The role of blood-based biomarkers in Parkinsonian disorders, Alzheimer's disease and frontotemporal dementia Marta Campagnolo, Eleonora Fiorenzato, Giulia Musso, Valentina Misenti, Simone Cauzzo, Annachiara Cagnin, Roberta Biundo, Cinzia Bussè, Carmelo Alessandro Fogliano, Stefano Mozzetta, Alessandra Codemo, Elisabetta Gasparoli, Stefania Moz, Marco Narici, Paola Pizzo, Maurizio Corbetta, Martina Montagnana, Angelo Antonini Journal of the Neurological Sciences, 2025 The complexity of neurodegenerative disorders necessitates an integrative approach that incorporates morphological, functional, and molecular biomarkers. The advent of highly sensitive single-molecule array (Simoa®) assays has significantly enhanced the accuracy of blood-based biomarker quantification, including glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and phosphorylated tau181 (p-tau181). This study evaluates the diagnostic utility of these biomarkers in neurodegenerative diseases. We analyzed data from 279 individuals from the PADUA-CESNE cohort: 120 with Parkinson's disease (PD), 88 with Alzheimer's disease (AD), 16 with frontotemporal dementia (FTD), 11 with multiple system atrophy (MSA), 14 with progressive supranuclear palsy (PSP), and 30 cognitively unimpaired controls. NfL levels were significantly lower in PD and AD compared to atypical parkinsonisms and FTD, effectively distinguishing MSA and PSP from controls. NfL also negatively correlated with Montreal Cognitive Assessment (MoCA) scores in AD and PD, indicating its association with cognitive decline. Elevated GFAP levels were observed in both PD and AD and inversely correlated with global cognition. Combining GFAP and p-tau181 improved AD differentiation from PD and other parkinsonian disorders, while the integration of all three biomarkers facilitated the distinction between AD and FTD. Notably, lower NfL levels (<20 ng/L) in conjunction with elevated p-tau181 were indicative of AD, whereas NfL levels below 40 ng/L were suggestive of PD. In conclusion, NfL serves as a sensitive indicator of neurodegeneration, albeit with limited specificity. However, by establishing biomarker concentration thresholds and integrating complementary biomarkers, blood-based assays may enhance the differential diagnosis of neurodegenerative diseases, providing valuable clinical insights.
Progranulin Mutation Manifesting as Parkinson Disease: A Case Series from the PADUA-CESNE Cohort Giulia Bonato, Marta Campagnolo, Aron Emmi, Valentina Misenti, Tommaso Carrer, Carmelo Fogliano, Leonardo Salviati, Miryam Carecchio, Angelo Antonini Movement Disorders Clinical Practice, 2025 BackgroundMutations in progranulin (GRN) are associated with frontotemporal dementia, although a Parkinson disease (PD) phenotype is uncommon, especially in young patients.CasesWe report three subjects from the PADUA‐CESNE cohort, meeting diagnostic criteria for PD, with onset under age 55. All had good response to dopaminergic therapy, abnormal dopamine transporter single‐photon emission computed tomography striatal uptake and a disease course consistent with PD, without clear atypical features, behavioral, or cognitive deficits. Genetic testing (next‐generation sequencing [NGS] panel) revealed three different variants in GRN gene. Skin biopsy immunohistochemistry analysis showed phosphorylated α‐synuclein deposition in two and was negative in one subject.ConclusionsOur findings expand the phenotypic spectrum of GRN mutations, showing that patients can present with clinical manifestations of PD, including phosphorylated synuclein pathology in the skin, with a relatively young age of onset. Our observations support the use of broad‐spectrum NGS panels to properly guide patients in counseling and accurately allocate them to disease‐modifying therapies.
