Targeting NLRP3-Mediated Neuroinflammation in Alzheimer’s Disease Treatment

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  • Tytuł: Targeting NLRP3-Mediated Neuroinflammation in Alzheimer’s Disease Treatment
  • Autor/Autorzy:
  • Nazwa czasopisma: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
  • Rok: 2022
  • Tom: 23
  • Numer: 16
  • ISSN: 1422-0067
  • e-ISSN: 1422-0067
  • DOI: 10.3390/ijms23168979
  • Adres www:: https://www.mdpi.com/1422-0067/23/16/8979
  • Strony od-do: 1-16
  • Język: angielski
  • Abstrakt: Alzheimer’s disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge. In the pathogenesis of AD, aggregates of amyloid β (Aβ) and neurofibrillary tangles (NFTs) containing Tau-microtubule-associated protein (tau) are known to trigger a neuroinflammatory response with subsequent formation of an inflammasome. In particular, the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is thought to play a crucial role in AD-related pathology. While the mechanisms for NLRP3 activation are not fully understood, it has been demonstrated that, after detection of protein aggregates, NLRP3 induces pro-inflammatory cytokines, such as interleukin 18 (IL-18) or interleukin 1β (IL-1β), that further potentiate AD progression. Specific inhibitors of NLRP3 that exhibit various mechanisms to attenuate the activity of NLRP3 have been tested in in vivo studies and have yielded promising results, as shown by the reduced level of tau and Aβ aggregates and diminished cognitive impairment. Herein, we would like to summarize the current state of knowledge on NLRP3 inflammasome priming, activation, and its actual role in AD pathogenesis, and to characterize the NLRP3 inhibitors that have been studied most and their impact on AD-related pathology.
  • Dyscyplina: nauki medyczne

MARC

  • 002 $a Targeting NLRP3-Mediated Neuroinflammation in Alzheimer’s Disease Treatment
  • 003 $b 0000-0001-8757-6958
  • 003 $b 0000-0002-0308-580X
  • 003 $a EWA KUCHARSKA (Autor)
  • 003 $a Ireneusz Majsterek (Autor)
  • 003 $a Julia Barczuk (Autor)
  • 003 $a Natalia Siwecka (Autor)
  • 003 $a Weronika Lusa (Autor)
  • 003 $a Wioletta Rozpedek-Kamińska (Autor)
  • 004 $a Oryginalny artykuł naukowy
  • 005 $a Praca oryginalna
  • 006 $a INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
  • 008 $a 2022
  • 009 $a 23
  • 010 $a 16
  • 011 $a 1422-0067
  • 012 $a 1422-0067
  • 013 $a 10.3390/ijms23168979
  • 014 $a https://www.mdpi.com/1422-0067/23/16/8979
  • 015 $a 1-16
  • 017 $a angielski
  • 020 $a Alzheimer’s disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge. In the pathogenesis of AD, aggregates of amyloid β (Aβ) and neurofibrillary tangles (NFTs) containing Tau-microtubule-associated protein (tau) are known to trigger a neuroinflammatory response with subsequent formation of an inflammasome. In particular, the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is thought to play a crucial role in AD-related pathology. While the mechanisms for NLRP3 activation are not fully understood, it has been demonstrated that, after detection of protein aggregates, NLRP3 induces pro-inflammatory cytokines, such as interleukin 18 (IL-18) or interleukin 1β (IL-1β), that further potentiate AD progression. Specific inhibitors of NLRP3 that exhibit various mechanisms to attenuate the activity of NLRP3 have been tested in in vivo studies and have yielded promising results, as shown by the reduced level of tau and Aβ aggregates and diminished cognitive impairment. Herein, we would like to summarize the current state of knowledge on NLRP3 inflammasome priming, activation, and its actual role in AD pathogenesis, and to characterize the NLRP3 inhibitors that have been studied most and their impact on AD-related pathology.
  • 022 $a Alzheimer’s disease
  • 022 $a Alzheimer’s disease treatment
  • 022 $a amyloid β
  • 022 $a neurofibrillary tangles
  • 022 $a NOD-like receptor pyrin domaincontaining 3;
  • 022 $a NOD-like receptor pyrin domain-containing 3 inflammasome
  • 022 $a NOD-like receptor pyrin domain-containing 3 inhibitors;
  • 966 $a nauki medyczne
  • 985 $a Wydział Pedagogiczny
  • 985 $b Instytut Nauk o Wychowaniu

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Kucharska_Targeting NLRP3.pdf (1,74 MB)

  • Licencja: CC BY 4.0
  • Wersja tekstu: Ostateczna opublikowana
  • Dostępność: Publiczny