المؤلفون: Elena Nardi Cesarini, Cinzia Costa, Paolo Calabresi, Paolo Maria Rossini, Michele Romoli, Francesca Miraglia, Fabrizio Vecchio, Francesca Alù

المصدر: Journal of Alzheimer's disease : JAD. 88(3)

مصطلحات موضوعية: Male, Pediatrics, medicine.medical_specialty, Population, Cognitive decline, Pilot Projects, Electroencephalography, Neuropsychological Tests, Risk Assessment, late onset epilepsy of unknown etiology, Epilepsy, mild cognitive impairment, Medicine, Dementia, Humans, Cognitive Dysfunction, Neuropsychological assessment, education, electroencephalography network small-world analysis, Aged, education.field_of_study, medicine.diagnostic_test, business.industry, General Neuroscience, Cognition, General Medicine, medicine.disease, Psychiatry and Mental health, Clinical Psychology, Neurology, Etiology, Female, Neurology (clinical), Geriatrics and Gerontology, business

الوصف: Background: Although people with late onset epilepsy of unknown etiology (LOEU) are at higher risk of cognitive decline compared to the general population, we still lack affordable tools to predict and stratify their risk of dementia. Objective: This pilot-study investigates the potential application of electroencephalography (EEG) network small-world (SW) properties in predicting cognitive decline among patients with LOEU. Methods: People diagnosed with LOEU and normal cognitive examination at the time of epilepsy diagnosis were included. Cerebrospinal fluid biomarkers, brain imaging, and neuropsychological assessment were performed at the time of epilepsy diagnosis. Baseline EEG was analyzed for SW properties. Patients were followed-up over time with neuropsychological testing to define the trajectory of cognitive decline. Results: Over 5.1 years of follow-up, among 24 patients diagnosed with LOEU, 62.5% were female, mean age was 65.3 years, thirteen developed mild cognitive impairment (MCI), and four developed dementia. Patients with LOEU developing MCI had lower values of SW coefficients in the delta (p = 0.03) band and higher SW values in the alpha frequency bands (p = 0.02) compared to patients having normal cognition at last follow-up. The two separate ANOVAs, for low and alpha bands, confirmed an interaction between SW and cognitive decline at follow-up. A similar gradient was confirmed for patients developing dementia compared to those with normal cognitive function as well as to those developing MCI. Conclusion: Baseline EEG analysis through SW is worth investigating as an affordable, widely available tool to stratify LOEU patients for their risk of cognitive decline.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6a8b818561c5a3971fc6e4304d1fd52eTest
https://pubmed.ncbi.nlm.nih.gov/34842184Test

المؤلفون: Chiara Bedetti, Claudio Liguori, Cinzia Costa, Andrea Romigi, Paolo Eusebi, Elena Nardi Cesarini, Lucia Farotti, Paolo Calabresi, Michele Romoli, Lucilla Parnetti, Sabrina Siliquini, Nicola Biagio Mercuri

المصدر: Neurobiology of Aging. 73:61-67

مصطلحات موضوعية: Male, 0301 basic medicine, Aging, medicine.medical_specialty, Time Factors, Amyloid, Disease, Late Onset Disorders, 03 medical and health sciences, Epilepsy, 0302 clinical medicine, Alzheimer Disease, Internal medicine, 80 and over, medicine, Humans, Dementia, Cognitive Dysfunction, Prospective Studies, Cognitive decline, Prospective cohort study, CSF biomarkers, Pathological, Aged, Aged, 80 and over, Neuroscience (all), Amyloid beta-Peptides, business.industry, General Neuroscience, Neuropsychology, Beta amyloid, Alzheimer's disease, Middle Aged, medicine.disease, Peptide Fragments, Settore MED/26 - NEUROLOGIA, 030104 developmental biology, Disease Progression, Neurology (clinical), Developmental Biology, Geriatrics and Gerontology, Female, business, Biomarkers, 030217 neurology & neurosurgery, Follow-Up Studies

