ArticleEuropean journal of nuclear medicine and molecular imaging2026
Loss of serotonergic function in carriers of PRKN mutations: a [
Article in European journal of nuclear medicine and molecular imaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeWe investigated serotonergic and dopaminergic terminal integrity role in PRKN-associated Parkinsonism (PRKN-PD) using [¹¹C]DASB Positron Emission Tomography (PET) and [¹²³I]FP-CIT Single Photon Emission Computerised Tomography (SPECT).
methodsFourteen PRKN-PD patients (mean age 49.70 ± 10.83, disease duration 10.95 ± 7.59 years, H&Y 2.0 ± 0.68), and twelve iPD patients (mean age 65.40 ± 7.48 years, disease duration 5.05 ± 4.50 years, H&Y 2.0 ± 0.93) underwent clinical assessments, 3-Tesla MRI, [11C]DASB PET-CT, and [123I]FP-CIT SPECT, and compared with previously acquired healthy control (HCs) data. [11C]DASB distribution volume ratio (DVR) parametric images were generated and DVR-1 values, equivalent to BPND, sampled from a priori selected regions-of-interest (ROIs) with the posterior cerebellum as reference. [123I]FP-CIT images underwent reconstruction and normalization to standard space, and striatal Specific Binding Ratio (SBR) calculated from the eight hottest consecutive slices.
resultsPRKN-PD patients showed 20.8% to 45.2% [11C]DASB BPND loss across several cortical and subcortical ROIs compared to HCs (p ≤ 0.01). After adjusting for age and disease duration, no differences in [11C]DASB BPND were observed between PRKN-PD and iPD. In PRKN-PD, higher [11C]DASB BPND in the raphe, brainstem, ventral striatum, and amygdala, correlated with higher scores on the Non-Motor Symptoms Scale (p < 0.05). Higher [11C]DASB BPND in the caudate and putamen correlated with higher scores on the Beck Depression Inventory II scale (p < 0.05). No correlation was detected between [11C]DASB BPND and [123I]FP-CIT SBR in the caudate and putamen.
conclusionsPRKN-PD is characterized by widespread serotonergic dysfunction, which is independent of dopaminergic degeneration and linked to key non-motor symptoms, particularly depression. These findings provide novel insights into the pathophysiology of PRKN-PD.
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