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  1. Book ; Online: Epilepsy

    Czuczwar, Stanislaw J

    2022  

    Keywords MJN ; Pathology of Epilepsy; Anatomical Basis of Seizures; Epilepsy Genetics; Epilepsy and Neurodevelopmental Disorders; Treatment of Status Epilepticus; CTRP Channels for Antiepileptic Drugs; GABAA Receptors in Epilepsy; Milk Nutrition in Epilepsy; Ketogenic Diet for in Epilepsy
    Language 0|e
    Size 1 electronic resource (133 pages)
    Publisher Exon Publications
    Publishing place Australia
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021609257
    ISBN 9780645332049 ; 0645332046
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Ischemia-Reperfusion Programming of Alzheimer's Disease-Related Genes-A New Perspective on Brain Neurodegeneration after Cardiac Arrest.

    Pluta, Ryszard / Czuczwar, Stanisław J

    International journal of molecular sciences

    2024  Volume 25, Issue 2

    Abstract: The article presents the latest data on pathological changes after cerebral ischemia caused by cardiac arrest. The data include amyloid accumulation, tau protein modification, neurodegenerative and cognitive changes, and gene and protein changes ... ...

    Abstract The article presents the latest data on pathological changes after cerebral ischemia caused by cardiac arrest. The data include amyloid accumulation, tau protein modification, neurodegenerative and cognitive changes, and gene and protein changes associated with Alzheimer's disease. We present the latest data on the dysregulation of genes related to the metabolism of the amyloid protein precursor, tau protein, autophagy, mitophagy, apoptosis, and amyloid and tau protein transport genes. We report that neuronal death after cerebral ischemia due to cardiac arrest may be dependent and independent of caspase. Moreover, neuronal death dependent on amyloid and modified tau protein has been demonstrated. Finally, the results clearly indicate that changes in the expression of the presented genes play an important role in acute and secondary brain damage and the development of post-ischemic brain neurodegeneration with the Alzheimer's disease phenotype. The data indicate that the above genes may be a potential therapeutic target for brain therapy after ischemia due to cardiac arrest. Overall, the studies show that the genes studied represent attractive targets for the development of new therapies to minimize ischemic brain injury and neurological dysfunction. Additionally,
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; tau Proteins/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Brain/metabolism ; Brain Ischemia/complications ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Amyloid/metabolism ; Amyloidogenic Proteins/metabolism ; Cerebral Infarction/pathology ; Reperfusion ; Heart Arrest/complications ; Heart Arrest/genetics ; Heart Arrest/pathology ; Amyloid beta-Peptides/metabolism
    Chemical Substances tau Proteins ; Amyloid beta-Protein Precursor ; Amyloid ; Amyloidogenic Proteins ; Amyloid beta-Peptides
    Language English
    Publishing date 2024-01-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25021291
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Trans

    Pluta, Ryszard / Czuczwar, Stanisław J

    International journal of molecular sciences

    2024  Volume 25, Issue 6

    Abstract: Recent evidence indicates that experimental brain ischemia leads to dementia with an Alzheimer's disease-like type phenotype and genotype. Based on the above evidence, it was hypothesized that brain ischemia may contribute to the development of Alzheimer' ...

    Abstract Recent evidence indicates that experimental brain ischemia leads to dementia with an Alzheimer's disease-like type phenotype and genotype. Based on the above evidence, it was hypothesized that brain ischemia may contribute to the development of Alzheimer's disease. Brain ischemia and Alzheimer's disease are two diseases characterized by similar changes in the hippocampus that are closely related to memory impairment. Following brain ischemia in animals and humans, the presence of amyloid plaques in the extracellular space and intracellular neurofibrillary tangles was revealed. The phenomenon of tau protein hyperphosphorylation is a similar pathological feature of both post-ischemic brain injury and Alzheimer's disease. In Alzheimer's disease, the phosphorylated Thr231 motif in tau protein has two distinct
    MeSH term(s) Animals ; Humans ; Alzheimer Disease/metabolism ; tau Proteins/metabolism ; Neurofibrillary Tangles/metabolism ; Brain/metabolism ; Phosphorylation ; Brain Ischemia/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2024-03-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25063091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Oxidative Stress and Neurodegeneration in Animal Models of Seizures and Epilepsy.

    Łukawski, Krzysztof / Czuczwar, Stanisław J

    Antioxidants (Basel, Switzerland)

    2023  Volume 12, Issue 5

    Abstract: Free radicals are generated in the brain, as well as in other organs, and their production is proportional to the brain activity. Due to its low antioxidant capacity, the brain is particularly sensitive to free radical damage, which may affect lipids, ... ...

