Mirella Russo

Scopus Publications

International consensus for the assessment of social cognition in neurocognitive disorders: framework definition and clinical recommendations of the SIGNATURE initiative
Alessandra Dodich, Andrea Panzavolta, Giulia Funghi, Claudia Meli, Cristina Festari, Thanos Chatzikostopoulos, Christian Chicherio, Florencia Clarens, Fabricio Ferreira de Oliveira, Marco Filardi, Agustin Ibanez, Laura Invernizzi, Thibaud Lebouvier, Giancarlo Logroscino, Sarah E. MacPherson, Riccardo Manca, Camillo Marra, Jordi A. Matias-Guiu, Maxime Montembeault, Costanza Papagno, Simone Pomati, Mario Possenti, Olivier Piguet, Leonardo Sacco, Ann-Katrin Schild, Marc Sollberger, Miguel Tábuas-Pereira, Marianna Tsatali, Magda Tsolaki, Esther van den Berg, Stefano F. Cappa, Maxime Bertoux, Fiona Kumfor, Jan Van den Stock, Marina Boccardi, Kathleen Anne Welsh-Bohmer, Chiara Cerami, , Federica Agosta, Elisa Canu, Ove Almkvist, Goran Hagman, Bengt Winblad, Daniele Altomare, Davide Angioni, Jean-Marie Annoni, Luca Beretta, Manfred Berres, Valentina Bessi, Ingo Fimm, Ingo Kilimann, Emre Bora, Andrea Brioschi-Guevara, Andreas Buchmann, Anton Gietl, Cinzia Bussè, Annachiara Cagnin, Russell Chander, Matthias Kliegel, Nathalie Mella, Alfredo Costa, Camille Coulangers, Pierre-Jean Ousset, Chiara Cupidi, Jean-François Démonet, Mira Didic, Francesco Di Lorenzo, Bruno Dubois, Alan Cronemberger Andrade, Bruno Fimm, Douglas Galasko, Nicola Girtler, Flavio Nobili, Matteo Pardini, Julie Henry, Renelle Bourdage, Lize Jiskoot, Jackie Poos, Haaro Seelaar, Stefan Klöppel, Christine Krebs, Walter A. Kukull, Richard Levy, Marisa Lima, Antonella Luca, Simona Luzzi, Marta Fernández Matarrubia, Patrizia Mecocci, Martina Pigliautile, Alina Menichelli, Micaela Mitolo, Andreas U. Monsch, Despoina Moraitou, Petr Novak, Miriam E. Ortiz, Sokratis Papageorgiou, Nikolaos Scarmeas, John Papatriantafyllou, Andrea Plutino, Davide Quaranta, Inez Ramakers, Stefania Rossi, Mirella Russo, Stefano Sensi, Perminder Sachdev, David P. Salmon, Pilar Sanchez, Florian Schöberl, Steven D. Shirk, Alessio Toraldo, Annalena Venneri, Dix Meiberth, Maurizio Gallucci, Fotini Kounti, Silvia Rodrigo Herrero, Pietro Marano, Tommaso Piccoli, Samrah Ahmed, Fabiola Böhm, Matthias Schroeter, Susanna Vestberg, Marie Söntgerath, Jennifer Thompson, Tamlyn Watermeyer, Hendrick-Jan van der Waal, Lucy Chrisman-Russell, Silvana Morson, Lucas Wolski, Renzo Dori, Andrea Fabbo, Chiara Galli, Claudia Bartels, Gert Geurtsen, Francesca Baglio, Sara Isernia, Cem Dogdu, Elisa Ruiu, Fijanne Strijkert, Nikki Zimmermann, Wendy Weidner, Helena Briales, Rita Pezzati, Anne Rita Oksengard, Angela Bradshaw
Alzheimer S Research and Therapy, 2026
BACKGROUND: Socio-cognitive assessment in neurocognitive disorders (NCDs) is rare in clinical practice and no consensus exists as to a uniform operationalization of socio-cognitive measures for NCDs in memory clinics. The SIGNATURE initiative aims to optimize the use of socio-cognitive measures in memory clinics, defining expert recommendations. We report consortium guidelines for the use of socio-cognitive measures in NCDs based on available evidence from the literature and the current state of practices in memory clinics. METHODS: Using a Delphi consensus method supported by a literature review and the results of an international survey, 22 specialists defined recommendations for the context of use, relevance in NCD diagnosis, priorities for future research and facilitators/obstacles of socio-cognitive assessment in major and mild NCDs. RESULTS: Overall, panelists recommended social cognition testing in routine diagnostic assessment to evaluate both socio-cognitive and socio-behavioral alterations. A set of clinical, methodological, implementation and external factors facilitating or hampering the use of socio-cognitive tasks was identified. CONCLUSIONS: This is the first focused endeavor to favor the implementation of socio-cognitive assessment, which is required by DSM-5 but seldom performed despite clear evidence of its clinical relevance for diagnosis and care. Our results provide an initial set of recommendations, refinable through the future actions of the SIGNATURE initiative. Future collaborative clinical research projects should overcome current limitations and foster the use of ecological and cross-culturally validated measures in clinics.
Plasma extracellular vesicles and phosphorylated tau 181 as early biomarkers of cognitive impairment in Alzheimer’s dementia
Viviana Brembati, Daniela Crescenti, Andrea Geviti, Elisa Rossini, Federico Angelo Cazzaniga, Fabio Moda, Elisa R. Zanier, Gisella Guerrera, Luca Battistini, Simone Baiardi, Alessandra Mandelli, Roberto Furlan, Federico Verde, Benedetta Nacmias, Chiara Adriana Elia, Maria Luisa Malosio, Alberto Imarisio, Franca Rosa Guerini, Chiara Fenoglio, Alessio Di Fonzo, Leonardo Biscetti, Margherita Squillario, Silvia Berra, Francesca Miraglia, Paolo Maria Rossini, Camillo Marra, Nicola Vanacore, Alberto Redolfi, Daniela Perani, Patrizia Spadin, Maria Cotelli, Stefano Cappa, Naike Caraglia, Fabrizio Vecchio, Pietro Tiraboschi, Federica Piras, Giovanni B. Frisoni, Cristina Muscio, Raffaele Lodi, Piero Parchi, Fabrizio Tagliavini, Enza Maria Valente, Gianluigi Forloni, Roberta Ghidoni, , /, Maurizio Belfiglio, Giacomina Rossi, Emanuela Maderna, Marcella Catania, Giuseppe Di Fede, Davide Quaranta, Emanuele Cassetta, Mario Barbagallo, Carlo Gabelli, Simona Luzzi, Fulvio Lauretani, Innocenzo Rainero, Carlo Ferrarese, Orazio Zanetti, Michela Marcon, Flavio Mariano Nobili, Matteo Pardini, Giuseppe Pelliccioni, Sabina Capellari, Elena Sinforiani, Alfredo Costa, Gioacchino Tedeschi, Carmen Gerace, Laura Bonanni, Sandro Sorbi, Lucilla Parnetti, , Ilaria Bizzozero, Paola Caroppo, Valeria Crepaldi, Giuseppe Di Fede, Giorgio Giaccone, Veronica Redaelli, Marcella Catania, Edoardo Bistaffa, Chiara Maria Giulia De Luca, Giacomina Rossi, Chiara Boiocchi, Sara Cimini, Maria Grazia Bruzzone, Luigi Antelmi, Stefania Ferraro, Ruben Gianeri, Jean Paul Medina, Anna Nigri, Cristina Rosazza, Domenico Arenella, Fabrizio Piras, Desiree Estela Porcari, Daniela Vecchio, Roberto Langella, Domenico Mancini, Giovanni Mancini, Marco Bozzali, Giovanni Giulietti, Laura Serr, Orazio Schillaci, Agostino Chiaravalloti, Valentino Bettinardi, Sandro Iannaccone, Federica Alemanno, Valerio Golzi, Anna Parma, Alessandra Marcone, Teresa Sikora, Cristina Festari, Valentino Nicolosi, Jorge Jovicich, Silvia De Francesco, Luisa Benussi, Guido Domingo, Roberta Zanardini, Daniela Galimberti, Elio Scarpini, Barbara Borroni, Elisa Bonomi, Viviana Cristillo, Silvia Pelizzari, Rosanna Turrone, Luca Rozzini, Roberto Gasparotti, Daniela Corbo, Lorella Mascaro, Barbara Paghera, Lucilla Parnetti, Elena Chipi, Chiara Montanucci, Lucia Farotti, Mirella Russo, Massimo Eugenio Dottorini, Cristina Tranfaglia, Roberto Tarducci, Andrea Chiappiniello, Pietro Chiarini, Pietro Floridi, Sandro Sorbi, Cristina Polito, Silvia Bagnoli, Gemma Lombardi, Alberto Pupi, Valentina Berti, Maria Teresa De Cristofaro, Alessandro Passeri, Enrico Fainardi, Andrea Ginestroni, Stefano Chiti, Roberto D’Alessandro, Ambra Fiorani, Simona Linarello, , Sonia Bellini, Antonio Longobardi, Valentina Bonetto, Ilaria Lisi, Laura Pasetto, Emiliano Giardina, Giulia Sancesario, Antonia Ratti, Vincenzo Silani, Nicola Ticozzi, Silvia Bagnoli, Assunta Ingannato, Michela Matteoli, Micol Avenali, Rosaria Calabrese, Cristina Agliardi, Daniela Galimberti, Michele Piana, Annarita Bentivoglio, Giulia Di Lazzaro, Stefano Gambardella
Alzheimer S Research and Therapy, 2026