الوصف: Although amyloid pathology plays a role in epilepsy, little is known about the relationship between beta amyloid and progression to Alzheimer's disease (AD) among patients with late-onset epilepsy of unknown origin (LOEU). This multicenter, observational, prospective study enrolled 40 consecutive nondemented adults diagnosed with LOEU, together with 43 age- and sex-matched healthy controls. All patients completed neuropsychological tests, core CSF AD biomarkers assessment (Aβ1-42, total tau, and phosphorylated tau), and follow-up for a mean of 3 years to verify cognitive decline. Despite age and baseline cognitive performance were similar to healthy controls, patients with LOEU had significant prevalence of CSF pathological Aβ1-42 (

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ec2ca354050b1c59c5fe4a05799c3addTest
https://doi.org/10.1016/j.neurobiolaging.2018.09.006Test

المؤلفون: Alessandro Mechelli, Salvatore Novello, Alessandro Tozzi, Paolo Calabresi, Valentina Durante, Michele Morari, Cinzia Costa, Guendalina Bastioli, Andrea Mancini, Petra Mazzocchetti, Massimiliano Di Filippo

المصدر: Neurobiology of Disease, Vol 118, Iss, Pp 1-8 (2018)

مصطلحات موضوعية: 0301 basic medicine, Male, Parkinson's disease, Dopamine, Inbred C57BL, Synaptic Transmission, Transgenic, Mice, 0302 clinical medicine, Receptors, Mice, Knockout, Chemistry, Electrophysiology, Settore MED/26 - NEUROLOGIA, Neurology, Dopamine Agonists, NMDA receptor, medicine.drug, medicine.medical_specialty, Quinpirole, Knockout, Lrrk2, Mouse model, Glutamic Acid, Mice, Transgenic, AMPA receptor, Neurotransmission, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, NO, lcsh:RC321-571, 03 medical and health sciences, Glutamatergic, Parkinsonian Disorders, Dopamine receptor D2, Internal medicine, Genetic model, Dopamine D2, medicine, Animals, Kinase activity, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Corpus Striatum, Excitatory Postsynaptic Potentials, Mice, Inbred C57BL, Receptors, Dopamine D2, nervous system diseases, 030104 developmental biology, Endocrinology, 030217 neurology & neurosurgery

الوصف: Among genetic abnormalities identified in Parkinson's disease (PD), mutations of the leucine-rich repeat kinase2 (LRRK2) gene, such as the G2019S missense mutation linked to enhanced kinase activity, are the most common. While the complex role of LRRK2 has not been fully elucidated, evidence that mutated kinase activity affects synaptic transmission has been reported. Thus, our aim was to explore possible early alterations of neurotransmission produced by the G2019S LRRK2 mutation in PD. We performed electrophysiological patch-clamp recordings of striatal spiny projection neurons (SPNs) in the G2019S-Lrrk2 knock-in (KI) mouse model of PD, in D1994S kinase-dead (KD), Lrrk2 knock-out (KO) and wild-type (WT) mice. In G2019S Lrrk2 KI mice, basal spontaneous glutamatergic transmission, synaptic facilitation, and NMDA/AMPA ratios were unchanged, whereas the stimulation of dopamine (DA) D2 receptor by quinpirole reduced the spontaneous and evoked excitatory postsynaptic currents (EPSC). Quinpirole reduced the EPSC amplitude of SPNs in KI but not in KD, KO and WT mice, suggesting that the enhanced LRRK2 kinase activity induced by the G2019S mutation is associated with the observed functional alteration of SPNs synaptic transmission. The effect of quinpirole was mediated by a phospholipase C (PLC)-dependent release of endocannabinoid, with subsequent activation of presynaptic cannabinoid receptor 1 and reduced release of glutamate. The key role of DA D2 receptor in reducing glutamatergic output in our LRRK2 genetic model of PD further supports the use of DA agonists in the treatment of early PD patients with LRRK2 mutations to counteract the disease progression.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f231f9567e956e7c3d6dd4ca5b8de3b8Test
http://www.sciencedirect.com/science/article/pii/S0969996118301852Test

