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Melli, G.

Publications and source records attributed to Melli, G..

3 recordsLinked to original sources

Plasmatic immune extracellular vesicle profiles identify prodromal and early stages of Parkinson's disease

Extracellular vesicles (EVs) hold promise as minimally invasive biomarkers for neurodegenerative proteinopathies, but disease- and stage-specific profiles remain unclear. For this study, we enrolled 378 participants across five centers and the MJFF-BioFIND cohort: 100 healthy controls [HC], 64 isolated REM sleep behavior disorder [iRBD], 41 DeNovo Parkinsons Disease [PD], 89 Late PD, 32 other Synucleinopathies, and 52 Tauopathies. All participants underwent clinical evaluation and blood collection. The 77 subjects from the BioFIND cohort also provided CSF samples. EV concentration and size were assessed by nanoparticle tracking analysis; flow cytometry quantified tetraspanins (CD9/CD63/CD81) and 37 surface markers. Multivariable logistic regression, receiver operating characteristic analyses (ROC), and repeated random forest (rRF) classifiers evaluated diagnostic utility. Late PD showed the highest EV concentrations compared to HC and other disease groups. Participants exhibited distinct EV surface immunophenotypes, with the iRBD group displaying the most extensive immune activation signature vs HC, followed by PD patients. Multivariate logistic regression analysis identified diagnostic marker panels: CD3/CD9/CD25/CD56 for iRBD, SSEA4 for Late PD, CD146/CD209 for Synucleinopathies, and CD8/CD45/CD62P for Tauopathies. ROC confirmed good discriminatory performance, with CD56 emerging as the strongest single predictor for iRBD vs HC, SSEA4 showing high sensitivity for Late PD, and marker combinations providing optimal balance for Synucleinopathy/Tauopathy classification vs HC. In the CSF BioFIND subset, Late PD EVs exhibited increased myeloid (CD1c), adhesion (CD29), activation (CD69), and epithelial (CD326) markers compared to HC. Among these, CD326 was independently associated with Late PD diagnosis. Machine learning classifiers using all 37 surface antigens achieved excellent training performance (91.7-94.3% accuracy for iRBD/Synucleinopathies vs HC) and maintained robust validation accuracy, particularly for iRBD (77.8%) and DeNovo PD (76.6%) vs HC. EV immuno-phenotyping reveals distinct signatures across the neurodegenerative proteinopathies spectrum, with the highest diagnostic utility for prodromal iRBD detection. Longitudinal validation and cell-of-origin refinement represent key next steps toward clinical translation.

neuroscience↗

Circulating extracellular vesicles drive microglial senescence and neurodegeneration in Parkinson`s disease

BackgroundExtracellular vesicles (EV), secreted membrane particles involved in cell-to-cell communication, carry important information on immunity and its dysregulation. Recent studies have demonstrated the crucial role of peripheral and central inflammation in causing Parkinsons disease (PD), as well as the involvement of EV in mediating neuron-glial interactions during neurodegeneration. However, the underlying mechanism of plasmatic EV in PD pathogenesis remains unknown. MethodsEV were isolated from pool of plasma of PD patients and age- and sex-matched healthy controls (HC) using size-exclusion chromatography and characterized by nanoparticle tracking analysis, western blot, and transmission electron microscopy. SH-SY5Y neurons and HMC3 microglia cells were treated with EV, and their impact was evaluated using flow cytometry and immunofluorescence. Conditioned medium (CM) from EV-treated HMC3 cells was applied to SH-SY5Y neurons to determine indirect neurotoxic effects. Cytokine profiling and senescence-like features of EV-treated HMC3 cells were assessed. Unbiased proteomic analysis of PD-EV and HC-EV were further performed. ResultsPD-EV induced axonal degeneration and cell death in SH-SY5Y neurons and increased levels of TNF-, IL-1{beta}, IFN-{gamma}, IL-8, and CCL11, accompanied by the expression of p16INK4a in HMC3 cells, suggesting a proinflammatory, senescence-associated secretory phenotype (SASP). Enrichment pathway analysis revealed that these changes were mainly related to inflammatory and immune responses. Moreover, CM from PD-EV-HMC3 cells increased apoptotic cell death in SH-SY5Y neurons more than direct PD-EV. Notably, proteomic analysis of PD-EV showed higher expression of proteins involved in complement cascades, immune response, phagocytosis, and post translational protein translation, further supporting the potential of EV to induce inflammatory changes in PD. ConclusionsThis study demonstrates that plasmatic PD-EV contributes to neuronal degeneration by reducing neuronal integrity and indirectly by activating microglia through the secretion of pro-inflammatory, senescence-associated mediators. Circulating EV exerts a role in bridging peripheral inflammation with microglia, modulating neuroinflammatory events.

neuroscience↗

Structure of ATTRv-F64S fibrils isolated from skin tissue of a living patient

Amyloid transthyretin-derived (ATTR) amyloidosis is a degenerative, systemic disease characterized by transthyretin fibril deposition in organs like the heart, kidneys, liver, and skin. We report the first cryo-EM structure of transthyretin fibrils isolated from skin tissue of a living patient carrying a rare genetic mutation (ATTRv F64S). The structure adopts a highly conserved fold previously observed in other ATTR fibrils from different tissues or genetic variants. Mass spectrometry was used to evaluate fibril content and identify post-translational modifications. The structural consistency between ATTR filaments validates non-invasive skin biopsy as a diagnostic tool.

biochemistry↗