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2. Plasma Aβ42 as biomarker of prodromal AD progression in patients with amnestic mild cognitive impairment: evidence from the PharmaCog/E-ADNI study

Author

Albani, Diego, Marizzoni, Moira, Ferrari, Clarissa, Fusco, Federica, Boeri, Lucia, Raimondi, Ilaria, Jovicich, Jorge, Babiloni, Claudio, Soricelli, Andrea, Lizio, Roberta, Galluzzi, Samantha, Cavaliere, Libera, Didic, Mira, Schönknecht, Peter, Molinuevo, José Luis, Nobili, Flavio, Parnetti, Lucilla, Payoux, Pierre, Bocchio, Luisella, Salvatore, Marco, Rossini, Paolo Maria, Tsolaki, Magda, Visser, Pieter Jelle, Richardson, Jill, Wiltfang, Jens, Bordet, Régis, Blin, Olivier, Forloni, Gianluigi, Frisoni, Giovanni, IRCCS - Istituto di Ricerche Farmacologiche 'Mario Negri' [Milan, Italy], Centro San Giovanni di Dio, Fatebenefratelli, Brescia (IRCCS), Università degli Studi di Brescia = University of Brescia (UniBs), University of Trento [Trento], Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), IRCCS-Hospital San Raffaele Pisana of Rome and Cassino, SDN - Istituto di Ricerca Diagnostica e Nucleare, Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital de la Timone [CHU - APHM] (TIMONE), Universität Leipzig, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Università degli studi di Genova = University of Genoa (UniGe), Università degli Studi di Perugia = University of Perugia (UNIPG), Imagerie cérébrale et handicaps neurologiques (ICHN), Institut des sciences du cerveau de Toulouse. (ISCT), Université Toulouse - Jean Jaurès (UT2J), Université de Toulouse (UT)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse - Jean Jaurès (UT2J), Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Università cattolica del Sacro Cuore = Catholic University of the Sacred Heart [Roma] (Unicatt), Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Aristotle University of Thessaloniki, Vrije Universiteit Medical Centre (VUMC), Vrije Universiteit Amsterdam [Amsterdam] (VU), GlaxoSmithKline [Stevenage, UK] (GSK), GlaxoSmithKline [Headquarters, London, UK] (GSK), Universität Duisburg-Essen = University of Duisburg-Essen [Essen], Georg-August-University = Georg-August-Universität Göttingen, CIDMA - University of Aveiro, Troubles cognitifs dégénératifs et vasculaires - U 1171 - EA 1046 (TCDV), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), CHU Lille, Institut de Neurosciences de la Timone (INT), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Université de Genève = University of Geneva (UNIGE), University of Duisburg-Essen, Troubles cognitifs dégénératifs et vasculaires - U 1171 (TCDV), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)

Subjects
Clinical trial, Clusterin, amnesic mild cognitive impairment (aMCI), [SCCO.NEUR]Cognitive science/Neuroscience, mental disorders, PharmaCog project, Amyloid-beta peptide, Biomarkers, Prodromal Alzheimer's disease
Abstract

International audience; It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. Here, we addressed this question starting from data of the European FP7 IMI-PharmaCog/E-ADNI longitudinal study in amnesic mild cognitive impairment (aMCI) patients including biological, clinical, neuropsychological (e.g., ADAS-Cog13), neuroimaging, and electroencephalographic measures. PharmaCog/E-ADNI patients were classified as "positive" (i.e., "prodromal AD" n = 76) or "negative" (n = 52) based on a diagnostic cut-off of Aβ42/P-tau in cerebrospinal fluid as well as APOE ε 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Aβ42, Aβ40) and apolipoprotein J (clusterin, CLU) were assessed. Linear Mixed Models found no significant differences in plasma molecules between the "positive" (i.e., prodromal AD) and "negative" groups at baseline. In contrast, plasma Aβ42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Aβ40 increased, but similarly in the two groups. Furthermore, plasma Aβ42 correlated with the ADAS-Cog13 score both in aMCI patients as a whole and the prodromal AD group alone. Finally, CLU correlated with the ADAS-Cog13 only in the whole aMCI group, and no association with ADAS-Cog13 was found for Aβ40. In conclusion, plasma Aβ42 showed disease progression-related features in aMCI patients with prodromal AD.

Published
2019

3. Plasma Aβ₄₂ as a biomarker of prodromal Alzheimer's disease progression in patients with amnestic mild cognitive impairment : Evidence from the PharmaCog/E-ADNI Study

Author

Albani, Diego, Marizzoni, Moira, Ferrari, Clarissa, Fusco, Federica, Boeri, Lucia, Raimondi, Ilaria, Jovicich, Jorge, Babiloni, Claudio, Soricelli, Andrea, Lizio, Roberta, Galluzzi, Samantha, Cavaliere, Libera, Didic, Mira, Schönknecht, Peter, Molinuevo, José Luis, Nobili, Flavio, Parnetti, Lucilla, Payoux, Pierre, Bocchio, Luisella, Salvatore, Marco, Rossini, Paolo Maria, Tsolaki, Magda, Visser, Pieter Jelle, Richardson, Jill C., Wiltfang, Jens, Bordet, Régis, Blin, Olivier, Forloni, Gianluigi, and Frisoni, Giovanni B.