Timely and accurate diagnosis of Alzheimer’s disease (AD) in clinical practice is a great challenge, especially during early disease stages with subtle or mild symptoms of cognitive decline. Moreover, robust and more accessible blood-based screening tests for early diagnosis are needed. In this study, we investigated the core AD blood biomarkers — amyloid beta 42 (Aβ42) and 40 (Aβ40) peptides, phosphorylated tau 181 (p-Tau181), neurofilament light chain (NfL), and total tau (t-Tau) — and extracellular vesicle (EVs) size and concentration in individuals characterized by different stages of cognitive decline to identify biochemical markers of dementia for early diagnosis. A total of n = 800 human plasma samples were analyzed. Plasma levels of NfL, t-Tau, p-Tau181, Aβ42, Aβ40 and plasma EVs were evaluated in n = 217 elderly healthy subjects (CTRL), in individuals with subjective cognitive complaints (SCC, n = 48), pre-mild cognitive impairment (pre-MCI, n = 58) and mild cognitive impairment (MCI, n = 426), and in n = 51 probable AD dementia patients (AD-dem), using ultrasensitive Single Molecule Array technology (Simoa®) and nanoparticle tracking analysis (NTA). Logistic regression and Receiver Operating Characteristic (ROC) analyses were employed. Plasma NfL displayed increased levels in AD-dem and MCI patients, while p-Tau181, Aβ42/Aβ40 ratio, Aβ42/p-Tau181 ratio, and EVs plasma levels were altered since the early stages of the pathology: in particular, p-Tau181 levels increased as cognitive symptoms worsened, already in the SCC and pre-MCI groups compared to CTRL, while the ratio of EVs concentration and size (EVs ratio) was decreased in all groups compared to CTRL. Plasma p-Tau181 best classified AD-dem patients from CTRL with an area under the curve (AUC) equal to 0.87, while EVs ratio best differentiated SCC from CTRL (AUC = 0.78). Combining p-Tau181 and EVs ratio with Aβ42/Aβ40 ratio and NfL, respectively, significantly improved the classification of pre-MCI and MCI from CTRL (AUCcomb = 0.79 and AUCcomb = 0.85). Combining biomarkers did not improve accuracy in discriminating MCI from SCC, pre-MCI and AD-dem. p-Tau181 and EVs ratio are promising biomarkers for the identification of individuals at risk of degenerative dementia. Combining the core AD plasma biomarkers with EVs ratio can aid in diagnosing the early stages of AD dementia.
Early Cenobamate as a Third-Line Option in Drug-Resistant Focal Epilepsy: A Paradigm Shift?
Fedele Dono, Mirella Russo, Rita Agosto, Giacomo Evangelista, Bruna Nucera, Giovanni Falcicchio, Stefano L. Sensi
Neurology and Therapy, 2026
INTRODUCTION: Drug-resistant epilepsy (DRE) affects nearly 30% of patients with epilepsy, and the optimal sequencing of adjunctive anti-seizure medications (ASMs) remains uncertain. Comparative real-world evidence on early use of newer ASM is limited. This study explores real-world comparative effectiveness, safety and 12-month retention of cenobamate (CNB) introduced as early third-line adjunctive therapy compared with perampanel (PER) and brivaracetam (BRV) in adults with focal-onset DRE. METHODS: This multicenter observational study included 34 CNB patients and 37 matched controls treated with PER or BRV, all after failure of two prior ASMs. Primary outcome was 12-month treatment retention; secondary outcomes included responder rates (≥ 50%, ≥ 75%, 100%) and adverse events at 3, 6 and 12 months. Comparative analyses were exploratory. Univariate analyses and longitudinal generalized linear mixed-effects models (GLMMs) were used to describe outcome trajectories over time. RESULTS: CNB showed a 12-month retention rate of 94.1%. Descriptively, seizure freedom was achieved in 62.5% of CNB patients at 12 months compared with 43.7% with PER and 16.6% with BRV. Adverse events were less frequent with CNB (9.4% at 12 months) than in controls (35.3%) and were generally non-treatment-limiting. GLMMs confirmed a significant time × treatment interaction for seizure frequency, indicating a steeper reduction in CNB patients, while no significant interaction emerged for adverse events. CONCLUSIONS: In this real-world study, early third-line CNB exhibits potentially favorable effectiveness compared with other commonly used third-line ASMs, and tolerability remained acceptable. These findings support the need for larger prospective studies to better define optimal treatment sequencing in focal-onset DRE.
Psychedelics and ketamine/esketamine in depressive disorders: biological mechanisms and associated neuroimaging and clinical changes
Giacomo d’Andrea, Stefania Chiappini, Laura Ciavoni, Rolando Tucci, Fabrizio Martino, Francesco Maria Semeraro, Daniele Di Battista, Alessio Mosca, Andrea Miuli, Francesco Di Carlo, Mirella Russo, Gilberto Di Petta, Michele Fornaro, Mauro Pettorruso, Stefano L. Sensi, Giovanni Martinotti
Translational Psychiatry, 2025
BACKGROUND: Over the past ten years, several psychedelic compounds, including tryptamines like lysergic acid diethylamide/LSD, psilocybin, ayahuasca, and dimethyltryptamine/DMT, have been tested in clinical trials for a range of psychiatric conditions, such as anxiety and depression. While these compounds are relatively available for treatment, ketamine and its S(+) enantiomer, esketamine, are increasingly used to manage treatment-resistant depression. The biological mechanisms set in motion by these compounds are still largely unexplored. Preliminary data indicate modulatory activity of distinct brain networks and selected neurotransmitter pathways (i.e., glutamate, serotonin). OBJECTIVE: This systematic review investigates functional changes in neural activity generated by these compounds (i.e., LSD, psilocybin, ayahuasca, and DMT or ketamine/esketamine) in depressive disorders. Studies involving different techniques (i.e. Positron Emission Tomography/PET, Single Photon Emission Computed Tomography/SPECT, functional Magnetic Resonance Imaging/fMRI and MRI) were included. METHOD: A literature search was conducted following preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines of 2015. The search was performed using PubMed Web of Science and Scopus databases, taking into consideration publications up to March 2022, without any time restrictions. RESULTS: The search produced a final set of 49 articles. Most were related to ketamine/esketamine (n = 44). A smaller number (n = 5) pertained to psychedelic tryptamines (one on ayahuasca and four on psilocybin). From the total of 49 studies, 9 were randomized-controlled trials, 25 were open-label studies, 4 were double-blind trials, 8 were observational studies, and 3 cross-over studies. CONCLUSIONS: Psylocibin seems to reset Default Mode Network (DMN) activity, thereby reducing depressive symptoms with long-term and sustainable antidepressant efficacy. Compared to psychedelics, ketamine exhibits a more specific action on networks involving prefrontal areas that act indirectly on the DMN. This effect may help explain ketamine's anti-anhedonic activity and its critical role in increasing cognitive control over emotional stimuli, thus reducing negative mood stages.
Neurological and neuropsychological correlates of Klippel-Feil syndrome
Sara Melchiorre, Mirella Russo, Matteo Santilli, Gaetano Polito, Consuelo Ciprietti, Dario Calisi, Valentina Panara, Loris Di Clemente, Astrid Thomas, Stefano L. Sensi
Neurological Sciences, 2025
Background Klippel-Feil syndrome is a rare congenital malformation caused by fusions of cervical vertebrae. In 50% of these patients, a triad of short neck, limited neck motion, and low posterior hairline characterizes the clinical presentation. In KFS, neurological deficits are common due to cervical canal stenosis and other deformities involving basicranial structures. Other congenital anomalies are also associated with the syndrome. Case presentation Our case describes a particular case of KFS, showing a disconnection between a severe involvement of the cervical-occipital structures indicated by magnetic resonance imaging and a mild clinical presentation. Moreover, a slight visual-spatial deficit was found in neuropsychological tests. No prior association between KFS and visuospatial impairment has been reported. Discussion and conclusions GDF6, a gene associated with KFS, plays a role in retinotectal mapping, which organizes visual stimuli in the brain. Early neurodevelopment abnormalities, such as atlanto-occipital anomalies in KFS, might affect related brain structures, which could explain the patient’s impaired visuospatial function. In addition, compensatory neuroplasticity underscores how the brain may adapt to congenital defects, even severe ones.
