Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023001
Arosh S Perera Molligoda Arachchige
The possibility of multimodality imaging with PET/MR and the availability of ultra-high field MRI has allowed to investigate novel aspects of neuropsychiatric conditions. One of the major barriers in current studies is the lack of an instrument that allows to accurately cover the temporal aspect under the same physiological conditions. The aim of this commentary is to provide our perspective on how the integration of EEG-PET-MR could be a solution to the current challenge in molecular imaging and seems to hold great promise in future pharmacological challenging-based studies, understanding different functional states of the brain, and could furthermore aid in the diagnostic and prognostic evaluations of neurocognitive disorders.
{"title":"Transitioning from PET/MR to trimodal neuroimaging: why not cover the temporal dimension with EEG?","authors":"Arosh S Perera Molligoda Arachchige","doi":"10.3934/Neuroscience.2023001","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023001","url":null,"abstract":"<p><p>The possibility of multimodality imaging with PET/MR and the availability of ultra-high field MRI has allowed to investigate novel aspects of neuropsychiatric conditions. One of the major barriers in current studies is the lack of an instrument that allows to accurately cover the temporal aspect under the same physiological conditions. The aim of this commentary is to provide our perspective on how the integration of EEG-PET-MR could be a solution to the current challenge in molecular imaging and seems to hold great promise in future pharmacological challenging-based studies, understanding different functional states of the brain, and could furthermore aid in the diagnostic and prognostic evaluations of neurocognitive disorders.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9383973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/neuroscience.2023024
Arosh S. Perera Molligoda Arachchige
{"title":"The blue brain project: pioneering the frontier of brain simulation","authors":"Arosh S. Perera Molligoda Arachchige","doi":"10.3934/neuroscience.2023024","DOIUrl":"https://doi.org/10.3934/neuroscience.2023024","url":null,"abstract":"<jats:p xml:lang=\"fr\" />","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134980161","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}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023016
Nicoletta Vegni, Caterina D'Ardia, Gloria Di Filippo, Francesco Maria Melchiori
Over the years, several interventions have been implemented, including Lego® Therapy, with the aim of supporting and implementing social and communication skills impairments in Autism Spectrum Disorders (ASD). Although recent studies have shown that the ability to learn implicitly is preserved in ASDs, no study related to Lego® Therapy has analyzed whether and how this training can also affect aspects not directly treated. In this study, we report a first attempt of assessment of Lego® Therapy's effect on the specific area of cognitive skills in an ASD child. Over a period of 12 months, a child with ASD had weekly meetings with an expert operator of Lego® aiming to improve the child's ability to communicate, reduce impulsiveness and hyper verbalism, and encourage pro-social behavior. The intervention resulted in positive outcomes that were assessed after 12 months.
{"title":"The impact of Lego® Therapy on cognitive skills in Autism Spectrum Disorders: a brief discussion.","authors":"Nicoletta Vegni, Caterina D'Ardia, Gloria Di Filippo, Francesco Maria Melchiori","doi":"10.3934/Neuroscience.2023016","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023016","url":null,"abstract":"<p><p>Over the years, several interventions have been implemented, including Lego® Therapy, with the aim of supporting and implementing social and communication skills impairments in Autism Spectrum Disorders (ASD). Although recent studies have shown that the ability to learn implicitly is preserved in ASDs, no study related to Lego® Therapy has analyzed whether and how this training can also affect aspects not directly treated. In this study, we report a first attempt of assessment of Lego® Therapy's effect on the specific area of cognitive skills in an ASD child. Over a period of 12 months, a child with ASD had weekly meetings with an expert operator of Lego® aiming to improve the child's ability to communicate, reduce impulsiveness and hyper verbalism, and encourage pro-social behavior. The intervention resulted in positive outcomes that were assessed after 12 months.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10323259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10187522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023014
Arosh S Perera Molligoda Arachchige
{"title":"Marijuana's potential in neurodegenerative diseases: an editorial.","authors":"Arosh S Perera Molligoda Arachchige","doi":"10.3934/Neuroscience.2023014","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023014","url":null,"abstract":"<jats:p xml:lang=\"fr\" />","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10323256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10187524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023005
Milad Khodavysi, Nejat Kheiripour, Hassan Ghasemi, Sara Soleimani-Asl, Ali Fathi Jouzdani, Mohammadmahdi Sabahi, Zahra Ganji, Zahra Azizi, Akram Ranjbar
Aluminum phosphide (ALP) is among the most significant causes of brain toxicity and death in many countries. Curcumin (CUR), a major turmeric component, is a potent protective agent against many diseases, including brain toxicity. This study aimed to examine the probable protection potential of nanomicelle curcumin (nanomicelle-CUR) and its underlying mechanism in a rat model of ALP-induced brain toxicity. A total of 36 Wistar rats were randomly divided into six groups (n = 6) and exposed to ALP (2 mg/kg/day, orally) + CUR or nanomicelle-CUR (100 mg/kg/day, orally) for 7 days. Then, they were anesthetized, and brain tissue samples were dissected to evaluate histopathological alterations, oxidative stress biomarkers, gene expression of SIRT1, FOXO1a, FOXO3a, CAT and GPX in brain tissue via hematoxylin and eosin (H&E) staining, biochemical and enzyme-linked immunosorbent assay (ELISA) methods and Real-Time PCR analysis. CUR and nanomicelle-CUR caused significant improvement in ALP-induced brain damage by reducing the MDA levels and induction of antioxidant capacity (TTG, TAC and SOD levels) and antioxidant enzymes (CAT, GPX), modulation of histopathological changes and up-regulation of gene expression of SIRT1 in brain tissue. It was concluded that nanomicelle-CUR treatment ameliorated the harmful effects of ALP-induced brain toxicity by reducing oxidative stress. Therefore, it could be considered a suitable therapeutic choice for ALP poisoning.
