(P27-027-23) Neurological Effects of Cannabidiol Supplementation in Cognitive Impaired Adult Male Wistar Rats

Objectives: Cognitive dysfunction is a major debilitating age-related disorder and also a common side effect of a number of medications and metabolic disorders. There is overwhelming evidence that one of the side effects of a number of antiretroviral drugs such as protease inhibitors (PI) is cognitive impairment. Cannabidiol (CBD), an isolate of Cannabis sativa is well reported for its antipsychotic, anxiolytic, anti-inflammatory, and neuroprotective effects. However, it is not known whether CBD is capable of preventing or ameliorating PI induced cognitive impairment. The present study was thus designed to ascertain the neuroprotective effects of CBD on ritonavir induced cognitive impairment in adult male albino Wister rat.

Methods: Adult male Wister rats weighing 160-180 g were divided into five groups (n=7). Group 1 animals served as control and were untreated. Group 2-5 were treated with PI (ritonavir 40 mg/Kg) and high fat diet (HFD) for 2 weeks. Concurrent treatment of apple cider vinegar (0.8 mg/Kg), CBD (10 and 25 mg/kg) were administered to groups 3-5 animals respectively. Cognitive functions, brain biochemical markers, histology and immunohistochemistry were determined.

Results: 2 weeks of HFD+PI treatment induced cognitive impairment evidenced by decreased discriminative index in Object recognition memory (ORM) and Object location memory (OLM) tests, significant elevated Glial fibrillary acidic protein (GFAP) expression in the prefrontal cortex and increased lipid peroxidation in the prefrontal cortex and the hippocampus. CBD treatment especially at the higher dose mitigated the HFD+PI induced cognitive impairment which was associated with reduced serum amyloid beta 1-42 levels, cortical lipid peroxidation, GFAP and Acetylcholinesterase (ACHE) expression.

Conclusions: In conclusion, CBD, depending on its dose, possesses remarkable cognitive preserving activity which is associated with decreased lipid peroxidation and down regulation of GFAP/ACHE pathways in rats treated with HFD+PI.

Funding Sources: Self-funded