Dietary Protein Supplementation Reverses Spinal Cord Neurodegeneration in a Rat Model of Bitter Cassava-Induced Konzo

Background: Konzo, a neurological disorder linked to consumption of improperly processed Bitter Cassava, is characterized by motor neuron damage and paralysis, yet effective dietary interventions remain poorly understood. This study investigated the potential protective and rehabilitative effects of an eggshell and brown bean protein supplement on spinal cord histoarchitecture in a rat model of Konzo. Methods: Twenty-five female Wistar rats (200–250 g) were randomly assigned into five groups (n=5). Group 1 received standard feed, while Group 2 was fed Bitter Cassava chow to induce Konzo. Group 3 received Cassava plus standard feed, Group 4 received Cassava plus eggshell and brown bean supplement, and Group 5 received the supplement alone. Feeding lasted four weeks. After sacrifice, spinal cords were harvested at the C4–C6 level and examined using qualitative histological assessment with Nissl staining to evaluate neuronal integrity. Results: Histological analysis revealed preserved cytoarchitecture in the control group, with intact anterior horn motor neurons containing abundant Nissl substances. Cassava-only rats displayed marked neurodegeneration, including distorted spinal cord structure, chromatolysis, and gliosis. In the Cassava plus standard feed group, partial preservation was observed, with some neurons retaining normal morphology alongside degenerative changes. The Cassava plus supplement group showed improved preservation, with well-organized grey and white matter, reduced degeneration, and restoration of motor neurons. Supplement-only rats exhibited generally normal spinal cord structure, with mild gliosis and occasional neuronal degeneration. Conclusion: Supplementation with eggshell + brown beans conferred notable neuroprotective and rehabilitative effects against Cassava-induced spinal cord damage. These findings suggest that simple dietary interventions may have practical translational value in populations at risk of Konzo and highlight the potential of nutritional neuroprotection as a low-cost strategy for mitigating Konzo-related neurotoxicity.