Angiotensin receptor blockers (ARBs) reduce the risk of developing epilepsy in patients with ischemic stroke and hypertension
Giacomo Evangelista, Fedele Dono, Sara Melchiorre, Clarissa Corniello, Davide Liviello, Paolo Quintieri, Martina Di Pietro, Mirella Russo, Catello Vollono, Stefano L. Sensi
Seizure, 2025
PURPOSE: Stroke is the most common cause of seizures in patients older than 60 years. About 10-30 % of new epilepsy diagnoses in elderly patients are associated with a brain ischemic event. Hypertension is a major risk factor for epilepsy and stroke, and 2 % of patients with epilepsy have hypertension. According to the European Society of Cardiology guidelines, Angiotensin-Converting Enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) are first-line hypertension treatment. ACEi and ARBs promote a protective effect against the development of seizures in the general population. However, no data are available about their possible preventive role in post-stroke epilepsy (PSE). In this study, we evaluated the relationship between different antihypertensive regimens and the risk of developing post-stroke epilepsy (PSE). METHODS: In this retrospective, observational study, we selected and evaluated data relative to patients with hypertension and a diagnosis of ischemic stroke (as confirmed by clinical and neuroimaging evaluations and who accessed our neurology ward between January 2016 and January 2022). All participants were followed up for a median period of 24 months. The PSE diagnosis was made according to the ILAE criteria. We excluded patients with acute symptomatic seizures. The details of the antihypertensive treatments, demographics, and clinical and neuroradiological data were analyzed. RESULTS: 528 patients (mean age: 71.37 ± 13.64, 302 men, 57.19 %) were enrolled. Thirty-eight (7.2 %) patients developed PSE. Anterior Cerebral Artery involvement (p = 0.05) and cortico-subcortical lesions (p = 0.001) were associated with a higher risk of PSE. A lower risk of PSE was observed in patients treated with ARBs, both before (p = 0.009) and after (p = 0.02) the stroke event. PSE incidence was higher in patients receiving Calcium Channel blockers (CCBs) (p = 0.019) and Beta-blockers (BBs) (p = 0.008) before the stroke event as well as BBS after the stroke event (p = 0.003). No differences were observed for ACEi if administered previous (p = 0.42) or after (p = 0.48) the stroke event. CONCLUSIONS: ARBs appear to offer a protective role against epilepsy development in patients with hypertension and stroke. These findings suggest that ARBs could be considered a promising target for future prospective studies evaluating PSE prevention in stroke patients.
Exploring the long-term effects of COVID-19 in patients with epilepsy: A multicenter Italian observational study
Fedele Dono, Mirella Russo, Giacomo Evangelista, Clarissa Corniello, Claudio Liguori, Carmen Calvello, Flavia Narducci, Catello Vollono, Stefano Sensi
Epilepsia Open, 2025
ObjectiveCoronavirus disease‐19 (COVID‐19), caused by SARS‐CoV‐2, has led to a global pandemic since December 2019. People with epilepsy (PwE) face higher risks of severe COVID‐19 outcomes and may be more vulnerable to long‐term neurological and psychiatric effects.MethodsThis multicenter, retrospective cohort study reviewed medical records of PwE with confirmed SARS‐CoV‐2 infection (COVID+) from four Italian hospitals (March 2020–December 2021). A control group (COVID−) included age‐ and sex‐matched PwE without infection. Demographics, epilepsy features, COVID‐19 severity, and neurological/psychiatric outcomes were assessed at baseline and at 6 and 12 months. Statistical analyses included regression and linear mixed model (LMM).ResultsAmong 130 patients (38 COVID+, 92 COVID−), no baseline differences were found in demographics, epilepsy characteristics, or comorbidities. At 6 months, the COVID+ group showed increased seizure frequency (p = 0.03) and higher rates of psychiatric (p < 0.01) and neurological symptoms (p < 0.01), requiring specific treatment (p = 0.01). At 12 months, psychiatric and neurological disorders persisted (p < 0.01), with more treated neurological symptoms (p < 0.01). LMM analysis found no significant seizure frequency differences over time (p = 0.47), but focal‐to‐bilateral tonic–clonic seizures showed a time‐dependent interaction (p = 0.025).SignificanceSARS‐CoV‐2 infection has lasting neurological and psychiatric effects in PwE. While acute seizure frequency changes are transient, cognitive impairment, insomnia, and depression persist, underscoring the need for continuous monitoring and personalized care.Plain Language SummaryThis study investigated long‐term neurological and psychiatric outcomes in people with epilepsy (PwE) after COVID‐19 infection. We compared 38 PwE with confirmed SARS‐CoV‐2 infection to 92 uninfected controls, matched by age and sex. At 6 months, infected patients showed increased seizure frequency and more psychiatric and neurological symptoms, often requiring treatment. At 12 months, seizure frequency stabilized, but cognitive issues, depression, and insomnia persisted. These findings highlight that while seizure changes may be temporary, COVID‐19 has lasting neuropsychiatric effects in PwE, emphasizing the importance of long‐term monitoring and individualized therapeutic strategies.
Understanding barriers and optimizing socio-cognitive assessment in the diagnosis of neurocognitive disorders
Chiara Cerami, Marina Boccardi, Claudia Meli, Andrea Panzavolta, Giulia Funghi, Cristina Festari, Stefano F. Cappa, Thanos Chatzikostopoulos, Christian Chicherio, Florencia Clarens, Fabricio Ferreira de Oliveira, Francesco Di Lorenzo, Marco Filardi, Agustin Ibanez, Nicola Girtler, Thibaud Lebouvier, Giancarlo Logroscino, Antonella Luca, Sarah E. MacPherson, Jordi A. Matias‐Guiu, Tommaso Piccoli, Olivier Piguet, Simone Pomati, Mirella Russo, Leonardo Sacco, Ann‐Katrin Schild, Stefano L. Sensi, Steven D. Shirk, Marc Sollberger, Miguel Tábuas‐Pereira, Magda Tsolaki, Esther van den Berg, Maxime Bertoux, Fiona Kumfor, Jan Van den Stock, Kathleen A. Welsh‐Bohmer, Alessandra Dodich, and
Journal of Neuropsychology, 2025
Harmonized neuropsychological assessment for neurocognitive disorders (NCDs) is an urgent priority in clinics. Neuropsychology assessments in NCDs seldom include tests exploring social cognitive skills. In 2022, we launched the SIGNATURE initiative to optimize socio‐cognitive assessment in NCDs. Here, we report findings from the first initiative phase, including consortium creation and evaluation of the state of the art in socio‐cognitive assessment in memory clinics. We developed an ad hoc online survey to explore practices and measures, relevance, and obstacles preventing the use of socio‐cognitive testing in clinics. The survey was distributed within the SIGNATURE network. National coordinators were identified to disseminate the survey to local collaborators and scientific societies active in the field of dementia and/or neuropsychology. Data were analysed in aggregate form and stratified by geographical area and variables of interest. Four hundred and thirteen (413) responses from 10 European and Latin American geographical regions were recorded. Responders were balanced between physicians and psychologists. Seventy‐eight (78) % of respondents reported no/limited experience with socio‐cognitive measures; more than 85% agreed on their relevance in clinics. Ekman‐60 faces was the most well‐known and/or used task, followed by the Faux‐Pas and Reading‐the‐Mind‐in‐the‐Eyes tests. Lack of clinical measures, assessment time, guidelines, and education/training were reported as main obstacles. Real‐life barriers prevent the adoption of socio‐cognitive testing in clinics. Bidirectional collaboration between clinicians and researchers is required to address clinical needs and constraints and facilitate consistent socio‐cognitive assessment.