Optical coherence tomography reveals retinal structural abnormalities in α-synucleinopathies: insights from the Padua-CESNE cohort M. Campagnolo, M. Puthenparampil, A. Emmi, L. Weis, E. Basili, V. Mauceri, A. Miscioscia, M. Carecchio, A. Guerra, V. Misenti, C. Fogliano, P. Gallo, A. Antonini Journal of Neural Transmission, 2025 The complexity of α-synucleinopathies, namely Parkinson’s disease (PD) and multiple system atrophy (MSA), calls for the adoption a multimodal approach integrating biological, morphological, and functional data. Phosphorylated α-synuclein (α-syn) detection in bodily fluids and tissues such as the skin helps provide biological characterization of the disease, but specific and accessible biomarkers are not available yet. The aim of this study was to define the role of Optical Coherence Tomography (OCT, a minimally invasive retinal imaging technique) patterns as possible biomarkers in the early stages of α-synucleinopathies, also supporting the differential diagnosis. Thirty-five (23 PD, 12 MSA), clinically, biologically and genetically characterized patients included in the PADUA-CESNE (Centro Studi per la Neurodegenerazione) cohort underwent OCT. A significant atrophy in the inferior, superior and temporal regions of the Retinal Nerve Fiber Layer (RNFL) and in the inner nuclear layer (INL) were observed in PD compared to controls, differently from MSA. Hyperreflective foci (HRF) counts were elevated across all retinal layers in all patients with PD exhibiting significantly higher numbers, suggesting microglial activation and greater retinal damage. Further research regarding OCT patterns in PD and MSA may consolidate the role of specific features, such as INL abnormalities and different HRF counts, in supporting the diagnosis and differential diagnosis in α-synucleinopathies. In light of the availability of potentially disease-modifying therapies, studies should focus on newly diagnosed patients, also undergoing thorough clinical, biological and genetic characterization.
Alpha-synuclein RT-QuIC assay in gastroduodenal and skin biopsies of Parkinson disease patients Aron Emmi, Angela Mammana, Michele Sandre, Simone Baiardi, Luca Weis, Marcello Rossi, Franco Magliocchetti, Edoardo Savarino, Francesco Paolo Russo, Andrea Porzionato, Miryam Carecchio, Marta Campagnolo, Angelo Antonini, Piero Parchi Annals of Clinical and Translational Neurology, 2025 In this study, we compared the value of pathological alpha‐synuclein (αSyn) seed amplification assay (SAA) in gastric and duodenal biopsies with skin biopsies in Parkinson disease (PD) patients with different disease duration. The accuracy of αSyn SAA was 87.7% in skin, 67.4% in duodenum, and 80.0% in gastric biopsies, with significantly higher sensitivity in advanced PD (skin: 81.8%; gastric: 88.9%; duodenal 58.8%). Misfolded αSyn was detected with higher sensitivity in advanced PD across all matrices, likely reflecting the progression of αSyn pathology. The seeding activity was lower in the duodenal than in the gastric wall, indicating differences in αSyn burden.
Genetic mutations in Parkinson’s disease: screening of a selected population from North-Eastern Italy Giulia Bonato, Angelo Antonini, Francesca Pistonesi, Marta Campagnolo, Andrea Guerra, Roberta Biundo, Manuela Pilleri, Cinzia Bertolin, Leonardo Salviati, Miryam Carecchio Neurological Sciences, 2025 Background Parkinson’s disease (PD) is a progressive neurodegenerative disorder with a multifactorial pathogenesis. Several genetic variants increase the risk of PD and about 5–10% of cases are monogenic. This study aims to define the genetic bases and clinical features of PD in a cohort of patients from Northeastern Italy, a peculiar geographical area previously not included in genetic screenings. Methods Using an NGS multigenic panel, 218 PD patients were tested based on age at onset, family history and development of atypical features. Results A total of 133 genetic variants were found in 103 patients. Monogenic PD was diagnosed in 43 patients (20% of the cohort); 28 (12.8%) carried mutations in GBA1, 10 in LRRK2 (4.6%) and 5 in PRKN (2.3%). In 17% of patients the genetic defect remained of uncertain interpretation. The selection criterion “age of onset < 55 years” was a significant predictor of a positive genetic test (OR 3.8, p 0.0037). GBA1 patients showed more severe symptoms and a higher burden of motor and non-motor complications compared to negative patients (dyskinesias OR 3, sleep disturbances OR 2.8, cognitive deficits OR 3.6; p < 0.05), with greater autonomic dysfunction (COMPASS-31 score 34.1 vs 20.2, p 0.03). Conclusions Applying simple clinical criteria for genetic testing allows to increase the probability to identify patients with monogenic PD and better allocate resources. This process is critical to widen the understanding of disease mechanisms and to increase the individuation of patients potentially benefitting from future disease-modifying therapies.
Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217 Giulia Musso, Eleonora Fiorenzato, Valentina Misenti, Simone Cauzzo, Roberta Biundo, Carmelo A. Fogliano, Giulia Bonato, Wassilios G. Meissner, Marta Campagnolo, Miryam Carecchio, Francesca Vianello, Andrea Guerra, Chiara Cosma, Annachiara Cagnin, Diego Cecchin, Martina Montagnana, Angelo Antonini Frontiers in Neurology, 2025 IntroductionPlasma phospho-tau 217 (pTau217) is a biomarker for Alzheimer’s disease (AD) pathology, reflecting amyloid (Aβ) and tau burden, but its role in Parkinson disease (PD) and 4-repeat(4R)-tauopathies remains incompletely understood. We measured plasma pTau217 across the cognitive spectrum of Lewy body diseases (PD, Dementia with Lewy bodies [DLB]) and in 4R-tauopathies, comparing these groups to cognitively unimpaired (CU) and mild cognitive impairment (MCI) individuals.MethodsParticipants included 18 cognitively normal PD (PD-NC), 32 PD with MCI, and 7 PD with dementia (PDD), alongside 4 DLB patients, grouped as PDD/DLB. The 4R-tauopathy group included 28 Progressive Supranuclear Palsy (PSP) and 4 corticobasal syndrome (CBS) patients, compared to 51 CU and 26 MCI individuals. Ptau217 was measured using the fully automated Lumipulse platform, with values adjusted for creatinine levels. Further, the presence of AD-pathology was defined using a validated cut-off based on Aβ-PET.ResultsPTau217 levels were significantly lower in PD-NC and CU individuals compared to those with greater cognitive impairment (PD-MCI, PDD/DLB, and PSP/CBS), and MCI individuals. AD co-pathology was identified in 28% of PDD/DLB and PSP/CBS patients, 16% of PD-MCI, and none of PD-NC. MCI showed the highest pTau217 positivity (35%), while 8% of CU individuals were positive despite normal cognition. In PD, pTau217 negatively correlated with cognitive performance, as assessed by Montreal Cognitive Assessment (MoCA: rs = −0.38, p = 0.004) and Mini-Mental State Examination (MMSE: rs = −0.37, p = 0.006).DiscussionPlasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. AD co-pathology independently contributes to cognitive deficits in PD, but not in PSP/CBS.
Repurposing chemotherapy-induced peripheral neuropathy grading Roser Velasco, Andreas A. Argyriou, David R. Cornblath, Pere Bruna, Paola Alberti, Emanuela Rossi, Ingemar S. J. Merkies, Dimitri Psimaras, Chiara Briani, Roy I. Lalisang, Angelo Schenone, Guido Cavaletti, Jordi Bruna, and European Journal of Neurology, 2024 Background and PurposeChemotherapy‐induced peripheral neuropathy (CIPN) is perceived differently by patients and physicians, complicating its assessment. Current recommendations advocate combining clinical and patient‐reported outcomes measures, but this approach can be challenging in patient care. This multicenter European study aims to bridge the gap between patients' perceptions and neurological impairments by aligning both perspectives to improve treatment decision‐making.MethodsData were pooled from two prospective studies of subjects (n = 372) with established CIPN. Patient and physician views regarding CIPN were assessed using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI‐CTCAE), Total Neuropathy Scale–clinical version (TNSc) items, and the disease‐specific quality of life ‐ Chemotherapy‐Induced Peripheral Neuropathy questionnaire (QLQ‐CIPN20) from the European Organization for Research and Treatment of Cancer (EORTC). To identify inherent neurotoxic severity patterns, we employed hierarchical cluster analysis optimized with k‐means clustering and internally validated by discriminant functional analysis.ResultsBoth NCI‐CTCAE and TNSc demonstrated a significant difference in the distribution of severity grades in relation to QLQ‐CIPN20 scores. However, a proportion of subjects with different neurotoxic severity grades exhibited overlapping QLQ‐CIPN20 scores. We identified three distinct clusters classifying subjects as having severely impaired, intermediately impaired, and mildly impaired CIPN based on TNSc and QLQ‐CIPN20 scores. No differences in demographics, cancer type distribution, or class of drug received were observed.ConclusionsOur results confirm the heterogeneity in CIPN perception between patients and physicians and identify three well‐differentiated subgroups of patients delineated by degree of CIPN impairment based on scores derived from TNSc and QLQ‐CIPN20. A more refined assessment of CIPN could potentially be achieved using the calculator tool derived from the cluster equations in this study. This tool, which facilitates individual patient classification, requires prospective validation.
