Parkinson’s disease (PD) is a neurodegenerative disorder characterized by both non-motor and motor symptoms, due to the loss of dopamine-producing neurons in the brain. Monoamine oxidase-B (MAO-B) inhibitors are essential in the treatment of PD, as they increase dopamine levels and could potentially slow down the progression of the disease. MAO-B inhibitors block the ability of the enzyme to degrade dopamine in the brain. MAO-B inhibitors work by inhibiting this enzyme, which raises dopamine levels and helps reduce motor symptoms, such as akinesia and stiffness in the muscles. In addition to their impact on dopamine levels, MAO-B inhibitors may possess neuroprotective properties. Research indicates that these inhibitors can shield neurons from the harmful byproducts of dopamine breakdown, such as dihydroxy acetaldehyde and hydrogen peroxide. This neuroprotective effect could potentially slow the progression of PD and protect against neuronal damage. MAO-B inhibitors are effective in treating both advanced and early stages of PD. They are recommended as initial treatments for individuals with early PD and can also be used as supplementary therapy in advanced PD to assist in managing motor complications. Additionally, MAO-B inhibitors have shown promise for the treatment of non-motor symptoms of PD, such as fatigue and sleep disturbances. MAO-B inhibitors are an important class of drugs for the treatment of PD, offering both symptomatic relief and potential disease-modifying effects. The goal of ongoing research and development of MAO-B inhibitors is to enhance their safety and selectivity profiles, which could lead to improved treatment approaches for PD and other neurodegenerative disorders.
{"title":"An overview of the role of monoamine oxidase-B in Parkinson’s disease: implications for neurodegeneration and therapy","authors":"Praveen Kumar Chandra Sekar, Sheena Mariam Thomas, Ramakrishnan Veerabathiran","doi":"10.37349/ent.2024.00085","DOIUrl":"https://doi.org/10.37349/ent.2024.00085","url":null,"abstract":"Parkinson’s disease (PD) is a neurodegenerative disorder characterized by both non-motor and motor symptoms, due to the loss of dopamine-producing neurons in the brain. Monoamine oxidase-B (MAO-B) inhibitors are essential in the treatment of PD, as they increase dopamine levels and could potentially slow down the progression of the disease. MAO-B inhibitors block the ability of the enzyme to degrade dopamine in the brain. MAO-B inhibitors work by inhibiting this enzyme, which raises dopamine levels and helps reduce motor symptoms, such as akinesia and stiffness in the muscles. In addition to their impact on dopamine levels, MAO-B inhibitors may possess neuroprotective properties. Research indicates that these inhibitors can shield neurons from the harmful byproducts of dopamine breakdown, such as dihydroxy acetaldehyde and hydrogen peroxide. This neuroprotective effect could potentially slow the progression of PD and protect against neuronal damage. MAO-B inhibitors are effective in treating both advanced and early stages of PD. They are recommended as initial treatments for individuals with early PD and can also be used as supplementary therapy in advanced PD to assist in managing motor complications. Additionally, MAO-B inhibitors have shown promise for the treatment of non-motor symptoms of PD, such as fatigue and sleep disturbances. MAO-B inhibitors are an important class of drugs for the treatment of PD, offering both symptomatic relief and potential disease-modifying effects. The goal of ongoing research and development of MAO-B inhibitors is to enhance their safety and selectivity profiles, which could lead to improved treatment approaches for PD and other neurodegenerative disorders.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141649600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A novel concept has been recently put forward in the mind/body interface (https://doi.org/10.37349/ent.2024.00074). The new concept has led to a new word: vitaction. Vitactions offer benefits to the brain and mind comparable to the advantages vitamins provide for the body’s overall health. The field of vitactions is as it was the vitamin field one century ago, i.e., without tools to make a complete classification. I propose to classify vitactions into five categories according to the behaviours necessary to maintain balanced brain functionality. A deficit of vitactions would contribute to the enormous prevalence in developed countries of diseases ranging from type 2 diabetes to neuropsychiatric diseases. The concept should help to identify which vitactions are deficient and to outline how they can be progressively implemented to improve the quality of life. The parallelism vitactions/vitamins also extends to overdosing; both hypervitaminosis and hypervitactinosis may be detrimental. This perspective article argues that vitactions should be considered at the practical and the scientific research levels, and that a balanced vitamin and vitaction supply is essential for a better life. In addition, reasons for proposing a synonym, “vitactin”, are given.
