Abstract

AbstractBackgroundNeurodegeneration diseases are a group of diseases like Alzheimer’s disease that are characterized by poor cognitive abilities, neuromuscular deficiencies and locomotion difficulties. The goal of biomedical research is to seek to explore suitable experimental models to study such neurological disorders. Such suitable models must underscore the 3Rs of alternative research models ‐ replacement, reduction and refinement. The lobster cockroach (Nauphoeta cinerea) is one such model that is gaining global attention for their suitability to study human‐related diseases. Therefore, this study aims to model neuromuscular deficiencies and neurodegeneration associated with impaired glucose homeostasis in lobster cockroach (Nauphoeta cinerea).MethodAcute neurotoxicity was achieved by injecting 74 and 740 nm streptozotocin (STZ) injection per cockroach head and the cockroaches were monitored for 7 days. Thereafter, their survival rate, mortality and behavioral profiles for neuromuscular function including the total time immobile, total distance traveled, time spent in periphery and average speed were assessed on the seventh day, after which the cockroaches were assayed for biomarkers of neurodegeneration and oxidative stress.ResultThe results showed that the survival rate, average speed and total distance traveled were reduced significantly, while STZ increased the mortality, time spent in periphery and total time immobile. Furthermore, STZ induced an increase in acetylcholinesterase activity, lipid peroxidation and total reactive oxygen species. In addition, the results also suggest an impairment in glucose‐trehalose conversation mechanism.ConclusionThese results are obvious indications of behavioral impairments and metabolic disruptions which affect neuromuscular function and are indices of neurodegeneration. This therefore, suggests that direct injection of STZ to cockroach head is a useful, effective and reproducible model in evaluating neuromuscular deficiencies and neurodegeneration associated with brain glucose metabolic dysregulation.

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