Immune landscape of the enteric nervous system differentiates Parkinson's disease patients from controls: The PADUA-CESNE cohort Marta Campagnolo, Luca Weis, Michele Sandre, Aleksandar Tushevski, Francesco Paolo Russo, Edoardo Savarino, Miryam Carecchio, Elena Stocco, Veronica Macchi, Raffaele De Caro, Piero Parchi, Luigi Bubacco, Andrea Porzionato, Angelo Antonini, Aron Emmi Neurobiology of Disease, 2024 BACKGROUND: Gastrointestinal dysfunction has emerged as a prominent early feature of Parkinson's Disease, shedding new light on the pivotal role of the enteric nervous system in its pathophysiology. However, the role of immune-cell clusters and inflammatory and glial markers in the gut pathogenetic process needs further elucidation. OBJECTIVES: We aimed to study duodenum tissue samples to characterize PD's enteric nervous system pathology further. Twenty patients with advanced PD, six with early PD, and 18 matched controls were included in the PADUA-CESNE cohort. METHODS: Duodenal biopsies from 26 patients with early to advanced stage PD and 18 age-matched HCs were evaluated for the presence of surface markers (CD3+, CD4+, CD8+, CD20+, CD68+, HLA-DR), presence of misfolded alpha-synuclein and enteric glial alteration (GFAP). Correlation of immulogic pattern and clinical characteristic were analyzed. RESULTS: The findings validate that in patients with Parkinson's Disease, the activation and reactive gliosis are linked to the neurodegeneration triggered by the presence of misfolded alpha-synuclein in the enteric nervous system. This process intensifies from the initial to the advanced stages of the disease. The clusters of T- and B-lymphocytes in the enteric system, along with the overall expression of HLA-DR in antigen-presenting cells, exceeded those in the control group. Conversely, no differences in terms of macrophage populations were found. CONCLUSIONS: These findings broaden our understanding of the mechanisms underlying the enteric nervous system's involvement in PD and point to the gastrointestinal system as a potential therapeutic target, especially in the early stages of the disease. Moreover, our results propose a role of T- and B-lymphocytes in maintaining inflammation and ultimately influencing alpha-synuclein misfolding and aggregation.
Inhibition of Protease-Activated Receptor-2 Activation in Parkinson’s Disease Using 1-Piperidin Propionic Acid Santina Quarta, Michele Sandre, Mariagrazia Ruvoletto, Marta Campagnolo, Aron Emmi, Alessandra Biasiolo, Patrizia Pontisso, Angelo Antonini Biomedicines, 2024 In Parkinson’s disease, neuroinflammation is a double-edged sword; when inflammation occurs it can have harmful effects, despite its important role in battling infections and healing tissue. Once triggered by microglia, astrocytes acquire a reactive state and shift from supporting the survival of neurons to causing their destruction. Activated microglia and Proteinase-activated receptor-2 (PAR2) are key points in the regulation of neuroinflammation. 1-Piperidin Propionic Acid (1-PPA) has been recently described as a novel inhibitor of PAR2. The aim of our study was to evaluate the effect of 1-PPA in neuroinflammation and microglial activation in Parkinson’s disease. Protein aggregates and PAR2 expression were analyzed using Thioflavin S assay and immunofluorescence in cultured human fibroblasts from Parkinson’s patients, treated or untreated with 1-PPA. A significant decrease in amyloid aggregates was observed after 1-PPA treatment in all patients. A parallel decrease in PAR2 expression, which was higher in sporadic Parkinson’s patients, was also observed both at the transcriptional and protein level. In addition, in mouse LPS-activated microglia, the inflammatory profile was significantly downregulated after 1-PPA treatment, with a remarkable decrease in IL-1β, IL-6, and TNF-α, together with a decreased expression of PAR2. In conclusion, 1-PPA determines the reduction in neuroglia inflammation and amyloid aggregates formation, suggesting that the pharmacological inhibition of PAR2 could be proposed as a novel strategy to control neuroinflammation.