المؤلفون: Massimiliano Di Filippo, Andrea Mancini, Laura Bellingacci, Lorenzo Gaetani, Petra Mazzocchetti, Teresa Zelante, Livia La Barbera, Antonella De Luca, Michela Tantucci, Alessandro Tozzi, Valentina Durante, Miriam Sciaccaluga, Alfredo Megaro, Davide Chiasserini, Nicola Salvadori, Viviana Lisetti, Emilio Portaccio, Cinzia Costa, Paola Sarchielli, Maria Pia Amato, Lucilla Parnetti, Maria Teresa Viscomi, Luigina Romani, Paolo Calabresi

مصطلحات موضوعية: Male, Encephalomyelitis, Autoimmune, Experimental, hippocampus, Knockout, Long-Term Potentiation, experimental autoimmune encephalomyelitis, Spatial Learning, neuroimmunology, multiple sclerosis, Inbred C57BL, p38 Mitogen-Activated Protein Kinases, General Biochemistry, Genetics and Molecular Biology, interleukin-17, Mice, Biozzi, Experimental, Mice, Cognition, Receptors, Animals, Hippocampal, Encephalomyelitis, CA1 Region, Hippocampal, cognitive impairment, Mice, Knockout, Behavior, synaptic plasticity, Receptors, Interleukin-17, Neuronal Plasticity, Behavior, Animal, Animal, CA1 Region, Mice, Inbred C57BL, inflammation, Synapses, Biozzi, Settore BIO/17 - ISTOLOGIA, Signal Transduction, Autoimmune

الوصف: Cognitive impairment (CI) is a disabling concomitant of multiple sclerosis (MS) with a complex and controversial pathogenesis. The cytokine interleukin-17A (IL-17A) is involved in the immune pathogenesis of MS, but its possible effects on synaptic function and cognition are still largely unexplored. In this study, we show that the IL-17A receptor (IL-17RA) is highly expressed by hippocampal neurons in the CA1 area and that exposure to IL-17A dose-dependently disrupts hippocampal long-term potentiation (LTP) through the activation of its receptor and p38 mitogen-activated protein kinase (MAPK). During experimental autoimmune encephalomyelitis (EAE), IL-17A overexpression is paralleled by hippocampal LTP dysfunction. An in vivo behavioral analysis shows that visuo-spatial learning abilities are preserved when EAE is induced in mice lacking IL-17A. Overall, this study suggests a key role for the IL-17 axis in the neuro-immune cross-talk occurring in the hippocampal CA1 area and its potential involvement in synaptic dysfunction and MS-related CI.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::350e0570178a4278a38ba221e16a2872Test
http://hdl.handle.net/10807/198244Test

المؤلفون: Magdalena Sauvage, Jill R. Crittenden, Shenyu Zhai, Cinzia Costa, Walker S. Jackson, Anne C. Smith, Veronica Ghiglieri, David E. Housman, David Sulzer, Ann M. Graybiel, Giuseppina Martella, D. James Surmeier, Takashi Kitsukawa, Eric Burguière, Karen A. Pescatore, Ellen M. Unterwald, Barbara Picconi, Hui Zhang, Morgane Thomsen, Paolo Calabresi, S. Barak Caine

المساهمون: McGovern Institute for Brain Research [Cambridge], Massachusetts Institute of Technology (MIT), Department of Brain and Cognitive Sciences, Feinberg School of Medicine, Northwestern University [Evanston], Graduate School of Frontier Biosciences [Osaka], Osaka University [Osaka], Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), McLean Hospital [Belmont, Ma.], Harvard Medical School [Boston] (HMS), New York State Psychiatric Institute, Columbia University [New York], Università degli Studi di Perugia (UNIPG), Fondazione Santa Lucia [IRCCS], Clinical and Behavioral Neurology [IRCCS Santa Lucia], Universita Vita Salute San Raffaele = Vita-Salute San Raffaele University [Milan, Italie] (UniSR), Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS San Raffaele Pisana), Temple University [Philadelphia], Pennsylvania Commonwealth System of Higher Education (PCSHE), Linköping University (LIU), Fondazione Policlinico Universitario Agostino Gemelli IRCCS, University of Arizona, Northwestern University Medical School [Chicago], CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Jefferson (Philadelphia University + Thomas Jefferson University), IRCCS San Raffaele Pisana, Temple University School of Medicine, Università cattolica del Sacro Cuore [Roma] (Unicatt), Gestionnaire, Hal Sorbonne Université, Institut du Cerveau = Paris Brain Institute (ICM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Università degli Studi di Perugia = University of Perugia (UNIPG)