    Abstract Free radicals are generated in the brain, as well as in other organs, and their production is proportional to the brain activity. Due to its low antioxidant capacity, the brain is particularly sensitive to free radical damage, which may affect lipids, nucleic acids, and proteins. The available evidence clearly points to a role for oxidative stress in neuronal death and pathophysiology of epileptogenesis and epilepsy. The present review is devoted to the generation of free radicals in some animal models of seizures and epilepsy and the consequences of oxidative stress, such as DNA or mitochondrial damage leading to neurodegeneration. Additionally, antioxidant properties of antiepileptic (antiseizure) drugs and a possible use of antioxidant drugs or compounds in patients with epilepsy are reviewed. In numerous seizure models, the brain concentration of free radicals was significantly elevated. Some antiepileptic drugs may inhibit these effects; for example, valproate reduced the increase in brain malondialdehyde (a marker of lipid peroxidation) concentration induced by electroconvulsions. In the pentylenetetrazol model, valproate prevented the reduced glutathione concentration and an increase in brain lipid peroxidation products. The scarce clinical data indicate that some antioxidants (melatonin, selenium, vitamin E) may be recommended as adjuvants for patients with drug-resistant epilepsy.
    Language English
    Publishing date 2023-05-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox12051049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Editorial: Epilepsy and endocrine function.

    Miziak, Barbara / Czuczwar, Stanisław J

    Frontiers in endocrinology

    2023  Volume 14, Page(s) 1288784

    MeSH term(s) Humans ; Epilepsy ; Seizures
    Language English
    Publishing date 2023-09-28
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2023.1288784
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Oxidative Stress and Neurodegeneration in Animal Models of Seizures and Epilepsy

    Łukawski, Krzysztof / Czuczwar, Stanislaw J.

    Antioxidants. 2023 May 05, v. 12, no. 5

    2023  

    Abstract: Free radicals are generated in the brain, as well as in other organs, and their production is proportional to the brain activity. Due to its low antioxidant capacity, the brain is particularly sensitive to free radical damage, which may affect lipids, ... ...

    Abstract Free radicals are generated in the brain, as well as in other organs, and their production is proportional to the brain activity. Due to its low antioxidant capacity, the brain is particularly sensitive to free radical damage, which may affect lipids, nucleic acids, and proteins. The available evidence clearly points to a role for oxidative stress in neuronal death and pathophysiology of epileptogenesis and epilepsy. The present review is devoted to the generation of free radicals in some animal models of seizures and epilepsy and the consequences of oxidative stress, such as DNA or mitochondrial damage leading to neurodegeneration. Additionally, antioxidant properties of antiepileptic (antiseizure) drugs and a possible use of antioxidant drugs or compounds in patients with epilepsy are reviewed. In numerous seizure models, the brain concentration of free radicals was significantly elevated. Some antiepileptic drugs may inhibit these effects; for example, valproate reduced the increase in brain malondialdehyde (a marker of lipid peroxidation) concentration induced by electroconvulsions. In the pentylenetetrazol model, valproate prevented the reduced glutathione concentration and an increase in brain lipid peroxidation products. The scarce clinical data indicate that some antioxidants (melatonin, selenium, vitamin E) may be recommended as adjuvants for patients with drug-resistant epilepsy.
    Keywords DNA ; animals ; antioxidant activity ; antioxidants ; brain ; death ; drug resistance ; epilepsy ; free radicals ; glutathione ; lipid peroxidation ; malondialdehyde ; melatonin ; mitochondria ; models ; neurodegenerative diseases ; neurons ; oxidative stress ; pathophysiology ; selenium ; vitamin E
    Language English
    Dates of publication 2023-0505
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox12051049
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Commentary on: Coadministered cannabidiol and clobazam: Preclinical evidence for both pharmacodynamic and pharmacokinetic interactions.

    Czuczwar, Stanislaw J

    Epilepsia

    2020  Volume 61, Issue 10, Page(s) 2063–2064

    MeSH term(s) Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Cannabidiol/pharmacology ; Cannabidiol/therapeutic use ; Clobazam ; Humans ; Lennox Gastaut Syndrome/drug therapy
    Chemical Substances Anticonvulsants ; Cannabidiol (19GBJ60SN5) ; Clobazam (2MRO291B4U)
    Language English
    Publishing date 2020-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 216382-2
    ISSN 1528-1167 ; 0013-9580
    ISSN (online) 1528-1167
    ISSN 0013-9580
    DOI 10.1111/epi.16660
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 517: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 475: Show issues

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  8. Article ; Online: Emerging therapeutic targets for epilepsy: preclinical insights.

    Łukawski, Krzysztof / Czuczwar, Stanisław J

    Expert opinion on therapeutic targets

    2022  Volume 26, Issue 3, Page(s) 193–206

    Abstract: Introduction: Around 30% of patients with epilepsy suffer from drug-resistant seizures. Drug-resistant seizures may have significant consequences such as sudden death in epilepsy, injuries, memory disturbances, and childhood learning and developmental ... ...

