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  1. Article ; Online: Innate immunity in neurons makes memories persist.

    Kelvington, Benjamin A / Abel, Ted

    Nature

    2024  Volume 628, Issue 8006, Page(s) 40–42

    MeSH term(s) Immunity, Innate ; Neurons/physiology
    Language English
    Publishing date 2024-03-27
    Publishing country England
    Document type News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-024-00679-4
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    In stock of ZB MED Cologne/Königswinter

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  2. Book ; Online ; E-Book: The neurobiology of schizophrenia

    Nickl-Jockschat, Thomas / Abel, Ted

    2016  

    Author's details edited by Ted Abel, Thomas Nickl-Jockschat
    Language English
    Size 1 Online-Ressource (xx, 449 Seiten), Illustrationen
    Publisher Elsevier AP
    Publishing place Amsterdam
    Publishing country Netherlands
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019473176
    ISBN 978-0-12-801877-4 ; 9780128018293 ; 0-12-801877-1 ; 0128018291
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Book: Sleep, neuronal plasticity and brain function

    Meerlo, Peter / Abel, Ted / Benca, Ruth M.

    (Current topics in behavioral neurosciences ; 25)

    2015  

    Author's details Peter Meerlo ; Ruth M. Benca ; Ted Abel
    Series title Current topics in behavioral neurosciences ; 25
    Collection
    Keywords Schlafforschung ; Schlaf ; Hirnfunktion ; Neuronale Plastizität
    Subject Neuroplastizität ; Gehirn ; Hirnleistung ; Hirnaktivität ; Hirnphysiologie ; Gehirnphysiologie ; Gehirnaktivität ; Gehirnfunktion ; Schlaf ; Schlafanalyse ; Schlafmedizin ; Somnologie
    Language English
    Size X, 559 S. : Ill., graph. Darst., 0 mm x 0 mm
    Publisher Springer
    Publishing place Berlin u.a.
    Publishing country Germany
    Document type Book
    HBZ-ID HT018674895
    ISBN 978-3-662-46877-7 ; 3-662-46877-8 ; 9783662468784 ; 3662468786
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2015 A 2272 available for loan (reading room) Lesesaal EG

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  4. Article ; Online: hnRNPH2 gain-of-function mutations reveal therapeutic strategies and a role for RNA granules in neurodevelopmental disorders.

    Kelvington, Benjamin A / Abel, Ted

    The Journal of clinical investigation

    2023  Volume 133, Issue 14

    Abstract: hnRNPH2-related neurodevelopmental disorder (NDD) is caused by mutations in the HNRNPH2 gene and is associated with substantial challenges, including developmental delay, intellectual disability, growth delay, and epilepsy. There is currently no ... ...

    Abstract hnRNPH2-related neurodevelopmental disorder (NDD) is caused by mutations in the HNRNPH2 gene and is associated with substantial challenges, including developmental delay, intellectual disability, growth delay, and epilepsy. There is currently no therapeutic intervention available to those with hnRNPH2-related NDD that addresses its underlying mechanisms. In this issue of the JCI, Korff et al. studied specific gain-of-function mutations associated with hnRNPH2-related NDD, with the help of mouse models that recapitulate key features of the condition in humans. Their work paves the way for therapeutic approaches that aim to reduce the expression of mutant hnRNPH2 and highlights a role for disrupted RNA granules in neurodevelopmental and neurodegenerative disorders.
    MeSH term(s) Animals ; Mice ; Humans ; Gain of Function Mutation ; Neurodevelopmental Disorders/genetics ; Neurodevelopmental Disorders/therapy ; Intellectual Disability/genetics ; Mutation ; Epilepsy/genetics
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI171499
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: hnRNPH2 gain-of-function mutations reveal therapeutic strategies and a role for RNA granules in neurodevelopmental disorders

    Benjamin A. Kelvington / Ted Abel

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Volume 14

    Abstract: hnRNPH2-related neurodevelopmental disorder (NDD) is caused by mutations in the HNRNPH2 gene and is associated with substantial challenges, including developmental delay, intellectual disability, growth delay, and epilepsy. There is currently no ... ...