{"title":"How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway.","authors":"Milad Khodavysi, Nejat Kheiripour, Hassan Ghasemi, Sara Soleimani-Asl, Ali Fathi Jouzdani, Mohammadmahdi Sabahi, Zahra Ganji, Zahra Azizi, Akram Ranjbar","doi":"10.3934/Neuroscience.2023005","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023005","url":null,"abstract":"<p><p>Aluminum phosphide (ALP) is among the most significant causes of brain toxicity and death in many countries. Curcumin (CUR), a major turmeric component, is a potent protective agent against many diseases, including brain toxicity. This study aimed to examine the probable protection potential of nanomicelle curcumin (nanomicelle-CUR) and its underlying mechanism in a rat model of ALP-induced brain toxicity. A total of 36 Wistar rats were randomly divided into six groups (n = 6) and exposed to ALP (2 mg/kg/day, orally) + CUR or nanomicelle-CUR (100 mg/kg/day, orally) for 7 days. Then, they were anesthetized, and brain tissue samples were dissected to evaluate histopathological alterations, oxidative stress biomarkers, gene expression of SIRT1, FOXO1a, FOXO3a, CAT and GPX in brain tissue via hematoxylin and eosin (H&E) staining, biochemical and enzyme-linked immunosorbent assay (ELISA) methods and Real-Time PCR analysis. CUR and nanomicelle-CUR caused significant improvement in ALP-induced brain damage by reducing the MDA levels and induction of antioxidant capacity (TTG, TAC and SOD levels) and antioxidant enzymes (CAT, GPX), modulation of histopathological changes and up-regulation of gene expression of SIRT1 in brain tissue. It was concluded that nanomicelle-CUR treatment ameliorated the harmful effects of ALP-induced brain toxicity by reducing oxidative stress. Therefore, it could be considered a suitable therapeutic choice for ALP poisoning.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9383977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023004
Arosh S Perera Molligoda Arachchige
{"title":"Neuroimaging with SPECT-MRI: a myth or reality?","authors":"Arosh S Perera Molligoda Arachchige","doi":"10.3934/Neuroscience.2023004","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023004","url":null,"abstract":"","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9385186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023003
Sara Arciniegas Ruiz, Eliav Tikochinsky, Vardit Rubovitch, Chaim G Pick, Bernard Attali
Background: In the fear memory network, the hippocampus modulates contextual aspects of fear learning while mutual connections between the amygdala and the medial prefrontal cortex are widely involved in fear extinction. G-protein-coupled receptors (GPCRs) are involved in the regulation of fear and anxiety, so the regulation of GPCRs in fear signaling pathways can modulate the mechanisms of fear memory acquisition, consolidation and extinction. Various studies suggested a role of M-type K+ channels in modulating fear expression and extinction, although conflicting data prevented drawing of clear conclusions. In the present work, we examined the impact of M-type K+ channel blockade or activation on contextual fear acquisition and extinction. In addition, regarding the pivotal role of the hippocampus in contextual fear conditioning (CFC) and the involvement of the axon initial segment (AIS) in neuronal plasticity, we investigated whether structural alterations of the AIS in hippocampal neurons occurred during contextual fear memory acquisition and short-time extinction in mice in a behaviorally relevant context.
Results: When a single systemic injection of the M-channel blocker XE991 (2 mg/kg, IP) was carried out 15 minutes before the foot shock session, fear expression was significantly reduced. Expression of c-Fos was increased following CFC, mostly in GABAergic neurons at day 1 and day 2 post-fear training in CA1 and dentate gyrus hippocampal regions. A significantly longer AIS segment was observed in GABAergic neurons of the CA1 hippocampal region at day 2.