    Abstract Introduction: Around 30% of patients with epilepsy suffer from drug-resistant seizures. Drug-resistant seizures may have significant consequences such as sudden death in epilepsy, injuries, memory disturbances, and childhood learning and developmental problems. Available antiepileptic drugs (AEDs) work via numerous mechanisms - mainly through inhibition of voltage-operated Na
    Areas covered: This article examines novel drug targets such as brain multidrug efflux transporters and inflammatory pathways; it progresses to discuss possible strategies for the management of drug-resistant seizures. Reduction of the consequences of blood brain barrier dysfunction and enhancement of anti-oxidative defense are discussed.
    Expert opinion: Novel drug targets comprise brain multidrug efflux transporters, TGF-β, Nrf2-ARE or m-TOR signaling and inflammatory pathways. Gene therapy and antagomirs seem the most promising targets. Epileptic foci may be significantly suppressed by viral-vector-mediated gene transfer, leading to an increased in situ concentration of inhibitory factors (for instance, galanin). Also, antagomirs offer a promising possibility of seizure inhibition by silencing micro-RNAs involved in epileptogenesis and possibly in seizure generation.
    MeSH term(s) Antagomirs/metabolism ; Antagomirs/therapeutic use ; Anticonvulsants/pharmacology ; Blood-Brain Barrier/metabolism ; Child ; Epilepsy/drug therapy ; Humans ; Seizures/drug therapy ; Seizures/metabolism
    Chemical Substances Antagomirs ; Anticonvulsants
    Language English
    Publishing date 2022-02-16
    Publishing country England
    Document type Journal Article
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2022.2039120
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5244: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Approaches for the discovery of drugs that target K Na 1.1 channels in KCNT1-associated epilepsy.

    Miziak, Barbara / Czuczwar, Stanisław J

    Expert opinion on drug discovery

    2022  , Page(s) 1–16

    Abstract: Introduction: There are approximately 70 million people with epilepsy and about 30% of patients are not satisfactorily treated. A link between gene mutations and epilepsy is well documented. A number of pathological variants of : Areas covered: ... ...

    Abstract Introduction: There are approximately 70 million people with epilepsy and about 30% of patients are not satisfactorily treated. A link between gene mutations and epilepsy is well documented. A number of pathological variants of
    Areas covered: Several methods for studies on KNa 1.1 channels have been reviewed - patch clamp analysis, Förster resonance energy transfer spectroscopy and whole-exome sequencing. The authors also review available drugs for the management of
    Expert opinion: The current methods enable deeper insights into electrophysiology of KNa 1.1 channels or its functioning in different activation states. It is also possible to identify a given
    Language English
    Publishing date 2022-11-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2259618-5
    ISSN 1746-045X ; 1746-0441
    ISSN (online) 1746-045X
    ISSN 1746-0441
    DOI 10.1080/17460441.2023.2150164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6388: Show issues Location:
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  10. Article ; Online: Apitherapy in Post-Ischemic Brain Neurodegeneration of Alzheimer's Disease Proteinopathy: Focus on Honey and Its Flavonoids and Phenolic Acids.

    Pluta, Ryszard / Miziak, Barbara / Czuczwar, Stanisław J

    Molecules (Basel, Switzerland)

    2023  Volume 28, Issue 15

    Abstract: Neurodegeneration of the brain after ischemia is a major cause of severe, long-term disability, dementia, and mortality, which is a global problem. These phenomena are attributed to excitotoxicity, changes in the blood-brain barrier, neuroinflammation, ... ...

    Abstract Neurodegeneration of the brain after ischemia is a major cause of severe, long-term disability, dementia, and mortality, which is a global problem. These phenomena are attributed to excitotoxicity, changes in the blood-brain barrier, neuroinflammation, oxidative stress, vasoconstriction, cerebral amyloid angiopathy, amyloid plaques, neurofibrillary tangles, and ultimately neuronal death. In addition, genetic factors such as post-ischemic changes in genetic programming in the expression of amyloid protein precursor, β-secretase, presenilin-1 and -2, and tau protein play an important role in the irreversible progression of post-ischemic neurodegeneration. Since current treatment is aimed at preventing symptoms such as dementia and disability, the search for causative therapy that would be helpful in preventing and treating post-ischemic neurodegeneration of Alzheimer's disease proteinopathy is ongoing. Numerous studies have shown that the high contents of flavonoids and phenolic acids in honey have antioxidant, anti-inflammatory, anti-apoptotic, anti-amyloid, anti-tau protein, anticholinesterase, serotonergic, and AMPAK activities, influencing signal transmission and neuroprotective effects. Notably, in many preclinical studies, flavonoids and phenolic acids, the main components of honey, were also effective when administered after ischemia, suggesting their possible use in promoting recovery in stroke patients. This review provides new insight into honey's potential to prevent brain ischemia as well as to ameliorate damage in advanced post-ischemic brain neurodegeneration.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; Apitherapy/adverse effects ; Honey ; Flavonoids/therapeutic use ; Flavonoids/metabolism ; Brain/metabolism ; tau Proteins/metabolism ; Ischemia/metabolism ; Amyloid beta-Peptides/metabolism
    Chemical Substances Flavonoids ; tau Proteins ; Amyloid beta-Peptides
    Language English
    Publishing date 2023-07-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules28155624
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 81: Show issues

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