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  1. Book ; Online: Experimental Models of Epilepsy and Related Comorbidities

    Farooq Shaikh, Mohd / Chakraborti, Ayanabha / Vezzani, Annamaria / Malin Abdullah, Jafri

    2019  

    Keywords Science: general issues ; Pharmacology ; experimental epilepsy ; comorbidities ; Animal Models ; antiepileptic drugs ; Anticonvulsant screening
    Size 1 electronic resource (175 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230788
    ISBN 9782889458431 ; 2889458431
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article: Brain Inflammation and Seizures: Evolving Concepts and New Findings in the Last 2 Decades.

    Vezzani, Annamaria

    Epilepsy currents

    2020  Volume 20, Issue 6_suppl, Page(s) 40S–43S

    Language English
    Publishing date 2020-10-05
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2270080-8
    ISSN 1535-7597
    ISSN 1535-7597
    DOI 10.1177/1535759720948900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book ; Conference proceedings: Proceedings of the First Meeting on Immunity and Inflammation in Epilepsy: Mechanistic Insights and Therapeutic Perspectives

    Vezzani, Annamaria / Rüegg, Stephan

    September 16 - 18, 2010, Milano, Italy

    (Epilepsia ; 52, Suppl. 3)

    2011  

    Event/congress Meeting on Immunity and Inflammation in Epilepsy (1, 2010, Mailand)
    Author's details guest ed.: Annamaria Vezzani and Stephan Rüegg
    Series title Epilepsia ; 52, Suppl. 3
    Collection
    Language English
    Size 53 S. : Ill.
    Publisher Wiley-Blackwell
    Publishing place Hoboken, NJ
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT016868738
    Database Catalogue ZB MED Medicine, Health

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    Zs A 517 -52,Suppl.3- not available for loan Zeitschriften-Lesesaal

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  4. Article ; Online: Neuroinflammation microenvironment sharpens seizure circuit.

    Villasana-Salazar, Benjamin / Vezzani, Annamaria

    Neurobiology of disease

    2023  Volume 178, Page(s) 106027

    Abstract: A large set of inflammatory molecules and their receptors are induced in epileptogenic foci of patients with pharmacoresistant epilepsies of structural etiologies or with refractory status epilepticus. Studies in animal models mimicking these clinical ... ...

    Abstract A large set of inflammatory molecules and their receptors are induced in epileptogenic foci of patients with pharmacoresistant epilepsies of structural etiologies or with refractory status epilepticus. Studies in animal models mimicking these clinical conditions have shown that the activation of specific inflammatory signallings in forebrain neurons or glial cells may modify seizure thresholds, thus contributing to both ictogenesis and epileptogenesis. The search for mechanisms underlying these effects has highlighted that inflammatory mediators have CNS-specific neuromodulatory functions, in addition to their canonical activation of immune responses for pathogen recognition and clearance. This review reports the neuromodulatory effects of inflammatory mediators and how they contribute to alter the inhibitory/excitatory balance in neural networks that underlie seizures. In particular, we describe key findings related to the ictogenic role of prototypical inflammatory cytokines (IL-1β and TNF) and danger signals (HMGB1), their modulatory effects of neuronal excitability, and the mechanisms underlying these effects. It will be discussed how harnessing these neuromodulatory properties of immune mediators may lead to novel therapies to control drug-resistant seizures.
    MeSH term(s) Animals ; Neuroinflammatory Diseases ; Seizures/complications ; Epilepsy/drug therapy ; Encephalitis/complications ; Inflammation Mediators
    Chemical Substances Inflammation Mediators
    Language English
    Publishing date 2023-02-02
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2023.106027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: mTOR and neuroinflammation in epilepsy: implications for disease progression and treatment.

    Ravizza, Teresa / Scheper, Mirte / Di Sapia, Rossella / Gorter, Jan / Aronica, Eleonora / Vezzani, Annamaria

    Nature reviews. Neuroscience

    2024  Volume 25, Issue 5, Page(s) 334–350

    Abstract: Epilepsy remains a major health concern as anti-seizure medications frequently fail, and there is currently no treatment to stop or prevent epileptogenesis, the process underlying the onset and progression of epilepsy. The identification of the ... ...

