Neuroprotective effects of dried camu-camu (Myrciaria dubia HBK McVaugh) residue in C. elegans

- Dried camu-camu residue extended the lifespan in C. elegans.
- Treatments with dried camu-camu residue increased the expression of antioxidant genes.
- Dried camu-camu residue promoted significant decreased neurotoxicity in C. elegans.
- Dried camu-camu residue is a bioactive-rich product with health-relevant potential.

The effect of hot air dried camu-camu (Myrciaria dubia HBK McVaugh) residue on modulating redox response signaling was evaluated in transgenic Caenorhabditis elegans. Camu-camu residue was fractionated into low and high molecular weight fractions and used as treatments. Relative fold changes in gene expression in response to camu-camu treatments were quantified using fluorescence microscopy. Also, the neuroprotective effects of camu-camu residue in experimentally induced neurodegeneration were evaluated in C. elegans models for Alzheimer's disease (AD) and Parkinson's disease (PD). For AD, time to thermally induced Aβ1-42 aggregation mediated paralysis was evaluated in transgenic C. elegans (CL4176). For PD, MPP + induced neurodegeneration was quantified by loss in motility due to paralysis. Results suggest a significant upregulation expression of superoxide dismutase (SOD-3 and SOD-4) and catalases (CTL-1; CTL-2; CTL-3) in response to treatment with camu-camu residue, especially with the low molecular weight fraction. Furthermore, treatment with this fraction significantly extended the life span in C. elegans by 20% and delayed Aβ1-42 induced paralysis by 21%. Additionally, treatment with camu-camu residue also abrogated MPP + induced neurodegeneration for PD by 15-21%.