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Oligodendrocytes in the aging brain

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TLDR
In this article, the authors discuss white matter changes, with focus on oligodendrocyte lineage cells and their ability to produce and maintain myelin to support normal brain homoeostasis.
Abstract
More than half of the human brain volume is made up of white matter: regions where axons are coated in myelin, which primarily functions to increase the conduction speed of axon potentials. White matter volume significantly decreases with age, correlating with cognitive decline. Much research in the field of non-pathological brain aging mechanisms has taken a neuron-centric approach, with relatively little attention paid to other neural cells. This review discusses white matter changes, with focus on oligodendrocyte lineage cells and their ability to produce and maintain myelin to support normal brain homoeostasis. Improved understanding of intrinsic cellular changes, general senescence mechanisms, intercellular interactions and alterations in extracellular environment which occur with aging and impact oligodendrocyte cells is paramount. This may lead to strategies to support oligodendrocytes in aging, for example by supporting myelin synthesis, protecting against oxidative stress and promoting the rejuvenation of the intrinsic regenerative potential of progenitor cells. Ultimately, this will enable the protection of white matter integrity thus protecting cognitive function into the later years of life.

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Spatial transcriptomic analysis reveals inflammatory foci defined by senescent cells in the white matter, hippocampi and cortical grey matter in the aged mouse brain

TL;DR: In this article , spatial transcriptomics (ST)-based method was used to identify microdomains containing senescent cells and were mapped to different anatomical brain regions to assess spatial distribution of cellular senescence in the aged mouse brain.
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The mechanism of ferroptosis regulating oxidative stress in ischemic stroke and the regulation mechanism of natural pharmacological active components.

TL;DR: In this article , the progress in the regulation mechanism of natural chemical components and herbal chemical components on ferroptosis in recent years is summarized, in order to provide reference information for future research on ferroidosis and lead compounds for the development of ferroidptosis inhibitors.
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Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin

TL;DR: The developmental cues and molecular drivers which regulate normal myelination both at the prenatal and postnatal periods are determined and the molecular pathways that can potentially be targets for pharmacological interventions in a variety of neurological disorders that exhibit demyelination are defined.
Journal ArticleDOI

Multiple Sclerosis and Aging: The Dynamics of Demyelination and Remyelination

Jorge Correale, +1 more
- 01 Jan 2022 - 
TL;DR: It is demonstrated that old mature OGDs lose their ability to produce and maintain healthy myelin over time, to induce de novo myelination, and to remodel pre-existing myelinated axons that contribute to neural plasticity in the CNS.
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Hallmarks of neurodegenerative disease: A systems pharmacology perspective

TL;DR: Formulating the mechanistic understanding of neurodegenerative pathophysiology as a mathematical model could aid in the identification and prioritization of drug targets and combinatorial treatment strategies, evaluate the role of patient characteristics on disease progression and therapeutic response, and serve as a central repository of knowledge.
References
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Journal ArticleDOI

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TL;DR: A consideration of the cause of the eventual degeneration of these strains leads to the hypothesis that non-cumulative external factors are excluded and that the phenomenon is attributable to intrinsic factors which are expressed as senescence at the cellular level.
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The limited in vitro lifetime of human diploid cell strains

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Telomeres shorten during ageing of human fibroblasts.

TL;DR: The amount and length of telomeric DNA in human fibroblasts does in fact decrease as a function of serial passage during ageing in vitro and possibly in vivo.
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The processing-speed theory of adult age differences in cognition.

TL;DR: A theory is proposed that increased age in adulthood is associated with a decrease in the speed with which many processing operations can be executed and that this reduction in speed leads to impairments in cognitive functioning because of what are termed the limited time mechanism and the simultaneity mechanism.
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The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression

TL;DR: A senescence-associated secretory phenotype (SASP) is acquired that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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