المصدر: Neurobiology of disease
Neurobiology of Disease
Neurobiology of Disease, Elsevier, 2021, 158, pp.105473. ⟨10.1016/j.nbd.2021.105473⟩
Neurobiology of Disease, Vol 158, Iss, Pp 105473-(2021)
Neurobiology of disease, 158:105473
Elsevier
Neurobiology of Disease, 2021, 158, pp.105473. ⟨10.1016/j.nbd.2021.105473⟩

مصطلحات موضوعية: Male, [SDV]Life Sciences [q-bio], [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Long-Term Potentiation, Striatum, Mice, 0302 clinical medicine, Cocaine, Extrapyramidal disorder, Drug addiction, Guanine Nucleotide Exchange Factors, Mice, Knockout, 0303 health sciences, Neuronal Plasticity, Self-administration, Long-term potentiation, M1 muscarinic receptor, 3. Good health, Neurology, Excitatory postsynaptic potential, LTP, Dendritic excitability, Amphetamine, Stereotypy, Kir2, Neurovetenskaper, RC321-571, Substance-Related Disorders, Neurosciences. Biological psychiatry. Neuropsychiatry, Biology, Hyperkinesis, Motor Activity, Medium spiny neuron, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Glutamatergic, Basal Ganglia Diseases, Parasympathetic Nervous System, Animals, 030304 developmental biology, Receptor, Muscarinic M1, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Neurosciences, Excitatory Postsynaptic Potentials, Dendrites, Neostriatum, Synaptic plasticity, Synapses, Cholinergic, Central Nervous System Stimulants, Neuroscience, 030217 neurology & neurosurgery

الوصف: CalDAG-GEFI (CDGI) is a protein highly enriched in the striatum, particularly in the principal spiny projection neurons (SPNs). CDGI is strongly down-regulated in two hyperkinetic conditions related to striatal dysfunction: Huntingtons disease and levodopa-induced dyskinesia in Parkinsons disease. We demonstrate that genetic deletion of CDGI in mice disrupts dendritic, but not somatic, M1 muscarinic receptors (M1Rs) signaling in indirect pathway SPNs. Loss of CDGI reduced temporal integration of excitatory postsynaptic potentials at dendritic glutamatergic synapses and impaired the induction of activity-dependent long-term potentiation. CDGI deletion selectively increased psychostimulant-induced repetitive behaviors, disrupted sequence learning, and eliminated M1R blockade of cocaine self-administration. These findings place CDGI as a major, but previously unrecognized, mediator of cholinergic signaling in the striatum. The effects of CDGI deletion on the selfadministration of drugs of abuse and its marked alterations in hyperkinetic extrapyramidal disorders highlight CDGIs therapeutic potential. Funding Agencies: William N. & Bernice E. Bumpus Foundation; Saks Kavanaugh Foundation; Simons Foundation; National Institute of Child Health and Development United States Department of Health & Human Services National Institutes of Health (NIH) - USANIH Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD) [R37 HD028341]; James and Pat Poitras Research Fund; Stanley Center for Psychiatric Research at the Broad Institute; National Institute of Mental Health United States Department of Health & Human Services National Institutes of Health (NIH) - USANIH National Institute of Mental Health (NIMH) [R01 MH071847, F32 MH065815]; National Institute on Aging United States Department of Health & Human Services National Institutes of Health (NIH) - USANIH National Institute on Aging (NIA) [R01 AG050548]; European Community FP7 - The-matic priority HEALTH contract [222918]; Ministry of Health; JPB Foundation; National Institute on Drug Abuse United States Department of Health & Human Services National Institutes of Health (NIH) - USANIH National Institute on Drug Abuse (NIDA) European Commission [R00 DA027825, R01 DA07418]

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0e9d40a8e94ed843df213514512c582cTest
http://europepmc.org/articles/PMC8486000Test

