AI Article Synopsis

  • Defective clearance of amyloid-β (Aβ) and inflammation contribute significantly to Alzheimer's disease (AD), with problems in transporting Aβ across the blood-brain barrier leading to plaque formation.
  • A study using porcine brain cells and murine hippocampal cultures showed that the antioxidant astaxanthin (ASX) improved the clearance of misfolded proteins and altered Aβ processing by promoting autophagy and enhancing specific transporters.
  • ASX also demonstrated anti-inflammatory properties by decreasing inflammatory cytokines and shifting microglial cells from a pro-inflammatory state (M1) to a protective state (M2), suggesting its potential as a treatment for AD-related issues.

Article Abstract

Defective degradation and clearance of amyloid-β as well as inflammation per se are crucial players in the pathology of Alzheimer's disease (AD). A defective transport across the blood-brain barrier is causative for amyloid-β (Aβ) accumulation in the brain, provoking amyloid plaque formation. Using primary porcine brain capillary endothelial cells and murine organotypic hippocampal slice cultures as in vitro models of AD, we investigated the effects of the antioxidant astaxanthin (ASX) on Aβ clearance and neuroinflammation. We report that ASX enhanced the clearance of misfolded proteins in primary porcine brain capillary endothelial cells by inducing autophagy and altered the Aβ processing pathway. We observed a reduction in the expression levels of intracellular and secreted amyloid precursor protein/Aβ accompanied by an increase in ABC transporters ABCA1, ABCG1 as well as low density lipoprotein receptor-related protein 1 mRNA levels. Furthermore, ASX treatment increased autophagic flux as evidenced by increased lipidation of LC3B-II as well as reduced protein expression of phosphorylated S6 ribosomal protein and mTOR. In LPS-stimulated brain slices, ASX exerted anti-inflammatory effects by reducing the secretion of inflammatory cytokines while shifting microglia polarization from M1 to M2 phenotype. Our data suggest ASX as potential therapeutic compound ameliorating AD-related blood brain barrier impairment and inflammation.

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http://dx.doi.org/10.1016/j.brainres.2023.148518DOI Listing

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