Nicotinamide adenine dinucleotide (NAD+) on H2O2-induced neuronal damage in Planarian
JSHS · 2020
Overview
Neurodegenerative diseases are characterized by a decline of motor and cognitive functions caused by the loss and degeneration of neurons. Nicotinamide adenine dinucleotide (NAD+) plays an important role in axonal degeneration. Indeed, decreased NAD+ levels were observed in Alzheimer’s and Parkinson’s diseases. Cell-based studies discovered that exogenous NAD+ protected cells from death induced by oxidative stress. Planarian's nervous system is composed of cephalic ganglia, two ventral nerve cords, and many sensory neurons, and possesses neurotransmitters and associated receptors found in vertebrates. Thus, this study investigated the potential role of NAD+ against neuronal damage using planarians as an animal model. Planarian’s cognitive ability and behavioral responses were measured by phototactic assays. The planarians were treated by Nicotinamide Riboside (NR), an NAD+ precursor, after sustaining neuronal damage by H2O2 exposure. They moved rapidly away from the light reaching >0.8 of the escape index values (θ) in 1 min showing the same responses as the control group. These responses were significantly different than those of untreated planarians which showed 0.22 of θ value in 1 min. Consequently, the NR treatment restored the photophobic resp onses of the H2O2exposed planarians, by enhancing the NAD+ level, thereby activating downstream factors such as NAD+- dependent Sirtuins (SIRT), and eventually repairing neuronal damage. This was supported by the restored photophobic responses of Resveratrol (a SIRT1 activator)-treated planarians. This study provides the first insight into the protective role of NAD+ and Sirtuin against neuronal damage in planarians and demonstrates that planarian can be a good animal model for neurodegenerative diseases.
Competition history
- JSHS 2020
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