المؤلفون: Cinzia Costa, Francesco Paciullo, Paolo Gresele

المصدر: Annals of Internal Medicine. 173:71-72

مصطلحات موضوعية: Male, Levetiracetam, medicine.drug_mechanism_of_action, Factor Xa Inhibitor, Blood plasma, Pharmacology, Rivaroxaban, Hematology and oncology, Internal Medicine, medicine, Humans, Drug Interactions, Transient ischemic attacks, Glycoproteins, Aged, Thrombocytosis, Drug administration, Ischemic Attack, Transient, business.industry, Anticoagulants, Drugs, Atrial fibrillation, General Medicine, Plasma levels, Epileptic seizures, medicine.disease, Ischemic Attack, Transient, Anticonvulsants, business, Factor Xa Inhibitors, medicine.drug

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2cbbf9fd36af05472ba4acf4967751f5Test
https://doi.org/10.7326/l19-0712Test

المؤلفون: Paolo Calabresi, Letizia M. Cupini, Chiara Bedetti, Paola Sarchielli, Cinzia Costa, Sabrina Siliquini, Ilenia Corbelli, Michele Romoli, Stefano Caproni, Paolo Eusebi

المصدر: Cephalalgia. 38:274-282

مصطلحات موضوعية: Adult, Male, Pediatrics, medicine.medical_specialty, Adolescent, Migraine Disorders, Lamotrigine, neuropharmacology, Young Adult, 03 medical and health sciences, Epilepsy, 0302 clinical medicine, Topiramate, medicine, Humans, migraine, antiepileptic drugs, 030212 general & internal medicine, Child, Adverse effect, Tolerability, adverse events, epilepsy, Neuropharmacology, Aged, Aged, 80 and over, business.industry, Valproic Acid, General Medicine, Middle Aged, medicine.disease, Settore MED/26 - NEUROLOGIA, Increased risk, Migraine, Anesthesia, Anticonvulsants, Female, Neurology (clinical), business, 030217 neurology & neurosurgery

الوصف: Background The impact of adverse events (AEs) of antiepileptic drugs (AEDs) have an impact on compliance and dropouts. We compared tolerability of AEs of AEDs among patients with migraine, epilepsy, or both. Methods Overall, 335 patients (epilepsy (n = 142), migraine (n = 131), and both (n = 62)), were evaluated with the Liverpool Adverse Events Profile (LAEP) to assess the magnitude, profile and occurrence rate of the AEs of valproate, topiramate, and lamotrigine. Results AEs were significantly more common with topiramate treatment (71.0%) and among migraineurs (69.5%), the latter being more prone to discontinue AEDs (46.6%). The profile of AEs with topiramate and valproate differed among groups. Moreover, treatment with both topiramate and valproate was associated, for all groups, with a worse tolerability profile compared to lamotrigine. Conclusion Our data suggest a specific drug and disease AE profile of AEDs. Specifically, migraineurs are the most affected by AEs, even though they receive very low dosages of AEDs. This finding might be considered a clinical implication of central sensitization mechanisms. Both the profile and tolerability of AEs, highly influencing quality of life, depended on the underlying conditions, and deeply impacted on treatment dropout. Therefore, before starting, switching or stopping AED treatment, all options need to be considered.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::96fe833894515203592d71dd302fb9dfTest
https://doi.org/10.1177/0333102416683925Test

المؤلفون: Massimiliano Di Filippo, Sabrina Siliquini, Claudio Liguori, Andrea Romigi, Cinzia Costa, Michela Tantucci, Annalisa Nobili, Paolo Calabresi, Petra Mazzocchetti, Virve Cavallucci, Marcello D'Amelio, Lucilla Parnetti, Alessandro Tozzi, Paolo Eusebi, Nicola Biagio Mercuri

