Adejoke Elizabeth Memudu

Rauvolfia vomitoria (RV) is recognised for its anti-seizure properties, largely due to its rich alkaloid content. In this study, we evaluated the effect of an aqueous extract of Rauvolfia vomitoria on PTZ-induced seizures in male Wistar rats and used in-silico methods to identify the most promising alkaloid compound for predictive analysis. Male Wistar rats (average weight: 160 g) were divided into four groups (n = 5): saline (control), 25 mg/kg PTZ i.p., 200 mg/kg oral RV pretreatment + 25 mg/kg PTZ i.p., and 40 mg/kg oral carbamazepine pretreatment + 25 mg/kg PTZ i.p. Following treatment, we assessed behaviour via the novel object recognition test (NORT) and evaluated antioxidant enzyme levels, brain electrolyte concentrations, and histomorphology changes. Additionally, we employed molecular docking and pharmacokinetic profiling to assess the drug-like properties of the compounds. NORT results revealed increased exploratory time and a non-significant discrimination index. Antioxidant defences were enhanced, while lipid peroxidation indices showed a non-significant reduction. Major electrolyte concentrations were preserved. Molecular docking identified serpentinine as a high-affinity NMDA receptor ligand, with several other Rauvolfia vomitoria alkaloids exhibiting favourable drug-like properties. Oral pretreatment with Rauvolfia vomitoria mitigates PTZ-induced seizure, potentially through antioxidant modulation and a slight trend towards recognition memory. In-silico analyses highlight Rauvolfia vomitoria alkaloids as promising candidates for further experimental validation.

Background: Ethnopharmacology of plant based dietary compounds with antioxidant activity such as lutein‐20, needs to be evaluated in animal model of Alzheimer's disease (AD) to assess the antioxidant and inflammatory indexes., in addition to histological changes in the prefrontal cortex (PFC) and hippocampus (HP). Method: Twenty (20) adult male Wistar rats grouped into four ( n = 5 viz; control, 20 mg/kg of Lutein‐20 treated group, AD model group exposed to 2 mg/kg of cadmium for 5 days, and the AD animal model group treated with 20 mg/kg of Lutein‐20 for 10 days. Serum was assayed for lipid peroxidation enzyme malondialdehyde (MDA), inflammatory marker total protein, pro‐inflammatory cytokines marker‐ tumour necrosis factor alpha (TNF alpha); antioxidant status of superoxidase dismutase (SOD), and Catalase (CAT) using spectrophotometric method. Statistical analysis was undertaken using one way ANOVA with significance set at p <0.05. Results: Our results demonstrated that cadmium significantly elevated markers of oxidative stress and pro‐inflammatory cytokines (MDA and TNF‐α), declined antioxidant enzyme activities (SOD, CAT, GSH), leading to neurodegeneration in the prefrontal cortex and hippocampus. However, administration of Lutein‐20 markedly reduced oxidative damage and suppressed neuroinflammatory responses through elevation of antioxidant enzyme activities resulting in a reduced disruption of the neuropil in the PFC and HP. Conclusion: Lutein‐20 attenuates pro‐inlnflammatory cytokines and improves antioxidant enzyme activity this underscores its neuroprotective potential as a therapeutic agent for neurodegeneration.

Alzheimer’s disease (AD) is the most common cause of age-related dementia and death, resulting from the aggregation of tau protein into insoluble neurofibrillary tangles (NFTs) composed of paired helical filaments and straight filaments. Graphene quantum dots (GQDs), a unique form of nanoparticles, have emerged as a crucial tool for the detection and diagnosis of AD. They are considered attractive due to their fluorescence-emitting capabilities, nanoscale size, chemical stability, solubility, and ease of synthesis. In this review, we investigated the potential of GQDs as a therapeutic tool in AD intervention, highlighting their recent developments, challenges, and future directions. A comprehensive and systematic search was conducted across electronic databases (Scopus, PubMed, Google Scholar, and Medline) for recent and up-to-date articles related to the keywords: “Alzheimer’s disease,” “graphene quantum dots,” “nanoparticles,” and “neuroscience.” Our findings indicate that QDs possess the ability to cross the blood–brain barrier, reduce disease symptoms, and facilitate drug delivery, cell labeling, and neuronal regeneration. In addition, early identification, prevention, and disassembly of tau protein aggregation in AD can be achieved using GQDs. In conclusion, the application of GQDs to improve the progression of AD neuropathology by disintegrating NFTs of tau protein presents a promising approach for diagnostic research in AD. The limitations of GQDs, particularly their long-term exposure to the brain, need to be thoroughly investigated. This includes minimizing the side effects through a multidisciplinary translational neuroscience approach for therapeutic applications in clinical trials.