Green kiwifruit extracts protect motor neurons from death in a spinal muscular atrophy model in Caenorhabditis elegans

Abstract

Kiwifruit is considered a functional food and a good source of nutraceuticals. Among the possible beneficial effects of kiwifruit species, a neuroprotective activity exerted in rats with learning and memory impairment induced by exposure to different chemicals was reported. We sought to investigate the neuroprotective activities of kiwifruit toward spinal muscular atrophy (SMA). To this purpose, we have used a recently developed Caenorhabditis elegans SMA model, displaying an age‐dependent degeneration of motor neurons detected as locomotory defects, disappearance of fluorescent markers, and apoptotic death of targeted neurons. Although an anti‐nematode activity is reported for kiwifruit, it has been verified that neither green ( Actinidia deliciosa , cultivar Hayward) nor gold ( Actinidia chinensis , cultivar Hort 16A) kiwifruit extracts cause detectable effects on wild‐type C. elegans growth and life cycle. Conversely, green kiwifruit extracts have a clear effect on the C. elegans SMA model by partially rescuing the degeneration and death of motor neurons and the locomotion impairment. The gold species does not show the same effect. The components responsible for the neuroprotection are macromolecules with a molecular weight higher than 3 kDa, present in the green and not in the yellow kiwifruit. In conclusion, this is the first study reporting a protective activity of green kiwifruit toward motor neurons. In addition, we demonstrate that C. elegans is an animal model suitable to study the biological activities contained in kiwifruit. Therefore, this model can be exploited for future investigations aimed at identifying kiwifruit molecules with potential applications in the field of human health.

Impairment of the neurotrophic signaling hub B-Raf contributes to motoneuron degeneration in spinal muscular atrophy

“…The B-Raf reduction was conserved in a C. elegans severe SMA model with reduced levels of the homolog lin-45. To avoid hindrances due to pleiotropic phenotypes observed in this severe model, we used a C. elegans conditional SMA model, through which we were already able to identify smn-1 interactors and factors playing a role in the prevention of neurodegeneration (60)(61)(62). In this model we could obtain a dose-dependent and cellautonomous rescue of the neurodegeneration with a wild-type and a hyperactive version of lin-45.…”

Divergent Effects of the Nonselective Adenosine Receptor Antagonist Caffeine in Pre-Manifest and Motor-Manifest Huntington’s Disease

“…Using preclinical models, the nematode Caenorhabditis elegans ( C. elegans ) was assessed as an animal model in manifold neurodegenerative disorders not only to evaluate effects of pharmacological or nutraceutical interventions and to identify neuroprotective candidates in neuronal cells, but also to gain insights into so-called “behavioral genetics” [ 21 , 22 ]. Manifold former research investigated different approaches of HD in C. elegans to investigate therapeutic effects of potential disease modifying targets or to identify underlying pathophysiological neurotoxic cascades [ 23 , 24 , 25 ].…”