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Serpa, M.

Publications and source records attributed to Serpa, M..

3 recordsLinked to original sources

Longitudinal White Matter Microstructure and Transition to Psychosis in Individuals at Clinical High Risk

Altered white matter microstructure, commonly indexed by fractional anisotropy (FA), has been reported in individuals at clinical high-risk of psychosis (CHR-P) across multiple white matter tracts. However, the relationship between these alterations and later transition to psychosis remains unclear. To address this gap, we investigated whether baseline and longitudinally updated FA measurements were associated with risk of transition to psychosis in a large cohort of individuals at CHR-P. We analysed diffusion tensor imaging data from N = 205 participants at CHR-P, 23 of whom developed psychosis within 3 years of follow-up. Data were collected at baseline, 6 months, and 12 months. Associations between global and tract-specific FA and transition risk were examined using Cox proportional hazards models of baseline data and longitudinally updated data. Point estimates were directionally consistent, with hazard ratios <1 for FA across all white matter tracts in both baseline and longitudinal models. Associations reached nominal significance in the hippocampal cingulum, anterior thalamic radiation, and forceps minor, but none of these remained significant after correcting for multiple comparisons (pcorr > .05). The directionally consistent estimates are compatible with small, distributed effects across multiple white matter pathways being associated with transition to psychosis, although this requires replication. Longitudinally updated FA measurements did not yield stronger associations than were available from baseline imaging data alone. Studies at an even larger scale are needed to establish whether these associations are robust and clinically meaningful.

neuroscience↗

Longitudinal White Matter Trajectories in Clinical High Risk and First-Episode Psychosis: Findings from the Multi-Centre PSYSCAN Study

Psychosis has been linked to changes in diffusion-derived fractional anisotropy (FA) across multiple white matter tracts, yet most evidence is cross-sectional. Longitudinal findings are inconsistent, and the clinical relevance of white matter changes over time remains unclear. To address this gap, we investigated longitudinal white matter changes and their clinical correlates in early psychosis in a large, multi-centre diffusion-tensor imaging study. Across 18 sites, 407 participants (healthy controls: n = 97, 59.8% men, mean age 23.9{+/-}4.6 years; clinical high risk of psychosis: n = 158, 53.5% men, mean age 23.0{+/-}4.9 years; first-episode psychosis: n = 152, 71.1% men, mean age 25.1{+/-}5.4 years) were scanned at up to three time points over 12 months. FA was assessed in the cingulum bundle, the superior longitudinal fasciculus, the inferior fronto-occipital fasciculus, and at the whole brain level. FA trajectories were analysed using linear mixed-effects models to test effects of group, social and occupational functioning, and (attenuated) psychotic symptoms, while controlling for demographic and socioeconomic covariates. No significant group differences in FA were observed, either globally or within tracts (p > .05). Longitudinal FA trajectories were not associated with changes in (attenuated) psychotic symptoms or functioning (p > .05). In contrast, higher baseline antipsychotic medication dose was significantly associated with lower FA (pcorr < .05). Overall, these findings indicate that white matter microstructure is relatively stable during the clinical-high-risk and first-episode phases of psychosis, and that it is not clearly associated with variation in symptom severity or functional outcomes over time.

neuroscience↗

Protective effect of P2Y receptors antagonism on stress-induced retinal degeneration

The death of retinal pigment epithelial (RPE) cells and photoreceptors (PR) is a hallmark of the progression of several degenerative ocular disorders. The precise molecular driver(s) behind RPE and PR cell death, however, remains unknown. Recent studies have suggested the involvement of ATP and purinergic signaling in the progression of age-related macular degeneration (AMD) and retinal degeneration. We have discovered that RPE cells release ATP when subjected to stress, which in turn exacerbates stress-related signaling via purinergic receptors that ultimately results in degeneration. Our findings demonstrate that blocking P2Y purinergic receptors using suramin can effectively prevent toxin-induced RPE cell death and dysfunction in vitro. Furthermore, we show efficacy of suramin in preventing photoreceptor degeneration in vivo using the RHO-P23H zebrafish model. This study reinforces the involvement of ATP and purinergic signaling in maintaining retinal health, and highlights the potential of purinergic receptor antagonism as a therapeutic strategy for retinal degeneration.

cell biology↗