Inflammation as a central mechanism in Alzheimer's disease

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  • Jefferson W. Kinney
    Department of Psychology University of Nevada Las Vegas Las Vegas NV USA
  • Shane M. Bemiller
    Stark Neurosciences Research Institute, Indiana University School of Medicine Indianapolis IN USA
  • Andrew S. Murtishaw
    Department of Psychology University of Nevada Las Vegas Las Vegas NV USA
  • Amanda M. Leisgang
    Department of Psychology University of Nevada Las Vegas Las Vegas NV USA
  • Arnold M. Salazar
    Department of Psychology University of Nevada Las Vegas Las Vegas NV USA
  • Bruce T. Lamb
    Stark Neurosciences Research Institute, Indiana University School of Medicine Indianapolis IN USA

書誌事項

公開日
2018-01
権利情報
  • http://creativecommons.org/licenses/by-nc-nd/4.0/
DOI
  • 10.1016/j.trci.2018.06.014
公開者
Wiley

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説明

<jats:title>Abstract</jats:title> <jats:p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia‐related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.</jats:p>

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