Assessment of diagnostic criteria for multifocal motor neuropathy in patients included in the Italian database Pietro Emiliano Doneddu, Luca Gentile, Dario Cocito, Raffaella Fazio, Marco Luigetti, Chiara Briani, Massimiliano Filosto, Gabriele Siciliano, Luana Benedetti, Giovanni Antonini, Sabrina Matà, Girolama Alessandra Marfia, Maurizio Inghilleri, Fiore Manganelli, Giuseppe Cosentino, Filippo Brighina, Marinella Carpo, Francesca Carta, Anna Mazzeo, Erdita Peci, Camilla Strano, Angela Romano, Marta Campagnolo, Stefano Cotti‐Piccinelli, Divina Valeria Viola, Francesco Germano, Luca Leonardi, Martina Sperti, Giorgia Mataluni, Marco Ceccanti, Emanuele Spina, Elisa Vegezzi, Vincenzo Di Stefano, Eduardo Nobile‐Orazio European Journal of Neurology, 2024 Background and purposeThis study aimed to assess the diagnostic criteria, ancillary investigations and treatment response using real‐life data in multifocal motor neuropathy (MMN) patients.MethodsClinical and laboratory data were collected from 110 patients enrolled in the Italian MMN database through a structured questionnaire. Twenty‐six patients were excluded due to the unavailability of nerve conduction studies or the presence of clinical signs and symptoms and electrodiagnostic abnormalities inconsistent with the MMN diagnosis. Analyses were conducted on 73 patients with a confirmed MMN diagnosis and 11 patients who did not meet the diagnostic criteria.ResultsThe European Federation of Neurological Societies/Peripheral Nerve Society (EFNS/PNS) diagnostic criteria were variably applied. AUTHOR:When applying the American Association of Electrodiagnostic Medicine criteria, an additional 17% of patients fulfilled the criteria for probable/definite diagnosis whilst a further 9.5% missed the diagnosis. In 17% of the patients only compound muscle action potential amplitude, but not area, was measured and subsequently recorded in the database by the treating physician. Additional investigations, including anti‐GM1 immunoglobulin M antibodies, cerebrospinal fluid analysis, nerve ultrasound and magnetic resonance imaging, supported the diagnosis in 46%–83% of the patients. Anti‐GM1 immunoglobulin M antibodies and nerve ultrasound demonstrated the highest sensitivity. Additional tests were frequently performed outside the EFNS/PNS guideline recommendations.ConclusionsThis study provides insights into the real‐world diagnostic and management strategies for MMN, highlighting the challenges in applying diagnostic criteria.
Unclassified clinical presentations of chronic inflammatory demyelinating polyradiculoneuropathy Pietro Emiliano Doneddu, Houseyin Akyil, Fiore Manganelli, Chiara Briani, Dario Cocito, Luana Benedetti, Anna Mazzeo, Raffaella Fazio, Massimiliano Filosto, Giuseppe Cosentino, Vincenzo Di Stefano, Giovanni Antonini, Girolama Alessandra Marfia, Maurizio Inghilleri, Gabriele Siciliano, Angelo Maurizio Clerici, Marinella Carpo, Angelo Schenone, Marco Luigetti, Giuseppe Lauria, Sabrina Matà, Tiziana Rosso, Giacomo Maria Minicuci, Marta Lucchetta, Guido Cavaletti, Giuseppe Liberatore, Emanuele Spina, Marta Campagnolo, Erdita Peci, Francesco Germano, Luca Gentile, Camilla Strano, Stefano Cotti Piccinelli, Elisa Vegezzi, Luca Leonardi, Giorgia Mataluni, Marco Ceccanti, Erika Schirinzi, Marina Romozzi, Eduardo Nobile-Orazio Journal of Neurology Neurosurgery and Psychiatry, 2023
