Introduction: There is a scarcity of epidemiological data on neurodegenerative diseases (NDs) in East Africa. This meta-analysis provides the regional prevalence of NDs, their contributing factors, and evidence of change over time concerning gender per age or year.Methods: Articles were retrieved from electronic databases following the PRISMA standard.Results: Forty-two studies were reviewed, and 25 were meta-analyzed with a random-effects model. The pool estimate proportion of 15.27%, 95% CI (0.09–0.23) (I² = 98.25%), (Q = 1,369.15, p < 0.0001) among a population of 15,813 male/female and 1,257 with NDs. Epidemiological characteristics associated with NDs include Dyskinesias prevalence 55.4%, 95% CI (13.5; 90.9), I² (96%) and subsistence farming prevalence 11.3%, 95% CI (5.8; 20.9), I² (99%). Publication bias by Egger test was (z = 4.1913, p < 0.0001), while rank correlation test using Kendall's model was (tau = 0.1237, p = 0.3873). Heterogeneity (R² design = 5.23%, p design < 0.0001; R² size = 52.163%, p size < 0.001; and R² period = 48.13, p period < 0.0001. Covariates (R² design + size + period = 48.41%, p < 0.001).Conclusion: There is a high prevalence of NDs in the East African region, which could impact life expectancy, morbidity, and quality of life. Thus, early screening and regular surveillance could assist in management strategies.

Background: The mechanisms involved in the spermatotoxic effect of Cannabis sativa are inconclusive. The involvement of oxidative stress in male factor infertility has been well documented, and the antioxidative potential of melatonin and vitamin C in many oxidative stress conditions has been well reported. This study sought to investigate whether melatonin and vitamin C will ameliorate C. sativa -induced spermatotoxicity or not. Methods: Fifty-five (55) male albino rats (250–300 g) were randomly divided in a blinded fashion into five oral treatment groups as follows: group I (control, n=5) received 1 mL/kg of 10% ethanol for 30 days; groups IIa, IIb, and IIc (n=5 each) received 2 mg/kg C. sativa for 20, 30, and 40 days, respectively; groups IIIa, IIIb, and IIIc (n=5 each) received a combination of 2 mg/kg C. sativa and 4 mg/kg melatonin for 20, 30, and 40 days, respectively; groups IVa, IVb, and IVc (n=5 each) received a combination of 2 mg/kg C. sativa and 1.25 g/kg vitamin C for 20, 30, and 40 days, respectively; group V (n=5) received a combination of 2 mg/kg C. sativa , 4 mg/kg melatonin, and 1.25 g/kg vitamin C for 30 days. Results: Cannabis treatments reduced the Johnsen score, sperm count, motility, morphology, paired testicular/body weight ratio, and total antioxidant capacity, but increased lactate dehydrogenase activity. In addition, supplementation of cannabis-treated rats with either melatonin or vitamin C exacerbates the effect of cannabis on those parameters, whereas combination of melatonin and vitamin C reversed the trend to the level comparable to control. Conclusions: This study further showed the gonadotoxic effect of C. sativa , which could be mediated by oxidative stress. It also showed that melatonin and vitamin C exacerbate C. sativa -induced testicular damage when administered separately but ameliorate it when combined in rats.

We investigated the effects of melatonin on sperm parameters and some biochemical markers in lead-exposed male Wistar rats. Lead (50 mg/kg bw/day) and/or melatonin (4 mg/kg or 10 mg/kg bw/day) was administered for 4 weeks, while 2-week lead exposure was preceded by or followed by 2-week treatment with both doses of melatonin in other groups. Lead reduced glutathione, catalase, adjusted testes weight, semen parameters but did not change malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, and total antioxidant capacity. Though independent of prolactin, lead-induced gonadotoxicity was both centrally and peripherally mediated, as it reduced gonadotropin-releasing hormone and testosterone levels, while gonadotropin levels did not change significantly probably due to negative feedback by elevated estradiol. However, pre-, simultaneous, or posttreatment of lead-exposed rats with melatonin reduced MDA, SOD, and estradiol but dose-dependently increased other parameters. Conclusively, lead causes male gonadotoxicity through oxidative stress and endocrine mechanisms, and these could be dose-dependently prevented and ameliorated by melatonin.