    Abstract hnRNPH2-related neurodevelopmental disorder (NDD) is caused by mutations in the HNRNPH2 gene and is associated with substantial challenges, including developmental delay, intellectual disability, growth delay, and epilepsy. There is currently no therapeutic intervention available to those with hnRNPH2-related NDD that addresses its underlying mechanisms. In this issue of the JCI, Korff et al. studied specific gain-of-function mutations associated with hnRNPH2-related NDD, with the help of mouse models that recapitulate key features of the condition in humans. Their work paves the way for therapeutic approaches that aim to reduce the expression of mutant hnRNPH2 and highlights a role for disrupted RNA granules in neurodevelopmental and neurodegenerative disorders.
    Keywords Medicine ; R
    Language English
    Publishing date 2023-07-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Sleep and memory: The impact of sleep deprivation on transcription, translational control, and protein synthesis in the brain.

    Lyons, Lisa C / Vanrobaeys, Yann / Abel, Ted

    Journal of neurochemistry

    2023  Volume 166, Issue 1, Page(s) 24–46

    Abstract: In countries around the world, sleep deprivation represents a widespread problem affecting school-age children, teenagers, and adults. Acute sleep deprivation and more chronic sleep restriction adversely affect individual health, impairing memory and ... ...

    Abstract In countries around the world, sleep deprivation represents a widespread problem affecting school-age children, teenagers, and adults. Acute sleep deprivation and more chronic sleep restriction adversely affect individual health, impairing memory and cognitive performance as well as increasing the risk and progression of numerous diseases. In mammals, the hippocampus and hippocampus-dependent memory are vulnerable to the effects of acute sleep deprivation. Sleep deprivation induces changes in molecular signaling, gene expression and may cause changes in dendritic structure in neurons. Genome wide studies have shown that acute sleep deprivation alters gene transcription, although the pool of genes affected varies between brain regions. More recently, advances in research have drawn attention to differences in gene regulation between the level of the transcriptome compared with the pool of mRNA associated with ribosomes for protein translation following sleep deprivation. Thus, in addition to transcriptional changes, sleep deprivation also affects downstream processes to alter protein translation. In this review, we focus on the multiple levels through which acute sleep deprivation impacts gene regulation, highlighting potential post-transcriptional and translational processes that may be affected by sleep deprivation. Understanding the multiple levels of gene regulation impacted by sleep deprivation is essential for future development of therapeutics that may mitigate the effects of sleep loss.
    MeSH term(s) Animals ; Child ; Humans ; Adolescent ; Sleep Deprivation/genetics ; Sleep Deprivation/metabolism ; Brain/metabolism ; Sleep/genetics ; Hippocampus/metabolism ; Protein Biosynthesis ; Mammals
    Language English
    Publishing date 2023-03-25
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/jnc.15787
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Chemogenetic Enhancement of cAMP Signaling Renders Hippocampal Synaptic Plasticity Resilient to the Impact of Acute Sleep Deprivation.

    Walsh, Emily Nicole / Shetty, Mahesh Shivarama / Diba, Kamran / Abel, Ted

    eNeuro

    2023  Volume 10, Issue 1

    Abstract: Sleep facilitates memory storage and even brief periods of sleep loss lead to impairments in memory, particularly memories that are hippocampus dependent. In previous studies, we have shown that the deficit in memory seen after sleep loss is accompanied ... ...

    Abstract Sleep facilitates memory storage and even brief periods of sleep loss lead to impairments in memory, particularly memories that are hippocampus dependent. In previous studies, we have shown that the deficit in memory seen after sleep loss is accompanied by deficits in synaptic plasticity. Our previous work has also found that sleep deprivation (SD) is associated with reduced levels of cyclic adenosine monophosphate (cAMP) in the hippocampus and that the reduction of cAMP mediates the diminished memory observed in sleep-deprived animals. Based on these findings, we hypothesized that cAMP acts as a mediator for not only the cognitive deficits caused by sleep deprivation, but also the observed deficits in synaptic plasticity. In this study, we expressed the heterologous
    MeSH term(s) Mice ; Animals ; Sleep Deprivation/metabolism ; Drosophila melanogaster/metabolism ; Hippocampus/metabolism ; Neuronal Plasticity/physiology ; Cyclic AMP/metabolism ; Long-Term Potentiation/physiology
    Chemical Substances Cyclic AMP (E0399OZS9N)
    Language English
    Publishing date 2023-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0380-22.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Sleep loss diminishes hippocampal reactivation and replay.