Subjects
Medizin
Published
2019

5. Neurobiological and clinical effect of metacognitive interpersonal therapy vs structured clinical model: study protocol for a randomized controlled trial.

Author

Magni, Laura Rosa, Carcione, Antonino, Ferrari, Clarissa, Semerari, Antonio, Riccardi, Ilaria, Nicolo', Giuseppe, Lanfredi, Mariangela, Pedrini, Laura, Cotelli, Maria, Bocchio, Luisella, Pievani, Michela, Gasparotti, Roberto, and Rossi, Roberta

Subjects
INTERPERSONAL psychotherapy, METACOGNITIVE therapy, RANDOMIZED controlled trials, FUNCTIONAL magnetic resonance imaging, BORDERLINE personality disorder
Abstract

Background: Borderline Personality Disorder (BPD) is a complex and debilitating disorder, characterized by deficits in metacognition and emotion dysregulation. The "gold standard" treatment for this disorder is psychotherapy with pharmacotherapy as an adjunctive treatment to target state symptoms. The present randomized clinical trial aims to assess the clinical and neurobiological changes following Metacognitive Interpersonal Therapy (MIT) compared with Structured Clinical Management (SCM) derived from specific recommendations in APA (American Psychiatric Association) guidelines for BPD. Methods: The study design is a randomized parallel controlled clinical trial and will include 80 BPD outpatients, aged 18–45 enrolled at 2 recruitment centers. Primary outcome will be the clinical change in emotion regulation capacities assessed with the Difficulties in Emotion Regulation Scale (DERS). We will also investigated the effect of psychotherapy on metacognitive abilities and several clinical features such as BPD symptomatology, general psychopathology, depression, personal functioning, and trait dimensions (anger, impulsivity, alexithymia). We will evaluate changes in brain connectivity patterns and during the view of emotional pictures. A multidimensional assessment will be performed at the baseline, at 6, 12, 18 months. We will obtain structural and functional Magnetic Resonance Images (MRIs) in MIT-Treated BPD (N = 30) and SCM-treated BPD (N = 30) at baseline and after treatment, as well as in a group of 30 healthy and unrelated volunteers that will be scanned once for comparison. Discussion: The present study could contribute to elucidate the neurobiological mechanisms underlying psychotherapy efficacy. The inclusion of a multidisciplinary study protocol will allow to study BPD considering different features that can affect the treatment response and their reciprocal relationships. Trial registration: NCT02370316. Registered 02/24/2015. [ABSTRACT FROM AUTHOR]

Published
2019
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8. Plasma Aβ42 as a Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study.

Author

Albani D, Marizzoni M, Ferrari C, Fusco F, Boeri L, Raimondi I, Jovicich J, Babiloni C, Soricelli A, Lizio R, Galluzzi S, Cavaliere L, Didic M, Schönknecht P, Molinuevo JL, Nobili F, Parnetti L, Payoux P, Bocchio L, Salvatore M, Rossini PM, Tsolaki M, Visser PJ, Richardson JC, Wiltfang J, Bordet R, Blin O, Forloni G, and Frisoni GB

Subjects
Aged, Alzheimer Disease blood, Alzheimer Disease physiopathology, Amnesia physiopathology, Biomarkers blood, Brain physiopathology, Cognitive Dysfunction physiopathology, Disease Progression, Electroencephalography, Female, Humans, Longitudinal Studies, Male, Middle Aged, Prodromal Symptoms, Alzheimer Disease diagnosis, Amnesia blood, Amyloid beta-Peptides blood, Cognitive Dysfunction blood, Peptide Fragments blood
Abstract

It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. Here, we addressed this question starting from data of the European FP7 IMI-PharmaCog/E-ADNI longitudinal study in amnesic mild cognitive impairment (aMCI) patients including biological, clinical, neuropsychological (e.g., ADAS-Cog13), neuroimaging, and electroencephalographic measures. PharmaCog/E-ADNI patients were classified as "positive" (i.e., "prodromal AD" n = 76) or "negative" (n = 52) based on a diagnostic cut-off of Aβ42/P-tau in cerebrospinal fluid as well as APOE ε 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Aβ42, Aβ40) and apolipoprotein J (clusterin, CLU) were assessed. Linear Mixed Models found no significant differences in plasma molecules between the "positive" (i.e., prodromal AD) and "negative" groups at baseline. In contrast, plasma Aβ42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Aβ40 increased, but similarly in the two groups. Furthermore, plasma Aβ42 correlated with the ADAS-Cog13 score both in aMCI patients as a whole and the prodromal AD group alone. Finally, CLU correlated with the ADAS-Cog13 only in the whole aMCI group, and no association with ADAS-Cog13 was found for Aβ40. In conclusion, plasma Aβ42 showed disease progression-related features in aMCI patients with prodromal AD.

Published
2019
Full Text
View/download PDF

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