Prasinezumab: A Bayesian Perspective on Its Efficacy
Mirella Russo, Tommaso Costa, Dario Calisi, Stefano L. Sensi
Movement Disorders, 2025
Parkinson's disease (PD) is a progressive neurodegenerative disorder featuring aberrant aggregation of α-synuclein (a presynaptic protein implicated in physiological synaptic vesicle trafficking and neurotransmitter release) as a critical modulator of the disease.1, 2 This notion has been further substantiated by the discovery of autosomal dominant variants of PD associated with mutation or triplication of the α-synuclein gene SNCA (PARK1 and PARK4, respectively).3 In PD, α-synuclein undergoes conformational changes (Fig. 1), leading to the formation of insoluble fibrils and intracellular inclusions known as Lewy bodies.4 One of the leading pathogenic theories postulates that these aggregates propagate in a prion-like manner, spreading throughout the brain in a pattern that correlates with disease progression.5-8 Although the link between α-synuclein anomalies and PD has been established, the modalities of this association are still unclear. A revised approach is considering that both a loss of function of a physiological (monomeric) protein9 and a gain of abnormal function could play a role.10, 11 On the one hand, α-synuclein oligomers and fibrils exhibit toxic properties as these aggregates disrupt cellular homeostasis, impair mitochondrial function, and induce oxidative stress, neuroinflammation, and synaptic dysfunction, ultimately leading to neuronal dysfunction and death.10 On the other hand, it has also been hypothesized that the loss of function of α-synuclein (synucleinopenia)9 may consistently affect PD pathophysiology. Due to its main localization at presynaptic terminals, the protein regulates neurotransmitter release and synaptic vesicle dynamics. Thus, its loss of function may impair synaptic transmission. Because α-synuclein is predominantly expressed in dopaminergic neurons, its loss of function may dysregulate dopaminergic signaling pathways.12 Furthermore, α-synuclein is involved in protein degradation pathways, including the ubiquitin-proteasome system and autophagy-lysosomal pathway.13 According to the model, a defective α-synuclein could favor the accumulation of misfolded proteins and protein aggregates, characteristic of PD pathology, thereby generating mixed neuropathology.14 α-Synuclein also interacts with mitochondria, influencing mitochondrial dynamics and function. Thus, a loss of function may disrupt mitochondrial bioenergetics and quality-control mechanisms, leading to mitochondrial impairment and oxidative stress.15 Moreover, α-synuclein has been linked to neuroprotection against excitotoxicity.16 Therefore, its loss of function could compromise neuronal resilience to stressors, making dopaminergic neurons more susceptible to degeneration. Several technical issues challenge the toxic role of α-synuclein. For instance, overexpression of α-synuclein due to SNCA gene multiplication does not necessarily lead to toxicity. High levels of α-synuclein are associated with better outcomes in some studies.9 Preclinical studies in knocked-out α-synuclein mice produced no substantial adverse effects. α-Synuclein knocked-out mice were fertile and showed normal neurodevelopment. However, dopaminergic dysfunction and abnormal motor responses were observed.17 The prion-like propagation of α-synuclein spreads is also questioned. It should also be underlined that the formation of α-synuclein aggregates is a passive, not active, process controlled by thermodynamic principles. Oligomers are indicated as toxic agents, but their real role is elusive because most experimental settings use supersaturated protein levels in which the presence of oligomers is transient, and they usually revert to monomers rather than forming fibers. This challenges the idea that oligomers can persist long enough to exert toxicity.9 This evidence has challenged the gain-of-function hypothesis and suggested that α-synuclein aggregation into Lewy bodies may be a protective mechanism rather than a toxic process. The recent development of disease-modifying therapies (DMTs) for PD has been a turning point. DMTs targeting α-synuclein are also crucial to confirm the “proteinopathy hypothesis,” whereas negative results could successfully be the Popperian “falsification element” against it (or at least could demonstrate that the matter is far more complex than a mere protein loss of function; see Fig. 1). One complicating factor is that currently, there are no precise biomarkers for PD, and the assessment of therapy-related changes can be challenging to assess in the short time span of clinical trials. Currently, no DMT has been approved for clinical use. More importantly, PD is still regarded as a disease, even though it better fits the construct of a syndrome.18 That point is worthwhile because it implies the challenging realization of homogeneous cohorts in PD clinical trials. Prasinezumab (PRX002) is a monoclonal immunoglobulin G1 antibody designed to selectively target the soluble and insoluble aggregated forms of α-synuclein, such as oligomers and fibrils, while sparing the physiological, soluble forms of the protein19 (see Supporting Information Data S1 [Preclinical Studies on Prasinezumab section] for the results of preclinical studies). In 2022, the PASADENA phase 2 trial20 assessed the efficacy of prasinezumab in patients with early-stage PD. The results were disappointing.20 Participants were randomly assigned to receive either a placebo or the compound (1500 or 4500 mg) every 4 weeks for 52 weeks. The primary outcome measured changes in the Movement Disorder Society–revised Unified Parkinson's Disease Rating Scale (MDS-UPDRS) scores, with secondary outcomes assessing dopamine transporter levels via single-photon emission computed tomography. Among 316 participants, the MDS-UPDRS scores and dopamine transporter levels did not differ when comparing the treatment and placebo groups.20 Overall, prasinezumab did not significantly affect PD progression compared with placebo, and optimism faded. Nonetheless, a new post hoc analysis was carried out and recently published.21 The post hoc analysis of the PASADENA study showed that the compound might slow motor progression in predefined subpopulations of patients with early-stage PD.21 Although the original study did not meet its primary endpoint (changes in MDS-UPDRS Parts I + II + III scores),20 in the subset of rapidly progressing patients,21 compared with placebo, drug-treated participants showed less worsening in motor signs (MDS-UPDRS Part III). The ongoing PADOVA study (NCT04777331) further investigates the impact of prasinezumab on motor progression in early-stage PD. However, methodological limitations must be accounted for, and longer trials might be required to observe effects in slowly progressing populations. Nonetheless, the recent post hoc analysis of the PASADENA trial raised many questions about the drug's efficacy because it indicated a numerical effect on motor progression in specific subpopulations (ie, fast progressing phenotypes). However, the lack of significant overall effects raises concerns about the robustness of these findings. First, the distinction between “diffuse malignant” and “nondiffuse malignant” phenotypes was made retrospectively and was data driven, which may have introduced a retrospective selection bias.21 The identification of “diffuse malignant” phenotypes at baseline with those with “more rapid” worsening is also problematic, because it conflates baseline features with outcomes. Moreover, the assessment of rapid progression was limited to the time of the observation and could carry a time-window bias and, as acknowledged by the authors of the original study,21 could reflect a different sensitivity to “signal-to-noise ratio” of the clinician's assessment (ie, the greater the change at scales, the greater the amplification of its perception, and vice versa). Furthermore, the prescription monoamine oxidase B inhibitors at baseline is not necessarily associated with a rapid progression of the disease but could depend on different factors, including the prescriber's preferences. Lastly, the mechanism of action of prasinezumab should counter a pathophysiological event that occurs relatively early in the disease course.19 Therefore, the association between drug efficacy and rapidity of clinical worsening, which is not necessarily associated with higher degree of α-synuclein deposition, is somehow confusing. Therefore, we used a Bayesian approach to test the effectiveness of prasinezumab for PD treatment. This provides a new angle on interpreting the trial results and offers critical elements for a constructive debate. This equation helps to calculate the BF for independent groups t test based on the most frequent t statistic. The null hypothesis ( H 0 $$ {H}_0 $$ ) in this test assumes that the population means of two independent groups are equal. Several assumptions underpin this method: the observations in both groups should be random samples, the dependent variable is normally distributed within each population, and the population variances should be equal (ie, the spreads of values in both groups are similar). The BF ( B F 01 $$ B{F}_{01} $$ ) can take values between 0 and infinity. When B F 01 < 1 $$ B{F}_{01}<1 $$ , the evidence favors the alternative hypothesis ( H 1 $$ {H}_1 $$ ); when B F 01 > 1 $$ B{F}_{01}>1 $$ , the evidence supports the null hypothesis ( H 0 $$ {H}_0 $$ ). Importantly, this approach allows for a full comparison of both hypotheses, modeling “what the data should look like when there is an effect.” The strength of the evidence depends on how far from 1 the BF is. Jeffreys (1939) proposed conventional thresholds: a BF greater than 3 or less than 1/3 is considered substantial evidence favoring one hypothesis over the other. Anything between 1/3 and 3 is interpreted as weak or anecdotal evidence. For example, if B F 01 = 6 $$ B{F}_{01}=6 $$ , this suggests that the null hypothesis ( H 0 $$ {H}_0 $$ ) is six times more likely than the alternative hypothesis ( H 1 $$ {H}_1 $$ ). In terms of posterior probabilities, this translates to an 86% probability for the null hypothesis ( H 0 $$ {H}_0 $$ ) (calculated as P 01 = B F 01 B F 01 + 1 = 6 7 $$ {P}_{01}=\frac{B{F}_{01}}{B{F}_{01}+1}=\frac{6}{7} $$ ), leaving a 14% probability for the alternative hypothesis ( H 1 $$ {H}_1 $$ ). All Bayesian analyses were performed using