{"title":"Vitactions: vitamins for the brain","authors":"Rafael Franco","doi":"10.37349/ent.2024.00084","DOIUrl":"https://doi.org/10.37349/ent.2024.00084","url":null,"abstract":"A novel concept has been recently put forward in the mind/body interface (https://doi.org/10.37349/ent.2024.00074). The new concept has led to a new word: vitaction. Vitactions offer benefits to the brain and mind comparable to the advantages vitamins provide for the body’s overall health. The field of vitactions is as it was the vitamin field one century ago, i.e., without tools to make a complete classification. I propose to classify vitactions into five categories according to the behaviours necessary to maintain balanced brain functionality. A deficit of vitactions would contribute to the enormous prevalence in developed countries of diseases ranging from type 2 diabetes to neuropsychiatric diseases. The concept should help to identify which vitactions are deficient and to outline how they can be progressively implemented to improve the quality of life. The parallelism vitactions/vitamins also extends to overdosing; both hypervitaminosis and hypervitactinosis may be detrimental. This perspective article argues that vitactions should be considered at the practical and the scientific research levels, and that a balanced vitamin and vitaction supply is essential for a better life. In addition, reasons for proposing a synonym, “vitactin”, are given.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141700347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Patrik Althoff, Friederike Rosenthal, Eva-Maria Dorsch, Daniel Drebinger, Radina Arsenova, Anna Chorschew, S. Rosenkranz, J. Bellmann-Strobl, Christoph Heesen, Friedemann Paul, M. Weygandt, Tanja Schmitz-Hübsch
Aim: This article is based on our previous research, which was presented as a poster at the ECTRIMS Congress 2018 and published as a conference abstract (https://www.professionalabstracts.com/ectrims2018/iplanner/#/presentation/1698). Cognitive-motor interference (CMI) has been observed in both healthy controls (HC) and persons with multiple sclerosis (pwMS), but limited and contradictory data is making it difficult to assess the impact of motor and cognitive functioning levels on CMI. The aim of this study was to investigate CMI in pwMS and HC by means of a dual task postural paradigm, to compare them between groups and to analyse the influence of motor and cognitive functioning levels assessed with complementary instruments on observed CMI. Methods: The dual task posturography paradigm serves to quantify the impact of a cognitive (i.e., performing serial subtractions), a motor challenge (closing eyes), or both challenges combined (triple task) on body sway during standing in an upright position feet closed. The data analysed were acquired in one interventional and four observational studies and selected based on predefined criteria and by systematic quality control. A total of 113 pwMS and 42 HC were selected for analysis. Results: Comparable changes in motor and cognitive performance due to cognitive or combined cognitive-motor challenges were observed in both HC and pwMS. Combining both tasks did not result in further changes in motor performance but resulted in a decrease in cognitive performance. This reduction in cognitive performance with an additional motor challenge correlated with lower levels of cognitive and motor functioning in pwMS. Unexpectedly, an increase in body sway due to a cognitive or combined cognitive-motor challenges was primarily observed in pwMS and HC with better cognitive and motor functioning. Conclusions: The results suggest that dual-task effects are not disease-specific but rather reflect individually different adaptation strategies depending on the specific motor and cognitive functioning levels.
