Journal
ACS CHEMICAL NEUROSCIENCE
Volume 8, Issue 9, Pages 1901-1912Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acschemneuro.7b00071
Keywords
Alzheimer's disease; amyloid beta peptide; Caenorhabditis elegans; cholinesterases; honokiol
Funding
- University of Queensland
- Australian Government Endeavour Fellowships and Scholarships Program
- UQ
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The biphenyl neolignan honokiol is a neuroprotectant which has been proposed as a treatment for central nervous system disorders such as Alzheimer's disease (AD). The death of cholinergic neurons in AD is attributed to multiple factors, including accumulation and fibrillation of amyloid beta peptide (A beta) within the brain; metal ion toxicity; and oxidative stress. In this study, we used a transgenic Caenorhabditis elegans model expressing full length A beta(42) as a convenient in vivo system for examining the effect of honokiol against A beta-induced toxicity. Furthermore, honokiol was evaluated for its ability to inhibit A beta(42) oligomerization and fibrillation; inhibit acetylcholinesterase and butyrylcholinesterase; scavenge 2,2diphenyl-1-picrylhydrazyl (DPPH) radicals; and chelate iron(II). Honokiol displayed activity similar to that of resveratrol and (-) epigallocatechin gallate (EGCG) in delaying A beta(42)-induced paralysis in C. elegans, and it exhibited moderate-to-weak ability to inhibit A beta(42) on-pathway aggregation, inhibit cholinesterases, scavenge DPPH radicals, and chelate iron(II). Moreover, honokiol was found to be chemically stable relative to EGCG, which was highly unstable. Together with its good drug-likeness and brain availability, these results suggest that honokiol may be amenable to drug development and that the synthesis of honokiol analogues to optimize these properties should be considered.
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