the JASP software.22 All results were also tested for robustness using a BF robustness check (see Supporting Information Data S1, Methods: Bayes Factor section). This study employed a Bayesian approach to examine the impact of prasinezumab on the progression of PD symptoms and signs. We used the BF in hypothesis testing. The BF is inherently comparative: it weighs the support for one model against that of another. Moreover, BFs do so by fully conditioning on the observed data. Otherwise, the P value depends on hypothetical outcomes that are more extreme than those observed in the sample. Such practice violates the likelihood principle and results in inconsistent or paradoxical conclusions. The BF can quantify evidence in favor of the null hypothesis. In the Bayesian framework, no special status is attached to either of the hypotheses under test; the BF assesses each model's predictive performance and expresses a preference for the model that made the most accurate forecasts. The fact that the BF can quantify evidence in favor of the null hypothesis can be of substantive importance. For instance, the hypothesis of interest may predict the absence of an effect across a varying set of conditions. Quantifying the null hypothesis is also important to learn whether the observed data provide evidence of absence or absence. Specifically, the possible outcomes of the BF can be assigned to three discrete categories: (1) evidence in favor of H 1 $$ {H}_1 $$ (ie, evidence in favor of the presence of an effect), (2) evidence in favor of H 0 $$ {H}_0 $$ (ie, evidence in favor of the absence of an effect), and (3) evidence that favors neither H 1 $$ {H}_1 $$ nor H 0 $$ {H}_0 $$ . Instead, the P value cannot provide a measure of evidence in favor of the null hypothesis. Finally, the BF is not affected by the sampling plan, that is, the intention with which the data were collected. This irrelevance follows from the likelihood principle, and it means that BFs may be computed and interpreted even when the intention with which the data are collected is ambiguous, unknown, or absent. All these advantages are not available if a classical analysis is performed as was done for the PASADENA trial data. Based on the findings shown in the first table of the source article21 (Table 1), a Bayesian analysis of the results obtained in these subpopulations was carried out. The results of the Bayesian analysis are shown in Table 2. The posterior probability column on the drug's effectiveness indicates no major and clinically relevant difference between the placebo and treated groups. The lack of efficacy applies to the population with and without rapid disease progression. The probability of efficacy is consistently less than 50% and near 50% only for the data-driven subphenotype diffuse malignant subgroup. The results support the notion that the drug's effects cannot be safely assessed. The findings are robust, as depicted in Figure 2, which shows no variation between the two hypotheses as the a priori changes; instead, there is only an increase in the BF for the same hypothesis. Additional analyses are described in Supporting Information Data S1 (Additional Bayesian Analyses section) and support the main results. Thus, there is no substantial evidence of a difference in efficacy between subpopulations with or without rapid progression. Ultimately, these results are consistent with the phase two PASADENA trial, which did not reach the primary end point at 52 weeks. In conclusion, the exploratory analysis to assess whether prasinezumab generates greater benefits on motor progression in prespecified subgroups with faster motor progression using the BF resulted in no supporting evidence. The negative findings related to the anti–α-synuclein approach confirm the many still unknown physiological and pathophysiological mechanisms controlled by the protein. Incorporation of the Bayesian approach in analyzing the efficacy of prasinezumab for the treatment of PD offers a number of important strategies for ongoing and future clinical trials, like adaptive designs to allow real-time decision-making and optimizing the trial parameters.23 The Bayesian framework also provides a probabilistic approach that quantifies uncertainty in treatment effects, thereby better informing decisions by stakeholders about modifications in trials, such as early stopping and expansion or changes in allocation ratios.24 Furthermore, Bayesian hierarchical models enable the assessment of individual variability in treatment responses, providing the groundwork for personalized treatment strategies.25 Beyond statistical and methodological issues, an additional point that should be considered when discussing the unsuccessful attempts to reach DMTs pertains to the disconnect between therapeutic strategies that are envisioned and tested in “clean and sanitized” clinical trials and the more difficult challenges offered by real-world settings. As recently discussed by Brett K. Beaulieu-Jones et al,26 research populations are studied among actively recruited individuals who often receive earlier diagnoses and comply with more consistent follow-ups. In contrast, in real-world populations, patients are diagnosed later in life and often exhibit a more rapid progression because of a combination of selection bias, multiple-hit comorbidity, late access to care, and intrinsic population differences.26 The study also highlighted bias in data collection. The mode of data gathering (actively recruited vs. passively recorded) introduces biases that must be carefully considered in clinical trial design and real-world analyses, ultimately affecting the validity of clinical outcomes. Somehow, the PASADENA trial mirrors findings from the Alzheimer's field in which multiple clinical trials targeting a single protein, amyloid, generated modest or null effects, substantially failing as disease-modifying intervention.27 In that regard, novel insights are promoting a reconceptualization of PD itself as more than a mere “synucleinopathy”, but rather a heterogeneous disorder arising from the convergence of multiple pathological processes but ultimately giving a variety of clinical manifestations. Most likely, “there is more than one Parkinson's Disease,”28 and our collective efforts should focus on dissecting the convergent and divergent mechanisms that act inside or outside the central nervous system. Research project: A. Conception, B. Organization, C. Execution; Statistical analysis: A. Design, B. Execution, C. Review and critique; Manuscript: A. Writing of the draft, B. Review and critique. MR: 1A, 1B, 1C, 2C, 3A, 3B. TC: 1A, 1C, 2A, 2B, 2C, 3A, 3B. DC: 1A, 1C, 2C, 3A, 3B. SLS: 1A, 1B, 1C, 2C, 3A, 3B. Open access publishing facilitated by Universita degli Studi Gabriele d'Annunzio Chieti Pescara, as part of the Wiley - CRUI-CARE agreement. S.L.S. is supported by research funding from the Italian Department of Health (RF-2013–02358785 and NET-2011-02346784-1), from the AIRAlzh Onlus (ANCC-COOP), from the Alzheimer’s Association—Part the Cloud: Translational Research Funding for Alzheimer’s Disease (18PTC-19-602325) and the Alzheimer’s Association—GAAIN Exploration to Evaluate Novel Alzheimer’s Queries (GEENA-Q-19-596282). The data that support the findings of this study are available from the corresponding author upon reasonable request. Data S1. Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Development of a diagnostic checklist to identify functional cognitive disorder versus other neurocognitive disorders
Verónica Cabreira, Jane Alty, Sonja Antic, Rui Araujo, Selma Aybek, Harriet A Ball, Gaston Baslet, Rohan Bhome, Jan Coebergh, Bruno Dubois, Mark Edwards, Sasa R Filipovic, Kristian Steen Frederiksen, Thomas Harbo, Bradleigh Hayhow, Robert Howard, Jonathan Huntley, Jeremy Darryl Isaacs, Curt LaFrance, Andrew Larner, Francesco Di Lorenzo, James Main, Elizabeth Mallam, Camillo Marra, João Massano, Emer R McGrath, Isabel Portela Moreira, Flavio Nobili, Suvankar Pal, Catherine M Pennington, Miguel Tábuas-Pereira, David Perez, Stoyan Popkirov, Dane Rayment, Martin Rossor, Mirella Russo, Isabel Santana, Jonathan Schott, Emmi P Scott, Ricardo Taipa, Tiago Teodoro, Michele Tinazzi, Svetlana Tomic, Sofia Toniolo, Caroline Winther Tørring, Tim Wilkinson, Martin Zeidler, Lisbeth Frostholm, Laura McWhirter, Jon Stone, Alan Carson
BMJ Neurology Open, 2025
BackgroundFunctional cognitive disorder (FCD) poses a diagnostic challenge due to its resemblance to other neurocognitive disorders and limited biomarker accuracy. We aimed to develop a new diagnostic checklist to identify FCD versus other neurocognitive disorders.MethodsThe clinical checklist was developed through mixed methods: (1) a literature review, (2) a three-round Delphi study with 45 clinicians from 12 countries and (3) a pilot discriminative accuracy study in consecutive patients attending seven memory services across the UK. Items gathering consensus were incorporated into a pilot checklist. Item redundancy was evaluated with phi coefficients. A briefer checklist was produced by removing items with >10% missing data. Internal validity was tested using Cronbach’s alpha. Optimal cut-off scores were determined using receiver operating characteristic curve analysis.ResultsA full 11-item checklist and a 7-item briefer checklist were produced. Overall, 239 patients (143 FCD, 96 non-FCD diagnoses) were included. The checklist scores were significantly different across subgroups (FCD and other neurocognitive disorders) (F(2, 236)=313.3, p<0.001). The area under the curve was excellent for both the full checklist (0.97, 95% CI 0.95 to 0.99) and its brief version (0.96, 95% CI 0.93 to 0.98). Optimal cut-off scores corresponded to a specificity of 97% and positive predictive value of 91% for identifying FCD. Both versions showed good internal validity (>0.80).ConclusionsThis pilot study shows that a brief clinical checklist may serve as a quick complementary tool to differentiate patients with neurodegeneration from those with FCD. Prospective blind large-scale validation in diverse populations is warranted.Cite Now
Neurological management of ischemic stroke in sickle cell disease– a case report with an updated review of the literature
C. Ciprietti, M. Russo, M. Santilli, S. Melchiorre, G. Polito, A. Thomas, S. L. Sensi
Neurological Sciences, 2025
Predicting conversion in cognitively normal and mild cognitive impairment individuals with machine learning: Is the CSF status still relevant?