    Abstract Epilepsy remains a major health concern as anti-seizure medications frequently fail, and there is currently no treatment to stop or prevent epileptogenesis, the process underlying the onset and progression of epilepsy. The identification of the pathological processes underlying epileptogenesis is instrumental to the development of drugs that may prevent the generation of seizures or control pharmaco-resistant seizures, which affect about 30% of patients. mTOR signalling and neuroinflammation have been recognized as critical pathways that are activated in brain cells in epilepsy. They represent a potential node of biological convergence in structural epilepsies with either a genetic or an acquired aetiology. Interventional studies in animal models and clinical studies give strong support to the involvement of each pathway in epilepsy. In this Review, we focus on available knowledge about the pathophysiological features of mTOR signalling and the neuroinflammatory brain response, and their interactions, in epilepsy. We discuss mitigation strategies for each pathway that display therapeutic effects in experimental and clinical epilepsy. A deeper understanding of these interconnected molecular cascades could enhance our strategies for managing epilepsy. This could pave the way for new treatments to fill the gaps in the development of preventative or disease-modifying drugs, thus overcoming the limitations of current symptomatic medications.
    MeSH term(s) Humans ; Epilepsy/drug therapy ; Animals ; TOR Serine-Threonine Kinases/metabolism ; Neuroinflammatory Diseases/drug therapy ; Neuroinflammatory Diseases/metabolism ; Disease Progression ; Signal Transduction/physiology ; Brain/metabolism ; Brain/pathology ; Anticonvulsants/therapeutic use ; Anticonvulsants/pharmacology
    Chemical Substances TOR Serine-Threonine Kinases (EC 2.7.11.1) ; MTOR protein, human (EC 2.7.1.1) ; Anticonvulsants
    Language English
    Publishing date 2024-03-26
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2034150-7
    ISSN 1471-0048 ; 1471-0048 ; 1471-003X
    ISSN (online) 1471-0048
    ISSN 1471-0048 ; 1471-003X
    DOI 10.1038/s41583-024-00805-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: An

    Cerovic, Milica / Di Nunzio, Martina / Craparotta, Ilaria / Vezzani, Annamaria

    Frontiers in neurology

    2023  Volume 14, Page(s) 1129138

    Abstract: Introduction: FIRES is a rare epileptic encephalopathy induced by acute unremitting seizures that occur suddenly in healthy children or young adults after a febrile illness in the preceding 2 weeks. This condition results in high mortality, neurological ...

    Abstract Introduction: FIRES is a rare epileptic encephalopathy induced by acute unremitting seizures that occur suddenly in healthy children or young adults after a febrile illness in the preceding 2 weeks. This condition results in high mortality, neurological disability, and drug-resistant epilepsy. The development of new therapeutics is hampered by the lack of validated experimental models. Our goal was to address this unmet need by providing a simple tool for rapid throughput screening of new therapies that target pathological inflammatory mechanisms in FIRES. The model was not intended to mimic the etiopathogenesis of FIRES which is still unknown, but to reproduce salient features of its clinical presentation such as the age, the cytokine storm and the refractoriness of epileptic activity to antiseizure medications (ASMs).
    Methods: We refined an
    Results: LPS induced a sustained neuroinflammatory response, as shown by increased mRNA levels of IL-1β, CXCL1 (IL-8), TNF, and increased IL-1β/IL-1Ra ratio. Epileptiform activity was exacerbated by neuroinflammation, also displaying increased resistance to maximal therapeutic concentrations of midazolam (100 μM), phenytoin (50 μM), sodium valproate (800 μM), and phenobarbital (100 μM). Treatment of LPS-exposed slices with two immunomodulatory drugs, a mouse anti-IL-6 receptor antibody (100 μM) corresponding to tocilizumab in humans, or anakinra (1.3 μM) which blocks the IL-1 receptor type 1, delayed the onset of epileptiform events and strongly reduced the ASM-resistant epileptiform activity evoked by neuroinflammation. These drugs were shown to reduce ASM-refractory seizures in FIRES patients.
    Discussion: The neuroinflammatory component and the pharmacological responsiveness of epileptiform events provide a proof-of-concept validation of this
    Language English
    Publishing date 2023-03-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2023.1129138
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Anti-inflammatory drugs in epilepsy: does it impact epileptogenesis?

    Vezzani, Annamaria

    Expert opinion on drug safety

    2015  Volume 14, Issue 4, Page(s) 583–592

    Abstract: Introduction: In the epilepsy therapeutic arena, there is urgent need for developing novel antiepileptogenesis treatments that offer a way to prevent the onset or the progression of the disease. Such treatments are still lacking, and their development ... ...