المصدر: Neurobiology of Aging. 48:161-171

مصطلحات موضوعية: Male, 0301 basic medicine, Aging, Transgenic, Mice, Epilepsy, chemistry.chemical_compound, 0302 clinical medicine, D1 dopamine receptor, Receptors, 80 and over, Transgenic mice, Receptor, Aβ, Aged, 80 and over, SCH-23390, Aβ1–42 oligomers, General Neuroscience, Alzheimer's disease, Middle Aged, Settore MED/26 - NEUROLOGIA, Dopamine receptor, Female, Epileptic threshold, Seizures, Neuroscience (all), Developmental Biology, Geriatrics and Gerontology, Neurology (clinical), Mice, Transgenic, 03 medical and health sciences, Dopamine receptor D1, Alzheimer Disease, Dopamine D1, medicine, Animals, Humans, oligomers, Aged, Amyloid beta-Peptides, Animal, business.industry, Receptors, Dopamine D1, Dentate gyrus, Neurotoxicity, 1–42, Benzazepines, medicine.disease, Peptide Fragments, Disease Models, Animal, 030104 developmental biology, chemistry, Disease Models, Synaptic plasticity, business, Neuroscience, 030217 neurology & neurosurgery

الوصف: Experimental and clinical observations indicate that amyloid-β1-42 (Aβ1-42) peptide not only represents a major actor in neurodegenerative mechanisms but also induce hyperexcitation in individual neurons and neural circuits. In this abnormal excitability, possibly leading to seizures, the D1 dopamine (DA) receptors may play a role. Cerebrospinal fluid levels of Aβ1-42 were measured in patients with late-onset epilepsy of unknown etiology. Moreover, the effect of amyloid peptide on the hippocampal epileptic threshold and synaptic plasticity and its link to D1 receptor function were tested in experimental mouse model of cerebral amyloidosis and in acute model of Aβ1-42-induced neurotoxicity. Among 272 evaluated epileptic patients, aged >55 years, 35 suffered from late-onset epilepsy of unknown etiology. In these subjects, cerebrospinal fluid Aβ1-42 levels were measured. The effects of Aβ1-42, amyloid oligomers, and D1 receptor modulation on epileptic threshold were analyzed by electrophysiological recordings in the dentate gyrus of mice hippocampal slices. We found that Aβ1-42 levels were significantly decreased in cerebrospinal fluid of patients with late-onset epilepsy of unknown etiology with respect to controls suggesting the cerebral deposition of this peptide in these patients. Aβ1-42 enhanced epileptic activity in mice through a mechanism involving increased surface expression of D1 receptor, and this effect was mimicked by D1 receptor stimulation and blocked by SCH 23390, a D1 receptor antagonist. Aβ1-42 may contribute to the pathophysiology of late-onset epilepsy of unknown origin. Our preclinical findings indicate that the D1 receptor is involved in mediating the epileptic effects of Aβ1-42. This novel link between Aβ1-42 and D1 receptor signaling might represent a potential therapeutic target.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::204e4111cba6085a394310fe4d21084bTest
https://doi.org/10.1016/j.neurobiolaging.2016.08.025Test

المؤلفون: Paolo Calabresi, Elena Nardi Cesarini, Andrea Mancini, Arjune Sen, Sarosh R. Irani, Diego Franciotta, Lucilla Parnetti, Paraskevi Krashia, Pasquale Nigro, Nicola Biagio Mercuri, Matteo Gastaldi, Massimiliano Di Filippo, Nicola Tambasco, Cinzia Costa, Annalisa Nobili, Marcello D'Amelio, Michele Romoli

المصدر: Annals of Clinical and Translational Neurology
Annals of Clinical and Translational Neurology, Vol 6, Iss 11, Pp 2261-2269 (2019)

مصطلحات موضوعية: 0301 basic medicine, Male, neurological disorders, Neurosciences. Biological psychiatry. Neuropsychiatry, Nerve Tissue Proteins, Hippocampal formation, Epileptogenesis, Autoantigens, Hippocampus, 03 medical and health sciences, Mice, 0302 clinical medicine, Autoimmune Diseases of the Nervous System, Medicine, Premovement neuronal activity, Animals, Humans, RC346-429, Research Articles, Autoantibodies, Autoimmune encephalitis, Neurons, Epilepsy, business.industry, General Neuroscience, autoimmune encephalitis, Glutamate receptor, Intracellular Signaling Peptides and Proteins, Membrane Proteins, 3. Good health, Mice, Inbred C57BL, Electrophysiology, Settore MED/26 - NEUROLOGIA, 030104 developmental biology, medicine.anatomical_structure, nervous system, Receptors, GABA-B, Schaffer collateral, Encephalitis, Neurology. Diseases of the nervous system, Neurology (clinical), business, Neuroscience, 030217 neurology & neurosurgery, Ex vivo, RC321-571, Research Article