Mirella Russo, Davide Nardini, Sara Melchiorre, Consuelo Ciprietti, Gaetano Polito, Miriam Punzi, Fedele Dono, Matteo Santilli, Astrid Thomas, Stefano L. Sensi, and
Alzheimer S and Dementia, 2025
Time to add two new disorders to neuropsychiatric aspects of Parkinson's disease
Stefano Luca Sensi, Matteo Alessandro De Rosa, Mirella Russo, Astrid Thomas, Marco Onofrj
Clinical Parkinsonism and Related Disorders, 2025
Perspectives on the diagnosis and management of functional cognitive disorder: An international Delphi study
Verónica Cabreira, Jane Alty, Sonja Antic, Rui Araújo, Selma Aybek, Harriet A. Ball, Gaston Baslet, Rohan Bhome, Jan Coebergh, Bruno Dubois, Mark Edwards, Saša R. Filipović, Kristian Steen Frederiksen, Thomas Harbo, Bradleigh Hayhow, Robert Howard, Jonathan Huntley, Jeremy Isaacs, William Curt LaFrance, Andrew J. Larner, Francesco Di Lorenzo, James Main, Elizabeth Mallam, Camillo Marra, João Massano, Emer R. McGrath, Laura McWhirter, Isabel Portela Moreira, Flavio Nobili, Catherine Pennington, Miguel Tábuas‐Pereira, David L. Perez, Stoyan Popkirov, Dane Rayment, Martin Rossor, Mirella Russo, Isabel Santana, Jonathan Schott, Emmi P. Scott, Ricardo Taipa, Michele Tinazzi, Svetlana Tomic, Sofia Toniolo, Caroline Winther Tørring, Tim Wilkinson, Lisbeth Frostholm, Jon Stone, Alan Carson
European Journal of Neurology, 2025
Psychiatric Disorders and Cognitive Fluctuations in Parkinson’s Disease: Changing Approaches in the First Decades of the 21st Century
Marco Onofrj, Matteo Alessandro De Rosa, Mirella Russo, Paola Ajdinaj, Dario Calisi, Astrid Thomas, Stefano Luca Sensi
Brain Sciences, 2024
Dancing sugar! A case of epilepsia partialis continua and subsequent belly dancing syndrome in a patient with a hyperosmolar hyperglycemic state
Davide Liviello, Sara Cipollone, Clarissa Corniello, Giacomo Evangelista, Laura Marzetti, Mirella Russo, Marco Onofrj, Fedele Dono, Stefano Sensi
Epileptic Disorders, 2024
Circulatory shock associated with left insular stroke and chronic steroid treatment
Mirella Russo, Fedele Dono, Marco Onofrj, Stefano L. Sensi
European Journal of Neurology, 2024
A case of benign recurrent abducens nerve palsy associated with chronic HBV infection
P. Quintieri, R. Speranza, M. Russo, F. Dono, M. Onofrj, S. L. Sensi
Neurological Sciences, 2024
A case of pediatric Guillain–Barré syndrome following hand–foot–and–mouth disease and the need for Brighton criteria revision in children
Giovanna Scorrano, Mirella Russo, Giovanni Prezioso, Stefano L. Sensi, Francesco Chiarelli
Acta Neurologica Belgica, 2023
The central role of the Thalamus in psychosis, lessons from neurodegenerative diseases and psychedelics
Marco Onofrj, Mirella Russo, Stefano Delli Pizzi, Danilo De Gregorio, Antonio Inserra, Gabriella Gobbi, Stefano L. Sensi
Translational Psychiatry, 2023
Autoimmune encephalitis during pregnancy: A diagnostic and therapeutic challenge—A systematic review with individual patients' analysis and clinical recommendations
Fedele Dono, Stefano Consoli, Maria Tappatà, Giacomo Evangelista, Mirella Russo, Jacopo Lanzone, Valeria Pozzilli, Bruna Nucera, Fabrizio Rinaldi, Martina Di Pietro, Lorenzo Tinti, Serena Troisi, Dario Calisi, Maria D'Apolito, Flavia Narducci, Giovanni Assenza, Francesca Anzellotti, Francesco Brigo, Catello Vollono, Marco Onofrj, Stefano L. Sensi, Roberto Michelucci
Epilepsia Open, 2023
Role of neurorehabilitation in the recovery of bilateral thalamic stroke related to the artery of Percheron anatomical variant
Gaetano Polito, Mirella Russo, Matteo Santilli, Cristina Cantarella, Carlo D'Aurizio, Stefano L Sensi
BMJ Case Reports, 2023
Heart rate variability modification as a predictive factor of sudden unexpected death in epilepsy: How far are we? A systematic review and meta-analysis
Giacomo Evangelista, Fedele Dono, Stefano Consoli, Jacopo Lanzone, Clarissa Corniello, Mirella Russo, Francesca Anzellotti, Marco Onofrj, Catello Vollono, Stefano L. Sensi
European Journal of Neurology, 2023
Diagnosis and treatment of late-onset myoclonic epilepsy in Down syndrome (LOMEDS): A systematic review with individual patients’ data analysis
Clarissa Corniello, Fedele Dono, Giacomo Evangelista, Stefano Consoli, Sibilla De Angelis, Sara Cipollone, Davide Liviello, Gaetano Polito, Sara Melchiorre, Mirella Russo, Alberto Granzotto, Francesca Anzellotti, Marco Onofrj, Astrid Thomas, Stefano L. Sensi
Seizure, 2023
Atypical progression of motor symptoms in facio-scapulo-humeral dystrophy: Clinical worsening or overlap?
Dario Calisi, Matteo A De Rosa, Mirella Russo, Stefano L Sensi
BMJ Case Reports, 2023
Heart rate variability modifications in adult patients with early versus late-onset temporal lobe epilepsy: A comparative observational study
Fedele Dono, Giacomo Evangelista, Stefano Consoli, Romina Venditti, Mirella Russo, Maria Vittoria De Angelis, Massimiliano Faustino, Angelo Di Iorio, Catello Vollono, Francesca Anzellotti, Marco Onofrj, Stefano L. Sensi
Neurophysiologie Clinique, 2023
Comparison of Machine Learning-based Approaches to Predict the Conversion to Alzheimer's Disease from Mild Cognitive Impairment
Raffaella Franciotti, Davide Nardini, Mirella Russo, Marco Onofrj, Stefano L. Sensi
Neuroscience, 2023
Correction to: Clinical presentation of strokes confined to the insula: a systematic review of literature (Neurological Sciences, (2021), 42, 5, (1697-1704), 10.1007/s10072-021-05109-1)
Vincenzo Di Stefano, Maria Vittoria De Angelis, Chiara Montemitro, Mirella Russo, Claudia Carrarini, Massimo di Giannantonio, Filippo Brighina, Marco Onofrj, David J. Werring, Robert Simister
Neurological Sciences, 2023
Biomarkers of diagnosis, prognosis, pathogenesis, response to therapy: Convergence or divergence? Lessons from Alzheimer's disease and synucleinopathies
Stefano L. Sensi, Mirella Russo, Pietro Tiraboschi
Handbook of Clinical Neurology, 2023
Functional Neurologic Disorders, disorders to be managed by neurologists, or are neurologists wandering in a dangerous field with inadequate resources?
Marco Onofrj, Paola Ajdinaj, Anna Digiovanni, Naveed Malek, Giovanni Martinotti, Filippo Maria Ferro, Mirella Russo, Astrid Thomas, Stefano Luca Sensi
Frontiers in Psychiatry, 2023
Bipolar spectrum disorders in neurologic disorders
Anna Digiovanni, Paola Ajdinaj, Mirella Russo, Stefano L. Sensi, Marco Onofrj, Astrid Thomas
Frontiers in Psychiatry, 2022
ECG monitoring of post-stroke occurring arrhythmias: an observational study using 7-day Holter ECG
Claudia Carrarini, V. Di Stefano, M. Russo, F. Dono, M. Di Pietro, N. Furia, M. Onofrj, L. Bonanni, M. Faustino, M. V. De Angelis
Scientific Reports, 2022
Altered Medial Prefrontal Connectivity in Parkinson's Disease Patients with Somatic Symptoms
Delli Pizzi Stefano, Raffaella Franciotti, Piero Chiacchiaretta, Antonio Ferretti, Richard A. Edden, Carlo Sestieri, Mirella Russo, Stefano L. Sensi, Marco Onofrj
Movement Disorders, 2022
Psychogenic non-epileptic seizures (PNES) in the COVID-19 pandemic era: A systematic review with individual patients' analysis.
