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  • 1
    UID:
    gbv_1778565786
    Format: 1 Online-Ressource (161 p.)
    ISBN: 9782889452538
    Series Statement: Frontiers Research Topics
    Content: Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function
    Note: English
    Additional Edition: Erscheint auch als ISBN 2889452530
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    UID:
    almafu_9958370253402883
    Format: 1 electronic resource (161 p.)
    Series Statement: Frontiers Research Topics
    Content: Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.
    Note: English
    Additional Edition: ISBN 2-88945-253-0
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Online Resource
    Online Resource
    [Erscheinungsort nicht ermittelbar] : Frontiers Media SA
    UID:
    b3kat_BV044802544
    Format: 1 Online-Ressource (159 Seiten) , Illustrationen, Diagramme
    ISBN: 9782889452538
    Note: Published in: Frontiers in aging neuroscience
    Language: English
    Subjects: Medicine
    RVK:
    Keywords: Nervendegeneration ; Metabolisches Syndrom ; Entzündung ; Gehirn ; Altern ; Aufsatzsammlung
    URL: Volltext  (kostenfrei)
    Library Location Call Number Volume/Issue/Year Availability
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