Affiliations 

  • 1 School of Health Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia; USM-RIKEN International Centre for Ageing Science (URICAS), Universiti Sains Malaysia, 11800 Penang, Malaysia. Electronic address: florence.hptan@aiesec.net
  • 2 School of Biological Sciences, Universiti Sains Malaysia, 11800 Penang, Malaysia; USM-RIKEN International Centre for Ageing Science (URICAS), Universiti Sains Malaysia, 11800 Penang, Malaysia
  • 3 USM-RIKEN International Centre for Ageing Science (URICAS), Universiti Sains Malaysia, 11800 Penang, Malaysia; Bioprobe Application Research Unit, RIKEN Centre for Sustainable Resource Science, RIKEN, Japan; Chemical Resource Development Research Unit, RIKEN CSRS, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan
  • 4 School of Health Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia; USM-RIKEN International Centre for Ageing Science (URICAS), Universiti Sains Malaysia, 11800 Penang, Malaysia; Nanobiotech Research Initiative, Institute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, Penang 11800, Malaysia
  • 5 School of Biological Sciences, Universiti Sains Malaysia, 11800 Penang, Malaysia; USM-RIKEN International Centre for Ageing Science (URICAS), Universiti Sains Malaysia, 11800 Penang, Malaysia; Malaysia Genome and Vaccine Institute (MGVI), National Institutes of Biotechnology Malaysia (NIBM), Jalan Bangi, 43000 Kajang, Selangor, Malaysia. Electronic address: ghows@usm.my
Behav Brain Res, 2023 Aug 24;452:114568.
PMID: 37414223 DOI: 10.1016/j.bbr.2023.114568

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative condition in civilizations worldwide. The distinctive occurrence of amyloid-beta (Aβ) accumulation into insoluble fibrils is part of the disease pathophysiology with Aβ42 being the most toxic and aggressive Aβ species. The polyphenol, p-Coumaric acid (pCA), has been known to boost a number of therapeutic benefits. Here, pCA's potential to counteract the negative effects of Aβ42 was investigated. First, pCA was confirmed to reduce Aβ42 fibrillation using an in vitro activity assay. The compound was next examined on Aβ42-exposed PC12 neuronal cells and was found to significantly decrease Aβ42-induced cell mortality. pCA was then examined using an AD Drosophila melanogaster model. Feeding of pCA partially reversed the rough eye phenotype, significantly lengthened AD Drosophila's lifespan, and significantly enhanced the majority of the AD Drosophila's mobility in a sex-dependent manner. The findings of this study suggest that pCA may have therapeutic benefits for AD.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.