Increased risk of neurodegenerative diseases (NDG) and reduced lifespan (LS) are liked to Type-2 diabetes mellitus (T2DM), dyslipidemia (DL) and inflammation (IF). Dysregulation in insulin/insulin-like growth factor-1 (IGF-1) (IIS) signaling, forkhead box O transcription factor (FOXO) and Silent Information Regulators or Sirtuins (SIRT) have been implicated as common etiological factors. We investigated the effect of three tropical fruits Jambolan (Eugenia jambolana Lam.), camu-camu (Myrciaria dubia HBK McVaugh) and Pitanga (Eugenia uniflora L.) fruit in Caenorhabditis elegans model for lifespan (LS) and NDG. For Alzheimer’s disease (AD), time to thermally induced amyloid b1-42 (Ab1-42) mediated paralysis was evaluated in transgenic C. elegans. For Parkinson’s Disease (PD), MPP+ (1-methyl-4-phenylpyridinium) induced neurodegeneration was quantified by loss in motility due to paralysis. Effect of fruit extracts and their respective fractions on modulating critical genes involved signaling pathways important in IIS, antioxidant response (AR), LS and NDG in transgenic C. elegans were quantified using fluorescence microscopy. Results suggest a statistically significant increase in lifespan coupled with a delay in Ab1-42 and MPP+ induced paralysis. Green fluorescent protein (GFP) tagged expression studies indicated a differential modulation of C. elegans homologs of genes relevant to IIS, AR and NDG by individual fruits and their fractions. In our preliminary evaluation, these tropical fruits conferred neuroprotection and prolonged lifespan in C. elegans. Further studies on elucidating the molecular mechanism of action and bioactive principles from these fruits are currently underway.

Evaluation of three tropical fruits on lifespan and experimentally induced neurodegeneration in Caenorhabditis elegans

251st National Meeting (2016)

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