• Medientyp: E-Artikel
  • Titel: The role of ATP-binding cassette subfamily A in the etiology of Alzheimer’s disease
  • Beteiligte: Bossaerts, Liene; Cacace, Rita; Van Broeckhoven, Christine
  • Erschienen: Springer Science and Business Media LLC, 2022
  • Erschienen in: Molecular Neurodegeneration
  • Sprache: Englisch
  • DOI: 10.1186/s13024-022-00536-w
  • ISSN: 1750-1326
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Alzheimer’s disease (AD) is the leading cause of dementia, clinically characterized by memory deficits and progressive cognitive decline. Despite decades of research effective therapies are lacking, and a large part of the genetic heritability remains unidentified.<jats:italic>ABCA7</jats:italic>and<jats:italic>ABCA1</jats:italic>, members of the ATP-binding cassette subfamily A (ABCA), were identified as AD risk genes in genome-wide association studies. Nevertheless, genetic and/or functional studies propose a link between AD and two other members of the ABCA subclass, i.e., ABCA2 and ABCA5.</jats:p></jats:sec><jats:sec><jats:title>Main body</jats:title><jats:p>Changes in expression or dysfunction of these transporters were found to increase amyloid β levels. This might be related to the common role of ABCA transporters in cellular cholesterol homeostasis, for which a prominent role in AD development has been suggested. In this review, we provide a comprehensive overview and discussion on the contribution of the ABCA subfamily to the etiopathogenesis of AD.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>A better understanding of the function and identification of disease-associated genetic variants in ABCA transporters can contribute to the development of novel therapeutic strategies for AD.</jats:p></jats:sec>
  • Zugangsstatus: Freier Zugang