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  1. Book: Metabolic and bioenergetic drivers of neurodegenerative disease: Treating neurodegenerative diseases as metabolic diseases

    Söderbom, Grażyna / Esterline, Russell / Oscarsson, Jan / Mattson, Mark P.

    (International review of neurobiology ; volume 155)

    2020  

    Author's details edited by Grażyna Söderbom, Russell Esterline, Jan Oscarsson, Mark P. Mattson
    Series title International review of neurobiology ; volume 155
    Collection
    Language English
    Size xviii, 301 Seiten, Illustrationen, Diagramme
    Edition First edition
    Publisher Academic Press, an imprint of Elsevier
    Publishing place Cambridge, MA
    Publishing country United States
    Document type Book
    HBZ-ID HT020608530
    ISBN 978-0-12-823121-0 ; 0-12-823121-1
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Ui II Zs 180 -155- verfügbar in Königswinter Königswinter

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  2. Article ; Online: The hormesis principle of neuroplasticity and neuroprotection.

    Mattson, Mark P / Leak, Rehana K

    Cell metabolism

    2024  Volume 36, Issue 2, Page(s) 315–337

    Abstract: Animals live in habitats fraught with a range of environmental challenges to their bodies and brains. Accordingly, cells and organ systems have evolved stress-responsive signaling pathways that enable them to not only withstand environmental challenges ... ...

    Abstract Animals live in habitats fraught with a range of environmental challenges to their bodies and brains. Accordingly, cells and organ systems have evolved stress-responsive signaling pathways that enable them to not only withstand environmental challenges but also to prepare for future challenges and function more efficiently. These phylogenetically conserved processes are the foundation of the hormesis principle, in which single or repeated exposures to low levels of environmental challenges improve cellular and organismal fitness and raise the probability of survival. Hormetic principles have been most intensively studied in physical exercise but apply to numerous other challenges known to improve human health (e.g., intermittent fasting, cognitive stimulation, and dietary phytochemicals). Here we review the physiological mechanisms underlying hormesis-based neuroplasticity and neuroprotection. Approaching natural resilience from the lens of hormesis may reveal novel methods for optimizing brain function and lowering the burden of neurological disorders.
    MeSH term(s) Animals ; Humans ; Hormesis/physiology ; Neuroprotection ; Neuronal Plasticity
    Language English
    Publishing date 2024-01-10
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2023.12.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Author Correction: How does hormesis impact biology, toxicology, and medicine?

    Calabrese, Edward J / Mattson, Mark P

    npj aging

    2023  Volume 9, Issue 1, Page(s) 6

    Language English
    Publishing date 2023-03-31
    Publishing country England
    Document type Published Erratum
    ISSN 2731-6068
    ISSN (online) 2731-6068
    DOI 10.1038/s41514-023-00101-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: Hormesis

    Mattson, Mark P.

    a revolution in biology, toxicology and medicine

    2010  

    Author's details Mark P. Mattson ... ed
    Keywords Hormesis ; Dose-response relationship (Biochemistry)
    Subject code 571.634
    Language English
    Size XIV, 213 S. : Ill., graph. Darst., 24 cm
    Publisher Springer u.a.
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT016116338
    ISBN 978-1-60761-494-4 ; 1-60761-494-4 ; 9781607614951 ; 1607614952
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2009 A 6136 order for loan Magazin

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  5. Article ; Online: Involvement of GABAergic interneuron dysfunction and neuronal network hyperexcitability in Alzheimer's disease: Amelioration by metabolic switching.

    Mattson, Mark P

    International review of neurobiology

    2020  Volume 154, Page(s) 191–205

    Abstract: Evidence accumulated over the past three decades suggests that the neurons that degenerate in Alzheimer's disease (AD) suffer metabolic compromise, hyperexcitability and consequent calcium ion ( ... ...

    Abstract Evidence accumulated over the past three decades suggests that the neurons that degenerate in Alzheimer's disease (AD) suffer metabolic compromise, hyperexcitability and consequent calcium ion (Ca
    MeSH term(s) Aging/metabolism ; Aging/pathology ; Alzheimer Disease/diet therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Animals ; Diet, Ketogenic ; Fasting ; GABAergic Neurons/metabolism ; GABAergic Neurons/pathology ; Humans ; Interneurons/metabolism ; Interneurons/pathology ; Ketones/metabolism ; NAD/metabolism ; Nerve Net/metabolism ; Nerve Net/pathology ; Nerve Net/physiopathology
    Chemical Substances Ketones ; NAD (0U46U6E8UK)
    Language English
    Publishing date 2020-07-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 209876-3
    ISSN 2162-5514 ; 0074-7742
    ISSN (online) 2162-5514
    ISSN 0074-7742
    DOI 10.1016/bs.irn.2020.01.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui II Zs.180: Show issues Location:
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  6. Article ; Online: Applying available knowledge and resources to alleviate familial and sporadic neurodegenerative disorders.

    Mattson, Mark P

    Progress in molecular biology and translational science

    2020  Volume 177, Page(s) 91–107

    Abstract: Here I present the scientific rationale and implementation strategies for elimination of early-onset neurodegenerative disorders (EONDD) from future generations, and for risk reduction and treatments for the more common late-onset neurodegenerative ... ...