Fedele Dono, Giacomo Evangelista, Stefano Consoli, Francesco Pasini, Mirella Russo, Bruna Nucera, Fabrizio Rinaldi, Giulia Battaglia, Catello Vollono, Francesco Brigo, Marco Onofrj, Stefano L. Sensi, Valerio Frazzini, Francesca Anzellotti
Journal of Psychosomatic Research, 2022
Migraine Pharmacological Treatment and Cognitive Impairment: Risks and Benefits
Mirella Russo, Matteo A. De Rosa, Dario Calisi, Stefano Consoli, Giacomo Evangelista, Fedele Dono, Matteo Santilli, Alberto Granzotto, Marco Onofrj, Stefano L. Sensi
International Journal of Molecular Sciences, 2022
COVID-19 and first manic episodes: a systematic review
Mirella Russo, Dario Calisi, Matteo A. De Rosa, Giacomo Evangelista, Stefano Consoli, Fedele Dono, Matteo Santilli, Francesco Gambi, Marco Onofrj, Massimo Di Giannantonio, Giustino Parruti, Stefano L. Sensi
Psychiatry Research, 2022
A Young Man with Cognitive Impairment and a Heart Condition
Mirella Russo, Matteo Santilli, Matteo A. De Rosa, Dario Calisi, Fedele Dono, Maria Vittoria Mattoli, Laura Bonanni, Marco Onofrj, Stefano L. Sensi
Journal of Alzheimer S Disease, 2022
Non convulsive refractory status epilepticus induced by thiocolchicoside (TCC) intrathecal injection: A case report
Giacomo Evangelista, Fedele Dono, Stefano Consoli, Valeria Pozzilli, Dario Calisi, Mirella Russo, Claudia D'Orazio, Anna D'Andreagiovanni, Giovanna Montesano, Sabina Rapini, Massimo Caulo, Marco Onofrj, Francesca Anzellotti
British Journal of Clinical Pharmacology, 2022
Perampanel enhances the cardiovagal tone and heart rate variability (HRV) in patients with drug-resistant temporal lobe epilepsy
Fedele Dono, Giacomo Evangelista, Stefano Consoli, Davide Rodorigo, Mirella Russo, Claudia Carrarini, Martina Di Pietro, Maria Vittoria De Angelis, Massimiliano Faustino, Francesca Anzellotti, Marco Onofrj, Angelo Di Iorio, Stefano L. Sensi, Valerio Frazzini, Catello Vollono
Seizure, 2022
Accuracy of the clinical diagnosis of dementia with Lewy bodies (DLB) among the Italian Dementia Centers: a study by the Italian DLB study group (DLB-SINdem)
Mirella Russo, Claudia Carrarini, Angelo Di Iorio, Raffaello Pellegrino, Amalia Cecilia Bruni, Salvatore Caratozzolo, Annalisa Chiari, Stefano Pretta, Camillo Marra, Maria Sofia Cotelli, Andrea Arighi, Giorgio G. Fumagalli, Tatiana Cataruzza, Francesca Caso, Cristina Paci, Mara Rosso, Serena Amici, David Giannandrea, Andrea Pilotto, Simona Luzzi, Annalisa Castellano, Fabrizia D’antonio, Antonina Luca, Giorgio Gelosa, Tommaso Piccoli, Marco Mauri, Federica Agosta, Claudio Babiloni, Barbara Borroni, Marco Bozzali, Massimo Filippi, Daniela Galimberti, Roberto Monastero, Cristina Muscio, Lucilla Parnetti, Daniela Perani, Laura Serra, Vincenzo Silani, Pietro Tiraboschi, Annachiara Cagnin, Alessandro Padovani, Laura Bonanni, Baschi Roberta, Fragiacomo Federica, Galantucci Sebastiano, Gaspari Caterina, Gazzola Gianmarco, Magnani Giuseppe, Mazzon Giulia, Mozzetta Stefano, Ravanelli Carmela, Ruggiero Marco, Salute Pierpaolo, Scamarcia Pietro Giuseppe, Turla Marinella, Verde Federico, Volontè Maria Antonietta, and
Neurological Sciences, 2022
Functional neurological disorder and somatic symptom disorder in Parkinson's disease
Marco Onofrj, Mirella Russo, Claudia Carrarini, Stefano Delli Pizzi, Astrid Thomas, Laura Bonanni, Alberto J. Espay, Stefano L. Sensi
Journal of the Neurological Sciences, 2022
Cortical network modularity changes along the course of frontotemporal and Alzheimer's dementing diseases
Raffaella Franciotti, Davide V Moretti, Alberto Benussi, Laura Ferri, Mirella Russo, Claudia Carrarini, Filomena Barbone, Dario Arnaldi, Nicola W Falasca, Giacomo Koch, Annachiara Cagnin, Flavio M Nobili, Claudio Babiloni, Barbara Borroni, Alessandro Padovani, Marco Onofrj, Laura Bonanni
Neurobiology of Aging, 2022
Levetiracetam Prophylaxis Therapy for Brain Tumor-Related Epilepsy (BTRE) Is Associated With a Higher Psychiatric Burden
Fedele Dono, Stefano Consoli, Giacomo Evangelista, Annalisa Ricci, Mirella Russo, Claudia Carrarini, Angelo Di Iorio, Laura Bonanni, Francesca Anzellotti, Marco Onofrj, Stefano L. Sensi
Frontiers in Neurology, 2022
Anti N-methyl-D-aspartate receptor (NMDAr) encephalitis during pregnancy: A case report
Fedele Dono, Giacomo Evangelista, Stefano Consoli, Giovanna Scorrano, Mirella Russo, Martina di Pietro, Marco Onofrj, Stefano L. Sensi, Francesca Anzellotti
Epilepsy and Behavior Reports, 2022
Muscarinic Receptors Expression in the Peripheral Blood Cells Differentiate Dementia with Lewy Bodies from Alzheimer's Disease
Marcella Reale, Claudia Carrarini, Mirella Russo, Fedele Dono, Laura Ferri, Martina Di Pietro, Erica Costantini, Annamaria Porreca, Marta Di Nicola, Marco Onofrj, Laura Bonanni
Journal of Alzheimer S Disease, 2022
A Machine Learning-Based Holistic Approach to Predict the Clinical Course of Patients within the Alzheimer's Disease Spectrum
Noemi Massetti, Mirella Russo, Raffaella Franciotti, Davide Nardini, Giorgio Maria Mandolini, Alberto Granzotto, Manuela Bomba, Stefano Delli Pizzi, Alessandra Mosca, Reinhold Scherer, Marco Onofrj, Stefano L. Sensi, , and
Journal of Alzheimer S Disease, 2022
Erratum to: A Machine Learning-Based Holistic Approach to Predict the Clinical Course of Patients within the Alzheimer's Disease Spectrum ([Journal of Alzheimer's Disease (2021) 85 (1639-1655) DOI: 10.3233/JAD-210573)
Noemi Massetti, Mirella Russo, Raffaella Franciotti, Davide Nardini, Giorgio Mandolini, et al.
Journal of Alzheimer S Disease, 2022
EEG Abnormalities During Delirium as a Prodromal Feature of Dementia with Lewy Bodies: A Case Report
Claudia Carrarini, Matteo Alessandro De Rosa, Dario Calisi, Anna Digiovanni, Pierpaolo Salute, Fedele Dono, Giacomo Evangelista, Stefano Consoli, Mirella Russo, Laura Ferri, Damiano D’Ardes, Maria Vittoria Mattoli, Francesco Cipollone, Marco Onofrj, Laura Bonanni
Journal of Alzheimer S Disease Reports, 2022
A case of Sars-Cov-2-related mania with prominent psychosis>
M. Russo, S. Consoli, M.A. De Rosa, D. Calisi, F. Dono, C. Carrarini, M. Onofrj, M.V. De Angelis, S.L. Sensi
Psychiatry Research, 2021
Preexisting Bipolar Disorder Influences the Subsequent Phenotype of Parkinson's Disease
Marco Onofrj, Angelo Di Iorio, Claudia Carrarini, Mirella Russo, Raffaella Franciotti, Alberto J. Espay, Laura S. Boylan, John‐Paul Taylor, Massimo Di Giannantonio, Giovanni Martinotti, Enza M. Valente, Astrid Thomas, Laura Bonanni, Stefano Delli Pizzi, Fedele Dono, StefanoL. Sensi
Movement Disorders, 2021
Late-onset Rasmussen encephalitis in Parry-Romberg syndrome: a case report
Giacomo Evangelista, Fedele Dono, Claudia Carrarini, Mirella Russo, Laura Bonanni
Neurological Sciences, 2021
The factitious/malingering continuum and its burden on public health costs: a review and experience in an Italian neurology setting
Marco Onofrj, Anna Digiovanni, Paola Ajdinaj, Mirella Russo, Claudia Carrarini, Massimo Di Giannantonio, Giovanni Martinotti, Stefano L. Sensi
Neurological Sciences, 2021
Visual evoked potential abnormalities in dementia with Lewy bodies
Claudia Carrarini, Mirella Russo, Giada Pagliaccio, Fedele Dono, Raffaella Franciotti, Giulia Deluca, Stefania Nanni, Antonio Saracino, Marco Onofrj, Laura Bonanni
Neurophysiologie Clinique, 2021
New daily persistent headache after SARS-CoV-2 infection: a report of two cases
Fedele Dono, Stefano Consoli, Giacomo Evangelista, Maria D’Apolito, Mirella Russo, Claudia Carrarini, Dario Calisi, Matteo De Rosa, Martina Di Pietro, Maria Vittoria De Angelis, Daniela Travaglini, Stefano L. Sensi, Marco Onofrj, Laura Bonanni
Neurological Sciences, 2021
Delirium in COVID-19 patients: a multicentric observational study in Italy
Giovanni Martinotti, Laura Bonanni, Stefano Barlati, Andrea Miuli, Gianna Sepede, Davide Prestia, Alice Trabucco, Claudia Palumbo, Alessandra Massaro, Martina Olcese, Damiano D’Ardes, Francesco Cipollone, Mario Amore, Emi Bondi, Mirella Russo, Claudia Carrarini, Marco Onofrj, Stefano Luca Sensi, Antonio Vita, Massimo di Giannantonio
Neurological Sciences, 2021
A Critical Review of Alien Limb-Related Phenomena and Implications for Functional Magnetic Resonance Imaging Studies
Martina Di Pietro, Mirella Russo, Fedele Dono, Claudia Carrarini, Astrid Thomas, Vincenzo Di Stefano, Roberta Telese, Laura Bonanni, Stefano L. Sensi, Marco Onofrj, Raffaella Franciotti
Frontiers in Neurology, 2021
An Atypical Presentation of CLIPPERS, a Challenging Diagnosis of Reversible Early-Onset Dementia
Mirella Russo, Alberto Piermartiri, Claudia Carrarini, Fedele Dono, Maria Vittoria De Angelis, Stefano L. Sensi, Marco Onofrj, Laura Bonanni
Case Reports in Neurology, 2021
Cognitive dysfunction in amyotrophic lateral sclerosis: can we predict it?