{"title":"Cognitive-motor interference in multiple sclerosis and healthy controls: results from single, dual, and triple task posturography","authors":"Patrik Althoff, Friederike Rosenthal, Eva-Maria Dorsch, Daniel Drebinger, Radina Arsenova, Anna Chorschew, S. Rosenkranz, J. Bellmann-Strobl, Christoph Heesen, Friedemann Paul, M. Weygandt, Tanja Schmitz-Hübsch","doi":"10.37349/ent.2024.00082","DOIUrl":"https://doi.org/10.37349/ent.2024.00082","url":null,"abstract":"Aim: This article is based on our previous research, which was presented as a poster at the ECTRIMS Congress 2018 and published as a conference abstract (https://www.professionalabstracts.com/ectrims2018/iplanner/#/presentation/1698). Cognitive-motor interference (CMI) has been observed in both healthy controls (HC) and persons with multiple sclerosis (pwMS), but limited and contradictory data is making it difficult to assess the impact of motor and cognitive functioning levels on CMI. The aim of this study was to investigate CMI in pwMS and HC by means of a dual task postural paradigm, to compare them between groups and to analyse the influence of motor and cognitive functioning levels assessed with complementary instruments on observed CMI. Methods: The dual task posturography paradigm serves to quantify the impact of a cognitive (i.e., performing serial subtractions), a motor challenge (closing eyes), or both challenges combined (triple task) on body sway during standing in an upright position feet closed. The data analysed were acquired in one interventional and four observational studies and selected based on predefined criteria and by systematic quality control. A total of 113 pwMS and 42 HC were selected for analysis. Results: Comparable changes in motor and cognitive performance due to cognitive or combined cognitive-motor challenges were observed in both HC and pwMS. Combining both tasks did not result in further changes in motor performance but resulted in a decrease in cognitive performance. This reduction in cognitive performance with an additional motor challenge correlated with lower levels of cognitive and motor functioning in pwMS. Unexpectedly, an increase in body sway due to a cognitive or combined cognitive-motor challenges was primarily observed in pwMS and HC with better cognitive and motor functioning. Conclusions: The results suggest that dual-task effects are not disease-specific but rather reflect individually different adaptation strategies depending on the specific motor and cognitive functioning levels.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141354871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The beneficial effects of gardening as a form of physical activity have garnered growing interest in recent years. This research aimed to evaluate the effect of gardening as a physical activity on promoting neuroplasticity and cognitive functioning in people. Methods: A systematic review was conducted on published articles between January 2010 to December 2022. The systematic search identified 3,470 records based on the PRISMA recommendations, 23 studies were eligible for inclusion in the review. Results: The study revealed the potential benefit of gardening physical activity on brain health. The evidence suggests that engaging in gardening physical activity not only boosts immunity and lowers inflammation but can also increase levels of growth neurotrophic factors like brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF), which are essential for promoting neuroplasticity and improving cognitive function. These results should be interpreted cautiously given the small number of included studies and few randomized controlled trials. Discussion: The study results of gardening physical activity are promising. However, to adequately comprehend the underlying mechanism of the physical activity of gardening on brain health, more well-designed research is still necessary.
{"title":"Effect of gardening physical activity on neuroplasticity and cognitive function","authors":"A. Lentoor","doi":"10.37349/ent.2024.00081","DOIUrl":"https://doi.org/10.37349/ent.2024.00081","url":null,"abstract":"Background: The beneficial effects of gardening as a form of physical activity have garnered growing interest in recent years. This research aimed to evaluate the effect of gardening as a physical activity on promoting neuroplasticity and cognitive functioning in people. Methods: A systematic review was conducted on published articles between January 2010 to December 2022. The systematic search identified 3,470 records based on the PRISMA recommendations, 23 studies were eligible for inclusion in the review. Results: The study revealed the potential benefit of gardening physical activity on brain health. The evidence suggests that engaging in gardening physical activity not only boosts immunity and lowers inflammation but can also increase levels of growth neurotrophic factors like brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF), which are essential for promoting neuroplasticity and improving cognitive function. These results should be interpreted cautiously given the small number of included studies and few randomized controlled trials. Discussion: The study results of gardening physical activity are promising. However, to adequately comprehend the underlying mechanism of the physical activity of gardening on brain health, more well-designed research is still necessary.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141386377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatically that a biochemical like tryptamine, for example, is converted into the hallucinogen dimethyltryptamine. Central to endogenous methylation activity is the folate cycle, which generates the primary transferable methyl groups in mammalian biochemistry. The relevance of this cycle to mental health becomes clear when the cycle is dysregulated, often leading to a buildup of both homocysteine and S-adenosylhomocysteine (SAH), while accompanied by a transient reduction in the intended physiologic target, S-adenosylmethionine (SAM). This paper includes an in-depth review of the causes of folate cycle perturbations associated with psychotic symptoms, expounding on alternative downstream pathways which are activated and pointing toward potential etiologic agents of the associated psychosis, the methylated tertiary amines N-methyl-salsolinol, N-methyl-norsalsolinol, and adrenochrome, which appear in scientific reports concerning their association with hallucinogenic and/or neurotoxic outcomes. Electrotopological state (E-state) data has been generated for these compounds, illustrating a strong similarity with hallucinogens, particularly in terms of the E-state of the nitrogen in their tertiary amine moieties. In light of the role the folate cycle plays in transmethylation, neuroprotective strategies to prevent the transition to psychosis are suggested, including the advisory that folate supplementation can be harmful depending on the status of other relevant biochemicals.
