The incidence of neurodegenerative diseases is directly proportional to age. The prevalence of non-communicable diseases, for example, Alzheimer’s and Parkinson’s, is expected to rise in the coming years. Understanding the etiopathology of these diseases is a crucial step that needs to be taken to develop drugs for their treatment. Animal models are being increasingly used to expand the knowledge and understanding on neurodegenerative diseases. Marine worms, known as polychaetes (phylum Annelida), which are abundantly and frequently found in benthic environments, possess a simple yet complete nervous system (including a true brain that is centralised and specialised) compared to other annelids. Hence, polychaetes can potentially be the next candidate for a nerve disease model. The ability to activate the entire nervous system regeneration (NSR) is among the remarkable features of many polychaetes species. However, the information on NSR in polychaetes and how it can potentially model neurodegenerative diseases in humans is still lacking. By exploring such studies, we may eventually be able to circumvent the developmental constraints that limit NSR in the human nervous system. This article is intended to briefly review responsible mechanisms and signalling pathways of NSR in marine polychaetes and to make a comparison with other established models of neurodegenerative disease.

Background: Mitragyna speciosa (MS) or ketum is primarily found in Southeast Asia, particularly in northern Malaysia and Thailand. The medicinal value of this plant has attracted significant attention from both herbal medicine practitioners and scientists worldwide. Despite having illegal consumption status, the plant merits study. We conducted a series of experiments to test our hypothesis that ketum impairs both learning and memory in rats. Methods: Ketum leaves were extracted using methanol and standardised for the amount of its pure compound, mitragynine. Rats were divided into groups for a passive avoidance task and long-term potentiation (LTP) extracellular recording. In the extracellular recording condition, rats were grouped into control, MS100 (100 mg/kg of ketum extract), MS200 (200 mg/kg of ketum extract), and MS500 (500 mg/kg of ketum extract) groups. An additional group that received morphine was included in the passive avoidance task (10 mg/kg), and there were six animals per group. Rats received daily treatments orally for 28 days for both experiments. Result: Using a passive avoidance task, our data revealed that the rats' memory significantly increased with increasing doses of MS compared to the morphine-treated group. Our findings from LTP recordings showed that LTP was fully blocked by the higher doses of MS. Conclusion: We speculate on the possibility that additional factors were involved in the passive avoidance task because it was an in vivo animal study, while the LTP experiment solely involved brain slices.