Risk of disease relapse, safety and tolerability of SARS-CoV-2 vaccination in patients with chronic inflammatory neuropathies Pietro Emiliano Doneddu, Chiara Briani, Dario Cocito, Fiore Manganelli, Gian Maria Fabrizi, Sabrina Matà, Anna Mazzeo, Raffaella Fazio, Luana Benedetti, Marco Luigetti, Maurizio Inghilleri, Elisa Ruiu, Gabriele Siciliano, Giuseppe Cosentino, Girolama Alessandra Marfia, Marinella Carpo, Massimiliano Filosto, Giovanni Antonini, Francesca Notturno, Stefano Sotgiu, Laura Cucurachi, Claudia Dell'Aquila, Elisa Bianchi, Tiziana Rosso, Andrea Giordano, Marco Fernandes, Marta Campagnolo, Erdita Peci, Emanuele Spina, Matteo Tagliapietra, Martina Sperti, Luca Gentile, Camilla Strano, Francesco Germano, Marina Romozzi, Federica Moret, Ignazio Roberto Zarbo, Divina Valeria Viola, Elisa Vegezzi, Giorgia Mataluni, Stefano Cotti‐Piccinelli, Luca Leonardi, Alessandra Carta, Eduardo Nobile‐Orazio, and European Journal of Neurology, 2023
Gastrointestinal barriers to levodopa transport and absorption in Parkinson's disease Valentina Leta, Lisa Klingelhoefer, Katherine Longardner, Marta Campagnolo, Hafize Çotur Levent, Federico Aureli, Vinod Metta, Roongroj Bhidayasiri, Guy Chung‐Faye, Cristian Falup‐Pecurariu, Fabrizio Stocchi, Peter Jenner, Tobias Warnecke, K. Ray Chaudhuri, and European Journal of Neurology, 2023
Duodenal alpha-Synuclein Pathology and Enteric Gliosis in Advanced Parkinson's Disease Aron Emmi, Michele Sandre, Francesco Paolo Russo, Giulia Tombesi, Federica Garrì, Marta Campagnolo, Miryam Carecchio, Roberta Biundo, Gaya Spolverato, Veronica Macchi, Edoardo Savarino, Fabio Farinati, Piero Parchi, Andrea Porzionato, Luigi Bubacco, Raffaele De Caro, Gabor G. Kovacs, Angelo Antonini Movement Disorders, 2023
Oligoclonal IgG bands in chronic inflammatory polyradiculoneuropathies Marta Ruiz, Marco Puthenparampil, Marta Campagnolo, Francesca Castellani, Alessandro Salvalaggio, Susanna Ruggero, Elisabetta Toffanin, Mario Cacciavillani, Paolo Gallo, Diego Franciotta, Chiara Briani Journal of Neurology Neurosurgery and Psychiatry, 2021
Nerve ultrasound in hereditary transthyretin amyloidosis: red flags and possible progression biomarkers Alessandro Salvalaggio, Daniele Coraci, Mario Cacciavillani, Laura Obici, Anna Mazzeo, Marco Luigetti, Francesca Pastorelli, Marina Grandis, Tiziana Cavallaro, Giulia Bisogni, Alessandro Lozza, Chiara Gemelli, Luca Gentile, Mario Ermani, Gian Maria Fabrizi, Rosaria Plasmati, Marta Campagnolo, Francesca Castellani, Roberto Gasparotti, Carlo Martinoli, Luca Padua, Chiara Briani Journal of Neurology, 2021
Clinician-rated measures for distal symmetrical axonal polyneuropathy: ACTTION systematic review Jennifer S. Gewandter, Christopher H. Gibbons, Marta Campagnolo, Joonho Lee, Jenna Chaudari, Nam Ward, Laurie Burke, Guido Cavaletti, David N. Herrmann, Justin C. McArthur, James W. Russell, A. Gordon Smith, Shannon M. Smith, Dennis C. Turk, Robert H. Dworkin, Roy Freeman Neurology, 2019
Peripheral nervous system involvement in lymphomas Chiara Briani, Andrea Visentin, Marta Campagnolo, Alessandro Salvalaggio, Sergio Ferrari, Tiziana Cavallaro, Renzo Manara, Roberto Gasparotti, Francesco Piazza Journal of the Peripheral Nervous System, 2019
Patients' and physicians' interpretation of chemotherapy-induced peripheral neurotoxicity Guido Cavaletti, David R. Cornblath, Ingemar S.J. Merkies, Tjeerd J. Postma, Emanela Rossi, Paola Alberti, Jordi Bruna, Andreas A. Argyriou, Chiara Briani, Roser Velasco, Haralabos P. Kalofonos, Dimitri Psimaras, Damien Ricard, Andrea Pace, Catharina G. Faber, Roy I. Lalisang, Dieta Brandsma, Susanne Koeppen, Simon Kerrigan, Angelo Schenone, Wolfgang Grisold, Anna Mazzeo, Luca Padua, Susan G. Dorsey, Marta Penas‐Prado, Maria G. Valsecchi, the CI‐PeriNomS Group Journal of the Peripheral Nervous System, 2019