{"title":"Diverse avenues of research support the transmethylation theory of psychosis: implications for neuroprotection","authors":"Christine L. Miller","doi":"10.37349/ent.2024.00079","DOIUrl":"https://doi.org/10.37349/ent.2024.00079","url":null,"abstract":"Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatically that a biochemical like tryptamine, for example, is converted into the hallucinogen dimethyltryptamine. Central to endogenous methylation activity is the folate cycle, which generates the primary transferable methyl groups in mammalian biochemistry. The relevance of this cycle to mental health becomes clear when the cycle is dysregulated, often leading to a buildup of both homocysteine and S-adenosylhomocysteine (SAH), while accompanied by a transient reduction in the intended physiologic target, S-adenosylmethionine (SAM). This paper includes an in-depth review of the causes of folate cycle perturbations associated with psychotic symptoms, expounding on alternative downstream pathways which are activated and pointing toward potential etiologic agents of the associated psychosis, the methylated tertiary amines N-methyl-salsolinol, N-methyl-norsalsolinol, and adrenochrome, which appear in scientific reports concerning their association with hallucinogenic and/or neurotoxic outcomes. Electrotopological state (E-state) data has been generated for these compounds, illustrating a strong similarity with hallucinogens, particularly in terms of the E-state of the nitrogen in their tertiary amine moieties. In light of the role the folate cycle plays in transmethylation, neuroprotective strategies to prevent the transition to psychosis are suggested, including the advisory that folate supplementation can be harmful depending on the status of other relevant biochemicals.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140976043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Short-chain fatty acids (SCFAs) play a key role regulating immune and metabolic homeostasis. Consequently, dysregulation in SCFA levels is involved in the pathogenesis of autoimmune, inflammatory, metabolic, and neurodegenerative disorders. These metabolites are generated by gut microbiota, and their production is influenced mainly by diet. Here, an overview is provided of how SCFA production is associated with diet and with neurological disorders. The mechanisms by which SCFAs exert beneficial effects are analysed, along with how their production may be boosted by diet and how the use of specific dietary interventions might improve the outcome of neurological diseases.
{"title":"Targeting short-chain fatty acids receptors signalling for neurological disorders treatment","authors":"C. Prado, Rodrigo Pacheco","doi":"10.37349/ent.2024.00073","DOIUrl":"https://doi.org/10.37349/ent.2024.00073","url":null,"abstract":"Short-chain fatty acids (SCFAs) play a key role regulating immune and metabolic homeostasis. Consequently, dysregulation in SCFA levels is involved in the pathogenesis of autoimmune, inflammatory, metabolic, and neurodegenerative disorders. These metabolites are generated by gut microbiota, and their production is influenced mainly by diet. Here, an overview is provided of how SCFA production is associated with diet and with neurological disorders. The mechanisms by which SCFAs exert beneficial effects are analysed, along with how their production may be boosted by diet and how the use of specific dietary interventions might improve the outcome of neurological diseases.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140230869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is significant in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transformation after recanalization predict poor prognosis of AIS. How to minimize reperfusion injury and hemorrhagic transformation, which greatly improves the prognosis of vascular recanalization, is becoming a hot topic in AIS research and an urgent problem to be solved. A wealth of neuroprotective drug studies is now available, while some of the neuroprotectants have met with failure in human studies. It is discussed in this review about the progress in neuroprotective therapy for AIS based on understanding the pathophysiologic mechanisms of reperfusion injury and hemorrhagic transformation, as well as challenges in exploring new neuroprotectants.