الوصف: Objective Autoantibody‐mediated forms of encephalitis (AE) include neurological disorders characterized by subacute memory loss, movement disorders, and, often, frequent, focal epileptic seizures. Yet, the electrophysiological effects of these autoantibodies on neuronal function have received little attention. In this study, we assessed the effects of CSF containing autoantibodies on intrinsic and extrinsic properties of hippocampal neurons, to define their epileptogenic potential. Methods We compared the effects of CSF containing leucine‐rich glioma inactivated 1 (LGI1), contactin‐associated protein‐like 2 (CASPR2), and γ‐aminobutyric acid receptor B (GABABR) antibodies on ex vivo electrophysiological parameters after stereotactic hippocampal inoculation into mice. Whole‐cell patch‐clamp and extracellular recordings from CA1 pyramidal neurons and CA3‐CA1 field recordings in ex vivo murine brain slices were used to study neuronal function. Results By comparison to control CSF, AE CSFs increased the probability of glutamate release from CA3 neurons. In addition, LGI1‐ and CASPR2 antibodies containing CSFs induced epileptiform activity at a population level following Schaffer collateral stimulation. CASPR2 antibody containing CSF was also associated with higher spontaneous firing of CA1 pyramidal neurons. On the contrary, GABABR antibody containing CSF did not elicit changes in intrinsic neuronal activity and field potentials. Interpretation Using patient CSF, we have demonstrated that the AE‐associated antibodies against LGI1 and CASPR2 are able to increase hippocampal CA1 neuron excitability, facilitating epileptiform activity. These findings provide in vivo pathogenic insights into neuronal dysfunction in these conditions.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e330a199b1df21ee1b37bf21473eab0bTest
https://pubmed.ncbi.nlm.nih.gov/31617317Test

المؤلفون: Jill C. Richardson, Flavio Nobili, Libera Cavaliere, Moira Marizzoni, Claudio Babiloni, Gianluigi Forloni, Giovanni B. Frisoniand, Mira Didic, Régis Bordet, Ludovico Minati, Jorge Jovicich, Susanna Lopez, Marco Salvatore, Jens Wiltfang, David Bartrés Faz, Claudio Del Percio, Camillo Marra, Giuseppe Noce, Andrea Soricelli, Diego Albani, Clarissa Ferrari, Tilman Hensch, Lucilla Parnetti, José Luis Molinuevo, Olivier Blin, Pierre Payoux, Cinzia Costa, Peter Schönknecht, Roberta Lizio, Pieter Jelle Visser, Magda Tsolaki, Lucia Farotti, Paolo Maria Rossini, Samantha Galluzzi, Ute Fiedler, Daniele Orlandi, Davide V. Moretti

المساهمون: University of Trento [Trento], Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), Centro San Giovanni di Dio, Fatebenefratelli, Brescia (IRCCS), Università degli Studi di Brescia = University of Brescia (UniBs), IRCCS SDN Napoli, IRCCS Istituto Nazionale dei Tumori [Milano], Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM), Universität Duisburg-Essen = University of Duisburg-Essen [Essen], Universität Leipzig, Pasqual Maragall Foundation, Universitat de Barcelona (UB), Università degli studi di Genova = University of Genoa (UniGe), Università degli Studi di Perugia = University of Perugia (UNIPG), Toulouse Neuro Imaging Center (ToNIC), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Toulouse Mind & Brain Institut (TMBI), Université Toulouse - Jean Jaurès (UT2J), Université de Toulouse (UT)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université Toulouse - Jean Jaurès (UT2J), Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT), Istituto Neurologico Mediterraneo (NEUROMED I.R.C.C.S.), Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA)-University of Naples Federico II = Università degli studi di Napoli Federico II, Aristotle University of Thessaloniki, VU University Medical Center [Amsterdam], GlaxoSmithKline, Glaxo Smith Kline, Université de 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), Universität Duisburg-Essen [Essen], Universität Leipzig [Leipzig], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Toulouse Mind & Brain Institut (TMBI), Université Toulouse - Jean Jaurès (UT2J)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse - Jean Jaurès (UT2J)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, University of Duisburg-Essen, Otten, Lisa, Neurology, Amsterdam Neuroscience - Neurodegeneration