    Giri, Bapun / Kaya, Utku / Maboudi, Kourosh / Abel, Ted / Diba, Kamran

    Research square

    2023  

    Abstract: Memories benefit from sleep, and sleep loss immediately following learning has a negative impact on subsequent memory storage. Several prominent hypotheses ascribe a central role to hippocampal sharp-wave ripples (SWRs), and the concurrent reactivation ... ...

    Abstract Memories benefit from sleep, and sleep loss immediately following learning has a negative impact on subsequent memory storage. Several prominent hypotheses ascribe a central role to hippocampal sharp-wave ripples (SWRs), and the concurrent reactivation and replay of neuronal patterns from waking experience, in the offline memory consolidation process that occurs during sleep. However, little is known about how SWRs, reactivation, and replay are affected when animals are subjected to sleep deprivation. We performed long duration (~12 h), high-density silicon probe recordings from rat hippocampal CA1 neurons, in animals that were either sleeping or sleep deprived following exposure to a novel maze environment. We found that SWRs showed a sustained rate of activity during sleep deprivation, similar to or higher than in natural sleep, but with decreased amplitudes for the sharp-waves combined with higher frequencies for the ripples. Furthermore, while hippocampal pyramidal cells showed a log-normal distribution of firing rates during sleep, these distributions were negatively skewed with a higher mean firing rate in both pyramidal cells and interneurons during sleep deprivation. During SWRs, however, firing rates were remarkably similar between both groups. Despite the abundant quantity of SWRs and the robust firing activity during these events in both groups, we found that reactivation of neurons was either completely abolished or significantly diminished during sleep deprivation compared to sleep. Interestingly, reactivation partially rebounded upon recovery sleep, but failed to reach the levels characteristic of natural sleep. Similarly, the number of replays were significantly lower during sleep deprivation and recovery sleep compared to natural sleep. These results provide a network-level account for the negative impact of sleep loss on hippocampal function and demonstrate that sleep loss impacts memory storage by causing a dissociation between the amount of SWRs and the replays and reactivations that take place during these events.
    Language English
    Publishing date 2023-02-16
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-2540186/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Neurobiological insights into twice-exceptionality: Circuits, cells, and molecules.

    Kelvington, Benjamin A / Nickl-Jockschat, Thomas / Abel, Ted

    Neurobiology of learning and memory

    2022  Volume 195, Page(s) 107684

    Abstract: Twice-exceptional learners face a unique set of challenges arising from the intersection of extraordinary talent and disability. Neurobiology research has the capacity to complement pedagogical research and provide support for twice-exceptional learners. ...

    Abstract Twice-exceptional learners face a unique set of challenges arising from the intersection of extraordinary talent and disability. Neurobiology research has the capacity to complement pedagogical research and provide support for twice-exceptional learners. Very few studies have attempted to specifically address the neurobiological underpinnings of twice-exceptionality. However, neurobiologists have built a broad base of knowledge in nervous system function spanning from the level of neural circuits to the molecular basis of behavior. It is known that distinct neural circuits mediate different neural functions, which suggests that 2e learning may result from enhancement in one circuit and disruption in another. Neural circuits are known to adapt and change in response to experience, a cellular process known as neuroplasticity. Plasticity is controlled by a bidirectional connection between the synapse, where neural signals are received, and the nucleus, where regulated gene expression can return to alter synaptic function. Complex molecular mechanisms compose this connection in distinct neural circuits, and genetic alterations in these mechanisms are associated with both memory enhancements and psychiatric disorder. Understanding the consequences of these changes at the molecular, cellular, and circuit levels will provide critical insights into the neurobiological bases of twice-exceptionality.
    MeSH term(s) Humans ; Neurobiology ; Synapses/physiology ; Neuronal Plasticity/physiology ; Learning/physiology ; Neurons/physiology
    Language English
    Publishing date 2022-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1223366-3
    ISSN 1095-9564 ; 1074-7427
    ISSN (online) 1095-9564
    ISSN 1074-7427
    DOI 10.1016/j.nlm.2022.107684
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Correction to: Selective role of the translin/trax RNase complex in hippocampal synaptic plasticity.

    Park, Alan Jung / Shetty, Mahesh Shivarama / Baraban, Jay M / Abel, Ted

    Molecular brain

    2021  Volume 14, Issue 1, Page(s) 48

    Language English
    Publishing date 2021-03-05
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2436057-0
    ISSN 1756-6606 ; 1756-6606
    ISSN (online) 1756-6606
    ISSN 1756-6606
    DOI 10.1186/s13041-021-00761-2
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