{"title":"Advances in neuroprotective therapy for acute ischemic stroke","authors":"Yang Yang, Dandan Guo, Yiming Liu, Yi Li","doi":"10.37349/ent.2024.00070","DOIUrl":"https://doi.org/10.37349/ent.2024.00070","url":null,"abstract":"Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is significant in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transformation after recanalization predict poor prognosis of AIS. How to minimize reperfusion injury and hemorrhagic transformation, which greatly improves the prognosis of vascular recanalization, is becoming a hot topic in AIS research and an urgent problem to be solved. A wealth of neuroprotective drug studies is now available, while some of the neuroprotectants have met with failure in human studies. It is discussed in this review about the progress in neuroprotective therapy for AIS based on understanding the pathophysiologic mechanisms of reperfusion injury and hemorrhagic transformation, as well as challenges in exploring new neuroprotectants.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140425064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aim: A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave birth to a cohort of infants with congenital Zika syndrome (CZS) originally defined by severe microcephaly, retinal scarring, joint deformities, and hypertonia. This study examines the nature, extent, and severity of all CZS clinicopathologic findings described to date, compiled and analyzed by system. It reviews studies monitoring disease progression and proposing classification schemes for CZS stages. The teratogenic cellular and molecular mechanisms implicated in CZS pathogenesis are also discussed. Methods: A systematic review was conducted by literature search through WorldCat.org and ProQuest Central databases to identify studies on case series from the 2015–2016 CZS outbreak. Results: Twenty-six reports were included describing radiologic, ophthalmologic, audiologic, orthopedic, and laboratory test results in CZS cases including stillborns between 2016 and 2023. CZS neuropathology included prenatal and postnatal microcephaly, cerebral calcifications, quadriparesis, epilepsy, ventriculomegaly, reduced cerebral parenchyma, malformation of cortical development, and sleep electroencephalogram disturbances. Visual deficits were due to retinal and optic nerve lesions. Conductive and sensorineural hearing deficits were stable. Hypertonia, hypotonia, and spasticity with foot, hip, knee, and shoulder deformities resulted in arthrogryposis and restricted joint mobility. There was enlargement of immune organs, increased leukocyte counts, and cytokine dysregulation. Oro-craniofacial deformities affected the midface and caused dental eruption delay. Additional studies proposed that these systemic teratogenic effects could be attributable to transplacental Zika virus infection of multiple fetal progenitor cell lineages. Conclusions: The CZS-associated impairments in brain, eye, musculoskeletal, and immunologic functions caused disabilities that varied from moderate to severe, and significantly increased age-specific mortality rates. Further research is warranted to assess progression, classify stages, elucidate the precise molecular mechanisms mediating Zika teratogenicity, develop suitable therapeutic strategies, and design supportive social policies.
{"title":"Analysis of congenital Zika syndrome clinicopathologic findings reported in the 8 years since the Brazilian outbreak","authors":"Dhaara Shah, Dhairavi Shah, Olivia Mua, Rana Zeine","doi":"10.37349/ent.2024.00072","DOIUrl":"https://doi.org/10.37349/ent.2024.00072","url":null,"abstract":"Aim: A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave birth to a cohort of infants with congenital Zika syndrome (CZS) originally defined by severe microcephaly, retinal scarring, joint deformities, and hypertonia. This study examines the nature, extent, and severity of all CZS clinicopathologic findings described to date, compiled and analyzed by system. It reviews studies monitoring disease progression and proposing classification schemes for CZS stages. The teratogenic cellular and molecular mechanisms implicated in CZS pathogenesis are also discussed. Methods: A systematic review was conducted by literature search through WorldCat.org and ProQuest Central databases to identify studies on case series from the 2015–2016 CZS outbreak. Results: Twenty-six reports were included describing radiologic, ophthalmologic, audiologic, orthopedic, and laboratory test results in CZS cases including stillborns between 2016 and 2023. CZS neuropathology included prenatal and postnatal microcephaly, cerebral calcifications, quadriparesis, epilepsy, ventriculomegaly, reduced cerebral parenchyma, malformation of cortical development, and sleep electroencephalogram disturbances. Visual deficits were due to retinal and optic nerve lesions. Conductive and sensorineural hearing deficits were stable. Hypertonia, hypotonia, and spasticity with foot, hip, knee, and shoulder deformities resulted in arthrogryposis and restricted joint mobility. There was enlargement of immune organs, increased leukocyte counts, and cytokine dysregulation. Oro-craniofacial deformities affected the midface and caused dental eruption delay. Additional studies proposed that these systemic teratogenic effects could be attributable to transplacental Zika virus infection of multiple fetal progenitor cell lineages. Conclusions: The CZS-associated impairments in brain, eye, musculoskeletal, and immunologic functions caused disabilities that varied from moderate to severe, and significantly increased age-specific mortality rates. Further research is warranted to assess progression, classify stages, elucidate the precise molecular mechanisms mediating Zika teratogenicity, develop suitable therapeutic strategies, and design supportive social policies.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140427171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes owing to their fascinating properties have the potential to revolutionize medicine and technology, particularly in the realm of drug delivery, biosensing, bioimaging, and as therapeutic agents to tackle complex neurological disorders such as Alzheimer’s and Parkinson’s disease. In this review, a summary of the use of carbon nanotubes for neuropathological outcomes such as alleviating oxidative stress and amyloid formation, which are well-studied molecular outcomes associated with Alzheimer’s and Parkinson’s disease. In the end, challenges associated with the clinical testing of carbon nanotubes and possible ways to overcome them are highlighted.
