abstract Importance: Psychosis is strongly associated with striatal dopamine dysfunction, but noninvasive measures that capture variation in dopamine remain limited. Hemodynamic latency, which quantifies the timing of low-frequency blood oxygen level-dependent (BOLD) fluctuations, may provide a way to indirectly probe dopamine dysfunction in psychosis. Objective: To determine whether striatal hemodynamic latency differs between individuals with early psychosis (EP) and healthy control (HC) participants and whether latency is associated with positive or negative symptom severity. Design: Cross-sectional analysis of resting-state functional magnetic resonance imaging (fMRI) data from the Human Connectome Project (HCP)-EP dataset. Setting: Multisite study at 4 sites using 3T Siemens Prisma MRI scanners. Participants: 105 individuals with EP and 55 HC participants with usable resting-state fMRI and hemodynamic latency data. Exposure: EP status. Main Outcomes and Measures: Voxel-wise hemodynamic latency was estimated using RapidTide and summarized within 6 striatal regions: nucleus accumbens core and shell, anterior and posterior caudate and putamen. Group differences were evaluated using linear mixed-effects models accounting for region and subject-level random effects and controlling for age, sex, and mean framewise displacement. Positive symptoms were measured using the Positive and Negative Syndrome Scale positive subscale; negative symptoms using the Clinical Assessment Interview for Negative Symptoms. Associations with symptoms were assessed using nested linear regressions within the EP group. Results: Latency was significantly lower in the dorsal than ventral striatum in HC and EP, with a greater difference in EP (b=-119.46 ms, SE=52.16, p=.022). Follow-up six-subregion models found significant main effects of group F(1,156.55)=7.79, p=.006, and region F(5,2760)=187.99; p< .001, but no group-by-region interaction F(5,2760)=1.74; p=.121. Region-specific contrasts showed lower latency in EP in the anterior caudate (p=.014), posterior caudate (p<.001), anterior putamen (p=.007), and posterior putamen (p=.029), but not NAc core or shell. Striatal latency was not significantly associated with positive or negative symptom severity among participants with EP. Conclusions and Relevance: EP was associated with broadly reduced striatal hemodynamic latency, with the strongest differences in the caudate and putamen. Altered striatal latency in psychosis warrants further evaluation as a noninvasive indirect marker of striatal pathophysiology linked to dopamine.
ER -