Fabiola De Marchi, , Claudia Carrarini, Antonio De Martino, Luca Diamanti, Antonio Fasano, Antonino Lupica, Mirella Russo, Simone Salemme, Edoardo Gioele Spinelli, Alessandro Bombaci
Neurological Sciences, 2021
Clinical presentation of strokes confined to the insula: a systematic review of literature
Vincenzo Di Stefano, Maria Vittoria De Angelis, Chiara Montemitro, Mirella Russo, Claudia Carrarini, Massimo di Giannantonio, Filippo Brighina, Marco Onofrj, David J. Werring, Robert Simister
Neurological Sciences, 2021
Status epilepticus and COVID-19: A systematic review
Fedele Dono, Bruna Nucera, Jacopo Lanzone, Giacomo Evangelista, Fabrizio Rinaldi, Rino Speranza, Serena Troisi, Lorenzo Tinti, Mirella Russo, Martina Di Pietro, Marco Onofrj, Laura Bonanni, Giovanni Assenza, Catello Vollono, Francesca Anzellotti, Francesco Brigo
Epilepsy and Behavior, 2021
Being the Family Caregiver of a Patient With Dementia During the Coronavirus Disease 2019 Lockdown
Milena Zucca, Valeria Isella, Raffaele Di Lorenzo, Camillo Marra, Annachiara Cagnin, Chiara Cupidi, Laura Bonanni, Valentina Laganà, Elisa Rubino, Nicola Vanacore, Federica Agosta, Paolo Caffarra, Renato Sambati, Davide Quaranta, Valeria Guglielmi, Ildebrando M. Appollonio, Giancarlo Logroscino, Massimo Filippi, Gioacchino Tedeschi, Carlo Ferrarese, Innocenzo Rainero, Amalia C. Bruni, and
Frontiers in Aging Neuroscience, 2021
Agitation and Dementia: Prevention and Treatment Strategies in Acute and Chronic Conditions
Claudia Carrarini, Mirella Russo, Fedele Dono, Filomena Barbone, Marianna G. Rispoli, Laura Ferri, Martina Di Pietro, Anna Digiovanni, Paola Ajdinaj, Rino Speranza, Alberto Granzotto, Valerio Frazzini, Astrid Thomas, Andrea Pilotto, Alessandro Padovani, Marco Onofrj, Stefano L. Sensi, Laura Bonanni
Frontiers in Neurology, 2021
Low molecular weight heparin in COVID-19 patients prevents delirium and shortens hospitalization
Damiano D’Ardes, Claudia Carrarini, Mirella Russo, Fedele Dono, Rino Speranza, Anna Digiovanni, Giovanni Martinotti, Angelo Di Iorio, Marco Onofrj, Francesco Cipollone, Laura Bonanni
Neurological Sciences, 2021
The Impact of COVID-19 Quarantine on Patients With Dementia and Family Caregivers: A Nation-Wide Survey
Innocenzo Rainero, Amalia C. Bruni, Camillo Marra, Annachiara Cagnin, Laura Bonanni, Chiara Cupidi, Valentina Laganà, Elisa Rubino, Alessandro Vacca, Raffaele Di Lorenzo, Paolo Provero, Valeria Isella, Nicola Vanacore, Federica Agosta, Ildebrando Appollonio, Paolo Caffarra, Cinzia Bussè, Renato Sambati, Davide Quaranta, Valeria Guglielmi, Giancarlo Logroscino, Massimo Filippi, Gioacchino Tedeschi, Carlo Ferrarese, and
Frontiers in Aging Neuroscience, 2021
New-onset refractory status epilepticus (NORSE) in post SARS-CoV-2 autoimmune encephalitis: a case report
Fedele Dono, Claudia Carrarini, Mirella Russo, Maria Vittoria De Angelis, Francesca Anzellotti, Marco Onofrj, Laura Bonanni
Neurological Sciences, 2021
Plasma neurofilament light chain predicts cognitive progression in prodromal and clinical dementia with lewy bodies
Andrea Pilotto, Alberto Imarisio, Claudia Carrarini, Mirella Russo, Stefano Masciocchi, Stefano Gipponi, Elisabetta Cottini, Dag Aarsland, Henrik Zetterberg, Nicholas J. Ashton, Abdul Hye, Laura Bonanni, Alessandro Padovani
Journal of Alzheimer S Disease, 2021
Hyperconnectivity in Dementia Is Early and Focal and Wanes with Progression
Laura Bonanni, Davide Moretti, Alberto Benussi, Laura Ferri, Mirella Russo, Claudia Carrarini, Filomena Barbone, Dario Arnaldi, Nicola Walter Falasca, Giacomo Koch, Annachiara Cagnin, Flavio Nobili, Claudio Babiloni, Barbara Borroni, Alessandro Padovani, Marco Onofrj, Raffaella Franciotti, and
Cerebral Cortex, 2021
Diaphragmatic myoclonus due to SARS-CoV-2 infection
Barbara Borroni, Stefano Gazzina, Fedele Dono, Valentina Mazzoleni, Paolo Liberini, Claudia Carrarini, Mirella Russo, Michela Pontolillo, Jacopo Vecchiet, M. Onofrj, Laura Bonanni
Neurological Sciences, 2020
Behavioral and psychological effects of coronavirus disease-19 quarantine in patients with dementia
Annachiara Cagnin, Raffaele Di Lorenzo, Camillo Marra, Laura Bonanni, Chiara Cupidi, Valentina Laganà, Elisa Rubino, Alessandro Vacca, Paolo Provero, Valeria Isella, Nicola Vanacore, Federica Agosta, Ildebrando Appollonio, Paolo Caffarra, Ilaria Pettenuzzo, Renato Sambati, Davide Quaranta, Valeria Guglielmi, Giancarlo Logroscino, Massimo Filippi, Gioacchino Tedeschi, Carlo Ferrarese, Innocenzo Rainero, Amalia C. Bruni, and
Frontiers in Psychiatry, 2020
Interictal Heart Rate Variability Analysis Reveals Lateralization of Cardiac Autonomic Control in Temporal Lobe Epilepsy
Fedele Dono, Giacomo Evangelista, Valerio Frazzini, Catello Vollono, Claudia Carrarini, Mirella Russo, Camilla Ferrante, Vincenzo Di Stefano, Luciano P. Marchionno, Maria V. De Angelis, Massimiliano Faustino, Laura Bonanni, Marco Onofrj, Stefano L. Sensi, Francesca Anzellotti
Frontiers in Neurology, 2020
Psychogenic Non-epileptic Seizures and Pseudo-Refractory Epilepsy, a Management Challenge
Francesca Anzellotti, Fedele Dono, Giacomo Evangelista, Martina Di Pietro, Claudia Carrarini, Mirella Russo, Camilla Ferrante, Stefano L. Sensi, Marco Onofrj
Frontiers in Neurology, 2020
Posterior variant of alien limb syndrome with sudden clinical onset as self-hitting associated with thalamic stroke
Mirella Russo, Claudia Carrarini, Fedele Dono, Vincenzo Di Stefano, Maria Vittoria De Angelis, Marco Onofrj, Stefano L. Sensi
Case Reports in Neurology, 2020
A stage-based approach to therapy in parkinson’s disease
Claudia Carrarini, Mirella Russo, Fedele Dono, Martina Di Pietro, Marianna G. Rispoli, Vincenzo Di Stefano, Laura Ferri, Filomena Barbone, Michela Vitale, Astrid Thomas, Stefano Luca Sensi, Marco Onofrj, Laura Bonanni
Biomolecules, 2019
Asymptomatic carotid acute dissection following focal status epilepticus
Fedele Dono, Francesca Anzellotti, Mirella Russo, Claudia Carrarini, Stefania Nanni, Camilla Ferrante, Maria Vittoria De Angelis, Marco Onofrj
Epilepsy and Behavior Case Reports, 2019
Somatic symptoms disorders in Parkinson's disease are related to default mode and salience network dysfunction
Raffaella Franciotti, Stefano Delli Pizzi, Mirella Russo, Claudia Carrarini, Danilo Carrozzino, Bernardo Perfetti, Marco Onofrj, Laura Bonanni
Neuroimage Clinical, 2019
Lateralized periodic discharges in insular status epilepticus: A case report of a periodic EEG pattern associated with ictal manifestation
Fedele Dono, Mirella Russo, Claudia Carrarini, Vincenzo Di Stefano, Stefania Nanni, Camilla Ferrante, Marco Onofrj, Francesca Anzellotti
Clinical Neurophysiology Practice, 2019
The pharmacology of visual hallucinations in synucleinopathies
Mirella Russo, Claudia Carrarini, Fedele Dono, Marianna Gabriella Rispoli, Martina Di Pietro, Vincenzo Di Stefano, Laura Ferri, Laura Bonanni, Stefano Luca Sensi, Marco Onofrj
Frontiers in Pharmacology, 2019
Case of posterior cortical atrophy (PCA) evolved to PCA-CBS
Nicola Salvadori, Mirella Russo, Leonardo Biscetti, Katia D’ Andrea, Massimo Eugenio Dottorini, Lucilla Parnetti
BMJ Case Reports, 2018
The Italian version of cognitive function instrument (CFI): reliability and validity in a cohort of healthy elderly
Elena Chipi, Giulia Frattini, Paolo Eusebi, Anita Mollica, Katia D’Andrea, Mirella Russo, Alice Bernardelli, Chiara Montanucci, Elisa Luchetti, Paolo Calabresi, Lucilla Parnetti
Neurological Sciences, 2018

Mirella Russo

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