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Photobiomodulation (PBM), also known as Low-level Laser Therapy (LLLT), involves the use of light from a laser or light-emitting diode (LED) in the treatment of various disorders and it has recently gained increasing interest. Progressive neuronal loss with attendant consequences such as cognitive and/or motor decline characterize neurodegenerative diseases. The available therapeutic drugs have only been able to provide symptomatic relief and may also present with some side effects, thus precluding their use in treatment. Recently, there has been an exponential increase in interest and attention in the use of PBM as a therapy in various neurodegenerative diseases in animal studies. Because of the financial and social burden of neurodegenerative diseases on the sufferers and the need for the discovery of potential therapeutic inventions in their management, it is pertinent to examine the beneficial effects of PBM and the various cellular mechanisms by which it modulates neural activity. Here, we highlight the various ways by which PBM may possess beneficial effects on neural activity and has been reported in various neurodegenerative conditions (Alzheimer's disease, Parkinson's disease, epilepsy, TBI, stroke) with the hope that it may serve as an alternative therapy in the management of neurodegenerative diseases because of the biological side effects associated with drugs currently used in the treatment of neurodegenerative diseases.
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Background: Despite widespread concerns about its possible side effects, notably on the prefrontal cortex (PFC), which mediates cognitive processes, the use of Cannabis sativa as a medicinal and recreational drug is expanding exponentially. This study evaluated possible behavioral alterations, neurotransmitter levels, histological, and immunohistochemical changes in the PFC of Wistar rats exposed to Cannabis sativa. Purpose: To evaluate the effect of graded doses of Cannabis sativa on the PFC using behavioural, histological, and immunohistochemical approaches. Methods: Twenty-eight juvenile male Wistar rats weighing between 70 g and 100 g were procured and assigned into groups A-D (n = 7 each). Group A served as control which received distilled water only as a placebo; rats in groups B, C, and D which were the treatment groups were orally exposed to graded doses of Cannabis sativa (10 mg/kg, 50 mg/kg, and 100 mg/kg, respectively). Rats in all experimental groups were exposed to Cannabis sativa for 21 days, followed by behavioral tests using the open field test for locomotor, anxiety, and exploratory activities, while the Y-maze test was for spatial memory assessment. Rats for biochemical analysis were cervically dislocated and rats for tissue processing were intracardially perfused following neurobehavioral tests. Sequel to sacrifice, brain tissues were excised and prefrontal cortices were obtained for the neurotransmitter (glutamate, acetylcholine, and dopamine) and enzymatic assay (Cytochrome C oxidase (CcO) and Glucose 6- Phosphate Dehydrogenase-G-6-PDH). Brain tissues were fixed in 10% Neutral Buffered Formalin (NBF) for histological demonstration of the PFC cytoarchitecture using H&E and glial fibrillary acidic protein (GFAP) for astrocyte evaluation. Results: Glutamate and dopamine levels were significantly increased (F = 24.44, P = .0132) in groups D, and B, C, and D, respectively, compared to control; likewise, the activities of CcO and G-6-PDH were also significantly elevated (F = 96.28, P = .0001) (F = 167.5, P = .0001) in groups C and D compared to the control. Cannabis sativa impaired locomotor activity and spatial memory in B and D and D, respectively. All Cannabis sativa exposed groups demonstrated evidence of neurodegeneration in the exposed groups; GFAP immunoexpression was evident in all groups with a marked increase in group D. Conclusion: Cannabis sativa altered neurotransmitter levels, energy metabolism, locomotor, and exploratory activity, and spatial working memory, with neuronal degeneration as well as reactive astrogliosis in the PFC.
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The high pathogenic nature of the Middle East Respiratory coronavirus (MER) and the associated high fatality rate demands an urgent attention from researchers. Because there is currently no approved drug for the management of the disease, research efforts have been intensified towards the discovery of a potent drug for the treatment of the disease. Papain Like protease (PLpro) is one of the key proteins involved in the viral replication. We therefore docked forty-six compounds already characterized from Azadirachta indica, Xylopia aethipica and Allium cepa against MERS-CoV-PLpro. The molecular docking analysis was performed with AutoDock 1.5.6 and compounds which exhibit more negative free energy of binding, and low inhibition constant (Ki) with the protein (MERS-CoV-PLpro) were considered potent. The physicochemical and pharmacokinetic properties of the compounds were predicted using the Swissadme web server. Twenty-two of the compounds showed inhibition potential similar to dexamethasone and remdesvir, which had binding affinity of -6.8 and -6.3 kcal/mol respectively. The binding affinity of the compounds ranged between -3.4 kcal/mol and -7.7 kcal/mol whereas; hydroxychloroquine had a binding affinity of -4.5 kcal/mol. Among all the compounds, nimbanal and verbenone showed drug likeliness, they did not violate the Lipinski rule neither were they inhibitors of drug-metabolizing enzymes. Both nimbanal and verbenone were further post-scored with MM/GBSA and the binding free energy of nimbanal (-25.51 kcal/mol) was comparable to that of dexamethasone (-25.46 kcal/mol). The RMSD, RMSF, torsional angle, and other analysis following simulation further substantiate the efficacy of nimbanal as an effective drug candidate. In conclusion, our study showed that nimbanal is a more promising therapeutic agent and could be a lead for the discovery of a new drug that may be useful in the management of severe respiratory coronavirus syndrome.
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This study assessed the effect of varying doses of aqueous extract of Aloe barbadensis on the cellular changes of hippocampal cells, oxidative and memory state of Wistar rats following monosodium glutamate-induced neurotoxicity. Eighty Wistar rats (8 weeks) were randomly as-signed into 4 groups of 20 rats; Group 1 received 3 mL/kg of distilled water. Groups 2, 3 and 4 received 3 g/kg/day of MSG. In addition, groups 3 and 4 received 100 and 200 mg/kg/day of AB ex-tract respectively. Administration was done orally for 28 days in all groups. Five rats per group were sacrificed weekly over a 4-week period. Memory was assessed using radial arm maze on the last day of administration. Following brain harvest, one cerebral hemisphere was homogenized for oxidative state assessment, while the other was fixed in 10% neutral buffered formalin and stained with H&E for hippocampal histomorphology. Data obtained were analyzed using student t-test and p value < 0.05 was considered significant. Across the 4-week period, group 2 rats showed significant increase in time spent to identify baited arms, significant reduction in density of apparentlynormal neurons and oligodendrocyte in CA 1-3 regions of hippocampus, and significant increase in reduced glutathione when compared with other groups. However, no significant differences were noted between groups 1, 3 and 4 for the above stated parameters. The study concluded that MSG caused hippocampal neuronal and oligodendrocytes degeneration and impairment of memory. These anomalies are prevented by 100 and 200 mg/kg of Aloe barbadensis
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