Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in diseaseassociated synaptic dysfunction could offer novel clues toward synapse-based therapeutic intervention for neurological and neuropsychiatric disorders.

Coronaviruses (CoV) are viruses widely known to cause severe respiratory distress due to the prominent clinical symptoms presented. These symptoms, which include fever and dry cough, are frequently found in individuals with CoV infection. Neurological manifestations of CoV have often been neglected; however, recent studies have reported neurological consequences of CoV infection. Here, we review these literatures and discuss the neurologic impact of CoV while highlighting potential implications of the novel SARS-CoV-2 in the nervous system. We also discuss the possible routes by which these viruses invade the nervous system and the mechanism by which they may induce neurological damage.

Due to many advantages Caenorhabditis elegans (C. elegans) has become a preferred model of choice in many fields, including neurodevelopmental toxicity studies. This review discusses the benefits of using C. elegans as an alternative to mammalian systems and gives examples of the uses of the nematode in evaluating the effects of major known neurodevelopmental toxins, including manganese, mercury, lead, fluoride, arsenic and organophosphorus pesticides. Reviewed data indicates numerous similarities with mammals in response to these toxins. Thus, C. elegans studies have the potential to predict possible effects of developmental neurotoxicants in higher animals, and may be used to identify new molecular pathways behind neurodevelopmental disruptions, as well as new toxicants.

A simple and cost-effective material composed of polyacrylonitrile nanofibers containing different concentrations of moringa (MR) leaf extracts was fabricated for antimicrobial properties and wound dressing. The fabricated materials were characterized by scanning electron microscopy, thermal gravimetric analysis, and Fourier transmission infrared spectroscopy. The antibacterial sensitivity of the developed polyacrylonitrile-moringa extract nanofibers was evaluated against Staphylococcus aureus and Escherichia coli by the agar diffusion method. A pronounced antibacterial activity was observed with the increase in the incorporated moringa leaf extract concentration within the polyacrylonitrile-moringa extract nanofibers against the bacterial strains. The best antibacterial sensitivity was observed for nanofibers containing 0.5 g of moringa leaf extract which had an inhibitory zone of 15 mm for E. coli and 12 mm for S. aureus. Furthermore, the cost-effective and biodegradable nanofibrous polyacrylonitrile–moringa extract nanofiber was also used to conduct further studies regarding wound dressing. The result reveals that the increase in the concentrations of moringa leaf extract influenced the healing properties of the material. For days 1, 4, and 7 of the wound dressing experiment, the % wound closure of the rat was the highest for the nanofiber containing 0.5 g of moringa leaf extract (35, 87, and 95%, respectively) compared to the positive control medical gauze (29, 75, and 93%, respectively).

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Manganese (Mn) is an essential trace element that is naturally found in the environment and is necessary as a cofactor for many enzymes and is important in several physiological processes that support development, growth, and neuronal function. However, overexposure to Mn may induce neurotoxicity and may contribute to the development of Alzheimer’s disease (AD) and Parkinson’s disease (PD). The present review aims to provide new insights into the involvement of Mn in the etiology of AD and PD. Here, we discuss the critical role of Mn in the etiology of these disorders and provide a summary of the proposed mechanisms underlying Mn-induced neurodegeneration. In addition, we review some new therapy options for AD and PD related to Mn overload.

Lead (Pb) is an environmental neurotoxicant, and has been implicated in several neurological disorders of dopaminergic dysfunction; however, the molecular mechanism of its toxicity has yet to be fully understood. This study investigated the effect of Pb exposure on dopaminergic neurodegeneration and function, as well as expression level of several dopaminergic signaling genes in wild type (N2) and protein kinase C ( pkc ) mutant Caenorhabditis elegans . Both N2 and pkc mutant worms were exposed to Pb 2+ for 1 h. Thereafter, dopaminergic (DAergic) neurodegeneration, behavior and gene expression levels were assessed. The results revealed that Pb 2+ treatment affects dopaminergic cell morphology and structure in worms expressing green fluorescent protein (GFP) under a DAergic cell specific promoter. Also, there was a significant impairment in dopaminergic neuronal function as tested by basal slowing response (BSR) in wild-type, N2 worms, but no effect was observed in pkc mutant worms. Furthermore, Pb 2+ exposure increased dat-1 gene expression level when compared with N2 worms, but no alteration was observed in the pkc mutant strains. LC–MS analysis revealed a significant decrease in dopamine content in worms treated with Pb 2+ when compared with controls. In summary, our results revealed that Pb 2+ exposure induced dopaminergic dysfunction in C. elegans by altering dat-1 gene levels, but pkc mutants showed significant resistance to Pb 2+ toxicity. We conclude that PKC activation is directly involved in the neurotoxicity of Pb.

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