المصدر: Journal of Alzheimer's Disease
Journal of Alzheimer's Disease, 2019, 69 (1), pp.15-35. ⟨10.3233/JAD-180158⟩
Jovicich, J, Babiloni, C, Ferrari, C, Marizzoni, M, Moretti, D V, Del Percio, C, Lizio, R, Lopez, S, Galluzzi, S, Albani, D, Cavaliere, L, Minati, L, Didic, M, Fiedler, U, Forloni, G, Hensch, T, Molinuevo, J L, Bartrés Faz, D, Nobili, F, Orlandi, D, Parnetti, L, Farotti, L, Costa, C, Payoux, P, Rossini, P M, Marra, C, Schönknecht, P, Soricelli, A, Noce, G, Salvatore, M, Tsolaki, M, Visser, P J, Richardson, J C, Wiltfang, J, Bordet, R, Blin, O & Frisoniand, G B 2019, ' Two-year longitudinal monitoring of amnestic mild cognitive impairment patients with prodromal Alzheimer's disease using topographical biomarkers derived from functional magnetic resonance imaging and electroencephalographic activity ', Journal of Alzheimer's Disease, vol. 69, no. 1, pp. 15-35 . https://doi.org/10.3233/JAD-180158Test
Journal of Alzheimer's Disease, 69(1), 15-35. IOS Press

مصطلحات موضوعية: 0301 basic medicine, Male, pharma cog project, Medizin, Prodromal Alzheimer's Disease, Electroencephalography, Audiology, Neuropsychological Tests, Amnesic Mild Cognitive Impairment (aMCI), 0302 clinical medicine, PharmaCog project, Alpha rhythms, prodromal alzheimer’s disease, Longitudinal Studies, Default mode network, ComputingMilieux_MISCELLANEOUS, medicine.diagnostic_test, General Neuroscience, Brain, clinical trial, General Medicine, Middle Aged, Magnetic Resonance Imaging, Clinical Trial, Psychiatry and Mental health, Clinical Psychology, Settore MED/26 - NEUROLOGIA, Resting State, alpha rhythms, amnesic mild cognitive impairment, biomarkers, electroencephalography, functional magnetic resonance imaging, oddball event-related potentials, resting state, Functional Magnetic Resonance Imaging (fMRI), Disease Progression, Evoked Potentials, Auditory, Female, prodromal Alzheimer’s disease, medicine.medical_specialty, Posterior parietal cortex, 03 medical and health sciences, Alzheimer Disease, medicine, Dementia, Humans, Cognitive Dysfunction, Electroencephalography (EEG), Aged, prodromal Alzheimer's disease, Resting state fMRI, business.industry, [SCCO.NEUR]Cognitive science/Neuroscience, [SCCO.NEUR] Cognitive science/Neuroscience, medicine.disease, Cortex (botany), 030104 developmental biology, Posterior cingulate, Amnesia, Geriatrics and Gerontology, Functional magnetic resonance imaging, business, 030217 neurology & neurosurgery, Oddball Event-Related Potentials (ERPs), Biomarkers

الوصف: Auditory "oddball" event-related potentials (aoERPs), resting state functional magnetic resonance imaging (rsfMRI) connectivity, and electroencephalographic (rsEEG) rhythms were tested as longitudinal functional biomarkers of prodromal Alzheimer's disease (AD). Data were collected at baseline and four follow-ups at 6, 12, 18, and 24 months in amnesic mild cognitive impairment (aMCI) patients classified in two groups: "positive" (i.e., "prodromal AD" n=81) or "negative" (n=63) based on a diagnostic marker of AD derived from cerebrospinal samples (Aβ 42 /P-tau ratio). A linear mixed model design was used to test functional biomarkers for Group, Time, and Group×Time effects adjusted by nuisance covariates (only data until conversion to dementia was used). Functional biomarkers that showed significant Group effects ("positive" versus "negative", p

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::37dbc7517269f82b3d05b09cfb6b1026Test
https://hal.science/hal-03609814Test