Introduction: Lead is the most used nonphysiological neurotoxic heavy metal in the world that has been indicated to interfere with the cognitive and noncognitive processes via numerous mechanisms. The neuroprotective effect of melatonin is well known, but the effect of its interaction with lead in the brain remains inconclusive.Objective: To assess the therapeutic role of melatonin on cognitive deficit, anxiety and depressive‐like symptoms in matured male Wistar rats exposed to a subchronic lead chloride (PbCl₂).Methods: Twenty male Wistar rats were blindly randomized into four groups (n = 5/group): group 1 to 4 underwent intragastric administration of physiological saline (10 ml/kg; vehicle), PbCl₂ (50 mg/kg), melatonin (10 mg/kg) and PbCl₂ + melatonin respectively for a period of 4 weeks during which neurobehavioral data were extracted, followed by neurochemical and histopathological evaluations.Results: Exposure to PbCl₂ reduced cognitive performance by increasing the escape latency and average proximity to the platform zone border, decreasing average path length in the platform zone, cognitive score, and time spent in probing. It raised the thigmotaxis percentage, time spent in rearing, number of pellet‐like feces, and time spent in the dark compartment of a bright/dark box which are predictors of anxiety. It also induced depressive‐like behavior as immobility time was enhanced. PbCl₂ deranged neurochemicals; malondialdehyde, interlukin‐1β, and tumor necrotic factor‐α were increased while superoxide dismutase and acetylcholinesterase were decreased without remarkable alteration in reduced glutathione and nitric oxide. Administration of PbCl₂ further disrupted neuronal settings of hippocampal proper and dentate gyrus. In contrast, the supplementation of melatonin reversed all the neurological consequences of PbCl₂ neurotoxicity by eliciting its properties against oxidative and nonoxidative action of PbCl₂.Conclusion: These findings suggest that melatonin down‐regulates neurotoxicant interplays in the brain systems. Therefore, this study suggests the use of melatonin as an adjuvant therapy in neuropathological disorders/dysfunctions.

Annona muricata and Khaya grandifoliola are ethnomedicinally used for the treatment of malaria and have been experimentally shown to have an anti-plasmodial effect, but the mechanisms involved are not fully understood. This study investigated the effect of the ethanol extracts of their leaves on parasitemia, radical scavenging and cytokines in Plasmodium berghei ANKA-infected BALB/c mice. BALB/c mice were infected with P. berghei and treated with chloroquine, A. muricata or K. grandifoliola extract for 4 days. The percentage of parasitemia and the level of cytokine expression were determined after treatment. Trace element, phytochemical and nitric oxide (NO) scavenging activity, 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging properties assays were done to study the antioxidant effects of AN and KG in vitro. P. berghei consistently increased parasitemia in BALB/c mice. The tested doses (100-, 200-, and 400 mg/kg) of A. muricata and K. grandifoliola attenuated the P. berghei-induced elevation of parasitemia and cytokines (TNF-α, IL-5, and IL-6) in vivo during the experimental period, though not as much as chloroquine. Moreover, both extracts scavenged the DPPH and NO radicals, though A. muricata had more anti-oxidant effect than K. grandifoliola in-vitro. The ethanol extracts of A. muricata and K. grandifoliola reduce parasitemia in P. berghei-treated mice BALB/c by scavenging free radicals and reducing cytokines, though the extracts were not as effective as chloroquine.

The role of oxidative stress in Cannabis sativa (CS)-associated reproductive toxicity is inconclusive. The present study employed reactive oxygen species (ROS)-total antioxidant capacity (TAC) score to understand the effect of CS on oxidative stress, while the possible anti-oxidative effect of melatonin and vitamin C were also investigated in rats receiving them alone or together with cannabis. Fifty-four male albino rats were randomized to 9 oral treatment groups (n = 6) as follow: Groups I and II served as control and received 1 ml/kg normal saline and 10% ethanol (vehicle for CS administration) respectively. Groups III–V received melatonin (4 mg/kg), vitamin C (1.25 g/kg) and their combination respectively. Group VI received CS (2 mg/kg), while groups VII–IX received melatonin, vitamin C, and their combination respectively in addition to CS. All treatment lasted for 30 days. The CS reduced the sperm parameters, TAC, and the ROS-TAC score but increase the ROS, while only melatonin and/or vitamin C improved these parameters. Supplementation of rats receiving CS with either melatonin or vitamin C exacerbated the CS-induced oxidative stress and spermatotoxicity but their combination (melatonin + vitamin C) prevented these conditions in them. Furthermore, ROS-TAC score better predicted the condition of sperm than either TAC or ROS. In conclusion, this study further implicates oxidative stress in CS-induced spermatotoxicity using the ROS-TAC score. It also provides evidences for the preventive effect of melatonin and vitamin C on oxidative stress and sperm toxicity when combined but not when administered separately in rats receiving CS