{"title":"Carbon nanotubes as neuroprotective agents","authors":"Daisy L. Wilson, J. Ahlawat, Mahesh Narayan","doi":"10.37349/ent.2024.00071","DOIUrl":"https://doi.org/10.37349/ent.2024.00071","url":null,"abstract":"Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes owing to their fascinating properties have the potential to revolutionize medicine and technology, particularly in the realm of drug delivery, biosensing, bioimaging, and as therapeutic agents to tackle complex neurological disorders such as Alzheimer’s and Parkinson’s disease. In this review, a summary of the use of carbon nanotubes for neuropathological outcomes such as alleviating oxidative stress and amyloid formation, which are well-studied molecular outcomes associated with Alzheimer’s and Parkinson’s disease. In the end, challenges associated with the clinical testing of carbon nanotubes and possible ways to overcome them are highlighted.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140424104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to cause a distinct disease called MOG antibody-associated disease (MOGAD). MOGAD accounts for approximately one-third of all demyelinating syndromes in children and is the second most common central nervous system (CNS) demyelinating disease after MS. The diagnosis is made by detecting anti-MOG IgG antibodies against the natural MOG antigen, in the presence of compatible clinical and neuroradiological features. However, due to controversies in the methodologies for detecting anti-MOG antibodies and their diagnostic cutoff values, as well as the expanding clinical spectrum, accurate diagnosis may be challenging, at least in a subset of patients. Clinical presentations of MOGAD vary by age; the highest rates are seen in acute disseminated encephalomyelitis in younger children and optic neuritis, myelitis, or brainstem symptoms in older children. Although it was previously thought to be a milder demyelinating disorder and to have a monophasic course in the majority of patients, recent studies have shown that relapses occur in about half of the patients and sequelae develop in a significant proportion of them, especially in those with persistently high antibody titers, leukodystrophy-like magnetic resonance imaging (MRI) lesions, and spinal cord involvement. However, due to the monophasic course in about half of the patients, long-term treatment is not recommended after the first clinical episode but is recommended for patients who experience relapse. Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. This review covers the challenges in the diagnosis of MOGAD in children.
{"title":"The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children","authors":"Ünsal Yılmaz","doi":"10.37349/ent.2024.00069","DOIUrl":"https://doi.org/10.37349/ent.2024.00069","url":null,"abstract":"Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to cause a distinct disease called MOG antibody-associated disease (MOGAD). MOGAD accounts for approximately one-third of all demyelinating syndromes in children and is the second most common central nervous system (CNS) demyelinating disease after MS. The diagnosis is made by detecting anti-MOG IgG antibodies against the natural MOG antigen, in the presence of compatible clinical and neuroradiological features. However, due to controversies in the methodologies for detecting anti-MOG antibodies and their diagnostic cutoff values, as well as the expanding clinical spectrum, accurate diagnosis may be challenging, at least in a subset of patients. Clinical presentations of MOGAD vary by age; the highest rates are seen in acute disseminated encephalomyelitis in younger children and optic neuritis, myelitis, or brainstem symptoms in older children. Although it was previously thought to be a milder demyelinating disorder and to have a monophasic course in the majority of patients, recent studies have shown that relapses occur in about half of the patients and sequelae develop in a significant proportion of them, especially in those with persistently high antibody titers, leukodystrophy-like magnetic resonance imaging (MRI) lesions, and spinal cord involvement. However, due to the monophasic course in about half of the patients, long-term treatment is not recommended after the first clinical episode but is recommended for patients who experience relapse. Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. This review covers the challenges in the diagnosis of MOGAD in children.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140426067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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