    Abstract Introduction: In the epilepsy therapeutic arena, there is urgent need for developing novel antiepileptogenesis treatments that offer a way to prevent the onset or the progression of the disease. Such treatments are still lacking, and their development requires a deep understanding of the mechanisms underlying the disease pathogenesis, in order to target them using appropriate drugs with timely interventions.
    Areas covered: Preclinical research highlighted glial cells in seizure-prone areas as key contributors to neuronal circuit hyperexcitability resulting in seizures. Microglia and astrocytes activated by epileptogenic insults increase their synthesis and release of pro-inflammatory molecules, thus contributing to the generation of neuroinflammation. This is now considered an established hallmark of epileptogenic foci in various forms of pharmaco-resistant epilepsies. Studies done in experimental models of non-genetic forms of epilepsy demonstrated that specific inflammatory molecules are involved in seizures, cell loss and co-morbidities.
    Expert opinion: Emerging findings highlight that specific inflammatory molecules are potential targets for drug intervention for preventing or arresting epileptogenesis. These drugs, by interfering with mechanisms implicated in disease development, may represent disease-modifying treatments. Clinical translation of anti-inflammatory intervention may take advantage of drugs already used in clinical practice for peripheral or other CNS disorders with a pathogenic neuroinflammatory component.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Astrocytes/metabolism ; Drug Design ; Drug Resistance ; Epilepsy/drug therapy ; Epilepsy/physiopathology ; Epilepsy/prevention & control ; Humans ; Inflammation/drug therapy ; Inflammation/physiopathology ; Microglia/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Anticonvulsants
    Language English
    Publishing date 2015-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2088728-0
    ISSN 1744-764X ; 1474-0338
    ISSN (online) 1744-764X
    ISSN 1474-0338
    DOI 10.1517/14740338.2015.1010508
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: A mathematical model of neuroimmune interactions in epileptogenesis for discovering treatment strategies.

    Batulin, Danylo / Lagzi, Fereshteh / Vezzani, Annamaria / Jedlicka, Peter / Triesch, Jochen

    iScience

    2022  Volume 25, Issue 6, Page(s) 104343

    Abstract: The development of epilepsy (epileptogenesis) involves a complex interplay of neuronal and immune processes. Here, we present a first-of-its-kind mathematical model to better understand the relationships among these processes. Our model describes the ... ...

    Abstract The development of epilepsy (epileptogenesis) involves a complex interplay of neuronal and immune processes. Here, we present a first-of-its-kind mathematical model to better understand the relationships among these processes. Our model describes the interaction between neuroinflammation, blood-brain barrier disruption, neuronal loss, circuit remodeling, and seizures. Formulated as a system of nonlinear differential equations, the model reproduces the available data from three animal models. The model successfully describes characteristic features of epileptogenesis such as its paradoxically long timescales (up to decades) despite short and transient injuries or the existence of qualitatively different outcomes for varying injury intensity. In line with the concept of degeneracy, our simulations reveal multiple routes toward epilepsy with neuronal loss as a sufficient but non-necessary component. Finally, we show that our model allows for
    Language English
    Publishing date 2022-05-04
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.104343
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Neuroimmunology of status epilepticus.

    Vezzani, Annamaria / Di Sapia, Rossella / Kebede, Valentina / Balosso, Silvia / Ravizza, Teresa

    Epilepsy & behavior : E&B

    2023  Volume 140, Page(s) 109095

    Abstract: Status epilepticus (SE) is a very heterogeneous clinical condition often refractory to available treatment options. Evidence in animal models shows that neuroinflammation arises in the brain during SE due to the activation of innate immune mechanisms in ... ...

    Abstract Status epilepticus (SE) is a very heterogeneous clinical condition often refractory to available treatment options. Evidence in animal models shows that neuroinflammation arises in the brain during SE due to the activation of innate immune mechanisms in brain parenchyma cells. Intervention studies in animal models support the involvement of neuroinflammation in SE onset, duration, and severity, refractoriness to treatments, and long-term neurological consequences. Clinical evidence shows that neuroinflammation occurs in patients with SE of diverse etiologies likely representing a common phenomenon, thus broadening the involvement of the immune system beyond the infective and autoimmune etiologies. There is urgent need for novel therapies for refractory SE that rely upon a better understanding of the basic mechanisms underlying this clinical condition. Preclinical and clinical evidence encourage consideration of specific anti-inflammatory treatments for controlling SE and its consequences in patients.
    MeSH term(s) Animals ; Neuroinflammatory Diseases ; Status Epilepticus/drug therapy ; Brain ; Models, Animal ; Anticonvulsants/therapeutic use
    Chemical Substances Anticonvulsants
    Language English
    Publishing date 2023-02-06
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2010587-3
    ISSN 1525-5069 ; 1525-5050
    ISSN (online) 1525-5069
    ISSN 1525-5050
    DOI 10.1016/j.yebeh.2023.109095
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Brain Autonomous Mechanisms of Seizure-Induced BBB Dysfunction.

    Vezzani, Annamaria

    Epilepsy currents

    2012  Volume 12, Issue 2, Page(s) 69–71

    Language English
    Publishing date 2012-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2270080-8
    ISSN 1535-7511 ; 1535-7597
    ISSN (online) 1535-7511
    ISSN 1535-7597
    DOI 10.5698/1535-7511-12.2.69
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