    Abstract Here I present the scientific rationale and implementation strategies for elimination of early-onset neurodegenerative disorders (EONDD) from future generations, and for risk reduction and treatments for the more common late-onset neurodegenerative disorders (LONDD). Young adults with a family history of an EONDD should be educated on the genetics and familial burden of EONDD. They can then be genotyped and, if positive for the mutation, counseled as to how they can ensure that none of their children will be affected by choosing either adoption or in vitro fertilization and preimplantation genetic testing. LONDD risk reduction will require education of physicians and patients on the benefits of regular intermittent bioenergetic and cognitive challenges (exercise, intermittent fasting, intellectual challenges and social engagement) for brain health, and on specific risk-reduction regimens. Regulations will be required to counteract the disease-promoting mercenary practices of the processed food and pharmaceutical industries. Clinical trials of pharmacological interventions should shift to small trials of agents that substantially mimic mechanisms of action of exercise and intermittent fasting to bolster neuronal bioenergetics and stress resistance.
    MeSH term(s) Brain ; Energy Metabolism ; Exercise ; Fasting ; Humans ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/therapy
    Language English
    Publishing date 2020-10-20
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2471995-X
    ISSN 1878-0814 ; 0079-6603 ; 1877-1173
    ISSN (online) 1878-0814
    ISSN 0079-6603 ; 1877-1173
    DOI 10.1016/bs.pmbts.2020.09.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: An Evolutionary Perspective on Why Food Overconsumption Impairs Cognition.

    Mattson, Mark P

    Trends in cognitive sciences

    2019  Volume 23, Issue 3, Page(s) 200–212

    Abstract: Brain structures and neuronal networks that mediate spatial navigation, decision-making, sociality, and creativity evolved, in part, to enable success in food acquisition. Here, I discuss evidence suggesting that the reason that overconsumption of energy- ...

    Abstract Brain structures and neuronal networks that mediate spatial navigation, decision-making, sociality, and creativity evolved, in part, to enable success in food acquisition. Here, I discuss evidence suggesting that the reason that overconsumption of energy-rich foods negatively impacts cognition is that signaling pathways that evolved to respond adaptively to food scarcity are relatively disengaged in the setting of continuous food availability. Obesity impairs cognition and increases the risk for some psychiatric disorders and dementias. Moreover, maternal and paternal obesity predispose offspring to poor cognitive outcomes by epigenetic molecular mechanisms. Neural signaling pathways that evolved to bolster cognition in settings of food insecurity can be stimulated by intermittent fasting and exercise to support the cognitive health of current and future generations.
    MeSH term(s) Cognitive Dysfunction/etiology ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/prevention & control ; Energy Intake/physiology ; Epigenesis, Genetic/physiology ; Exercise/physiology ; Fasting/physiology ; Humans ; Obesity/complications ; Obesity/genetics ; Obesity/prevention & control ; Signal Transduction/physiology
    Language English
    Publishing date 2019-01-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2010989-1
    ISSN 1879-307X ; 1364-6613
    ISSN (online) 1879-307X
    ISSN 1364-6613
    DOI 10.1016/j.tics.2019.01.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The potential of gene editing for Huntington's disease.

    Duan, Wenzhen / Urani, Ece / Mattson, Mark P

    Trends in neurosciences

    2023  Volume 46, Issue 5, Page(s) 365–376

    Abstract: Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the huntingtin gene resulting in long stretches of polyglutamine repeats in the huntingtin protein. The disease involves ... ...

    Abstract Huntington's disease (HD) is a dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the huntingtin gene resulting in long stretches of polyglutamine repeats in the huntingtin protein. The disease involves progressive degeneration of neurons in the striatum and cerebral cortex resulting in loss of control of motor function, psychiatric problems, and cognitive deficits. There are as yet no treatments that can slow disease progression in HD. Recent advances in gene editing using clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein 9 (Cas9) systems and demonstrations of their ability to correct gene mutations in animal models of a range of diseases suggest that gene editing may prove effective in preventing or ameliorating HD. Here we describe (i) potential CRISPR-Cas designs and cellular delivery methods for the correction of mutant genes that cause inherited diseases, and (ii) recent preclinical findings demonstrating the efficacy of such gene-editing approaches in animal models, with a focus on HD.
    MeSH term(s) Animals ; Gene Editing/methods ; Huntington Disease/genetics ; Huntington Disease/therapy ; CRISPR-Cas Systems/genetics ; Neurodegenerative Diseases/genetics ; Mutation ; Disease Models, Animal
    Language English
    Publishing date 2023-03-10
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 282488-7
    ISSN 1878-108X ; 0378-5912 ; 0166-2236
    ISSN (online) 1878-108X
    ISSN 0378-5912 ; 0166-2236
    DOI 10.1016/j.tins.2023.02.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Book: Sleep and aging

    Mattson, Mark P.

    (Advances in cell aging and gerontology ; 17)

    2005  

    Author's details vol. ed.: Mark P. Mattson
    Series title Advances in cell aging and gerontology ; 17
    Collection
    Keywords Schlaf ; Alter
    Subject Alter Mensch ; Betagter ; Senioren ; Senior
    Language English
    Size VIII, 194 S. : Ill., graph. Darst.
    Edition 1. ed.
    Publisher Elsevier
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT014360700
    ISBN 0-444-51876-2 ; 978-0-444-51876-7
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 1881 -17- verfügbar in Königswinter Königswinter

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  10. Book: Membrane microdomain signaling

    Mattson, Mark P.

    lipid rafts in biology and medicine

    2005  

    Author's details ed. by Mark P. Mattson
    Keywords Membrane Microdomains / physiology ; Membrane Microdomains / pathology ; Signal Transduction ; Apoptosis ; Synapses / metabolism ; Lipids / metabolism ; Membranlipide ; Signaltransduktion
    Subject Signalübertragung ; Signalvermittlung
    Language English
    Size X, 214 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place Totowa, NJ
    Publishing country United States
    Document type Book
    HBZ-ID HT014039648
    ISBN 1-58829-354-8 ; 978-1-58829-354-1
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2004 A 5809 order for loan Magazin

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