Functioning and quality of life in patients with neuropathy associated with anti-MAG antibodies Yuri M. Falzone, Marta Campagnolo, Mariangela Bianco, Patrizia Dacci, Daniele Martinelli, Marta Ruiz, Silvia Bocci, Federica Cerri, Angelo Quattrini, Giancarlo Comi, Luana Benedetti, Fabio Giannini, Giuseppe Lauria, Eduardo Nobile-Orazio, Chiara Briani, Raffaella Fazio, Nilo Riva Journal of Neurology, 2018
Pentraxin-3 and VEGF in POEMS syndrome: A 2-year longitudinal study Chiara Briani, Chiara Dalla Torre, Federica Lessi, Tiziana Cavallaro, Marina Scarlato, Sergio Ferrari, Marta Campagnolo, Marta Lucchetta, Ilaria Cabrini, Michela Morbin, Giuseppe Lauria, Fausto Adami, Angelo A. Manfredi Journal of Neuroimmunology, 2014
Long-term course of oxaliplatin-induced polyneuropathy: A prospective 2-year follow-up study Chiara Briani, Andreas A. Argyriou, Cristina Izquierdo, Roser Velasco, Marta Campagnolo, Paola Alberti, Barbara Frigeni, Mario Cacciavillani, Francesca Bergamo, Diego Cortinovis, Marina Cazzaniga, Jordi Bruna, Guido Cavaletti, Haralabos P. Kalofonos Journal of the Peripheral Nervous System, 2014
Correspondence between neurophysiological and clinical measurements of chemotherapy-induced peripheral neuropathy: Secondary analysis of data from the CI-PeriNomS study Kathleen A. Griffith, Susan G. Dorsey, Cynthia L. Renn, Shijun Zhu, Mary E. Johantgen, David R. Cornblath, Andreas A. Argyriou, Guido Cavaletti, Ingemar S. J. Merkies, Paola Alberti, Tjeerd J. Postma, Emanuela Rossi, Barbara Frigeni, Jordi Bruna, Roser Velasco, Haralabos P. Kalofonos, Dimitri Psimaras, Damien Ricard, Andrea Pace, Edvina Galie, Chiara Briani, Chiara Dalla Torre, Catharina G. Faber, Roy I. Lalisang, Willem Boogerd, Dieta Brandsma, Susanne Koeppen, Joerg Hense, Dawn J. Storey, Simon Kerrigan, Angelo Schenone, Sabrina Fabbri, Maria Grazia Valsecchi, the CI‐PeriNomS Group Journal of the Peripheral Nervous System, 2014
The chemotherapy-induced peripheral neuropathy outcome measures standardization study: From consensus to the first validity and reliability findings G. Cavaletti, D.R. Cornblath, I.S.J. Merkies, T.J. Postma, E. Rossi, B. Frigeni, P. Alberti, J. Bruna, R. Velasco, A.A. Argyriou, H.P. Kalofonos, D. Psimaras, D. Ricard, A. Pace, E. Galiè, C. Briani, C. Dalla Torre, C.G. Faber, R.I. Lalisang, W. Boogerd, D. Brandsma, S. Koeppen, J. Hense, D. Storey, S. Kerrigan, A. Schenone, S. Fabbri, M.G. Valsecchi, A. Mazzeo, A. Pace, A. Pessino, A. Schenone, A. Toscano, A.A. Argyriou, B. Brouwer, B. Frigeni, B. Piras, C. Briani, C. Dalla Torre, C. Dominguez Gonzalez, C.G. Faber, C. Tomasello, D. Binda, D. Brandsma, D. Cortinovis, D. Psimaras, D. Ricard, D. Storey, D.R. Cornblath, E. Galiè, E. Lindeck Pozza, E. Rossi, E.K. Vanhoutte, F. Lanzani, F. Pastorelli, G. Altavilla, G. Cavaletti, G. Granata, H.P. Kalofonos, I. Ghignotti, I.S.J. Merkies, J. Bruna, J. Hense, J.J. Heimans, L. Mattavelli, L. Padua, L. Reni, M. Bakkers, M. Boogerd, M. Campagnolo, M. Cazzaniga, M. Eurelings, M. Leandri, M. Lucchetta, M. Penas Prado, M. Russo, M.G. Valsecchi, M.L. Piatti, P. Alberti, P. Bidoli, R. Grant, R. Plasmati, R. Velasco, R.I. Lalisang, R.J. Meijer, S. Fabbri, S.G. Dorsey, S. Galimberti, S. Kerrigan, S. Koeppen, T.J. Postma, W. Boogerd, W. Grisold Annals of Oncology, 2013