Conclusions: Our results underscore the role of M-type K + channels in CFC and the importance of hippocampal GABAergic neurons in fear expression.
{"title":"Contextual fear response is modulated by M-type K+ channels and is associated with subtle structural changes of the axon initial segment in hippocampal GABAergic neurons.","authors":"Sara Arciniegas Ruiz, Eliav Tikochinsky, Vardit Rubovitch, Chaim G Pick, Bernard Attali","doi":"10.3934/Neuroscience.2023003","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023003","url":null,"abstract":"<p><strong>Background: </strong>In the fear memory network, the hippocampus modulates contextual aspects of fear learning while mutual connections between the amygdala and the medial prefrontal cortex are widely involved in fear extinction. G-protein-coupled receptors (GPCRs) are involved in the regulation of fear and anxiety, so the regulation of GPCRs in fear signaling pathways can modulate the mechanisms of fear memory acquisition, consolidation and extinction. Various studies suggested a role of M-type K+ channels in modulating fear expression and extinction, although conflicting data prevented drawing of clear conclusions. In the present work, we examined the impact of M-type K+ channel blockade or activation on contextual fear acquisition and extinction. In addition, regarding the pivotal role of the hippocampus in contextual fear conditioning (CFC) and the involvement of the axon initial segment (AIS) in neuronal plasticity, we investigated whether structural alterations of the AIS in hippocampal neurons occurred during contextual fear memory acquisition and short-time extinction in mice in a behaviorally relevant context.</p><p><strong>Results: </strong>When a single systemic injection of the M-channel blocker XE991 (2 mg/kg, IP) was carried out 15 minutes before the foot shock session, fear expression was significantly reduced. Expression of c-Fos was increased following CFC, mostly in GABAergic neurons at day 1 and day 2 post-fear training in CA1 and dentate gyrus hippocampal regions. A significantly longer AIS segment was observed in GABAergic neurons of the CA1 hippocampal region at day 2.</p><p><strong>Conclusions: </strong>Our results underscore the role of M-type K + channels in CFC and the importance of hippocampal GABAergic neurons in fear expression.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9383970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This review aims to perform a bibliometric analysis of the research related to brain-derived neurotrophic factor (BDNF) in schizophrenia and offer suggestions for further work. Based on the keywords used, our study retrieved 335 documents for further analysis using a combination of three bibliometric techniques: co-word analysis, document co-citation analysis, and bibliographic coupling. A general rising trend in the number of publications was found in BDNF and schizophrenia research. Researchers from China and the United States have mostly researched BDNF and schizophrenia. Molecular Psychiatry is the most prestigious journal in the field of BDNF and schizophrenia research. The main topics and important research areas are cognition and the involvement of BDNF as a neurobiological marker (pathogenesis, therapy monitoring, and risk factors). Future research is anticipated to concentrate on relevant subjects, such as factors that affect BDNF levels or are connected to BDNF dysfunction in schizophrenia, as well as animal models of schizophrenia, in addition to cognition in schizophrenia.
{"title":"Brain-derived neurotrophic factor (BDNF) in schizophrenia research: a quantitative review and future directions.","authors":"Rozaziana Ahmad, Khairunnuur Fairuz Azman, Rosliza Yahaya, Nazlahshaniza Shafin, Norsuhana Omar, Asma Hayati Ahmad, Rahimah Zakaria, Adi Wijaya, Zahiruddin Othman","doi":"10.3934/Neuroscience.2023002","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023002","url":null,"abstract":"<p><p>This review aims to perform a bibliometric analysis of the research related to brain-derived neurotrophic factor (BDNF) in schizophrenia and offer suggestions for further work. Based on the keywords used, our study retrieved 335 documents for further analysis using a combination of three bibliometric techniques: co-word analysis, document co-citation analysis, and bibliographic coupling. A general rising trend in the number of publications was found in BDNF and schizophrenia research. Researchers from China and the United States have mostly researched BDNF and schizophrenia. Molecular Psychiatry is the most prestigious journal in the field of BDNF and schizophrenia research. The main topics and important research areas are cognition and the involvement of BDNF as a neurobiological marker (pathogenesis, therapy monitoring, and risk factors). Future research is anticipated to concentrate on relevant subjects, such as factors that affect BDNF levels or are connected to BDNF dysfunction in schizophrenia, as well as animal models of schizophrenia, in addition to cognition in schizophrenia.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9383975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023006
Scott Mendoza
Treating neurological patients during the pandemic period has become extremely challenging. At the same time, responding properly to these challenges has been diverse around the world, with varying levels of readiness, discipline, and approach. Additionally, there are significant differences in healthcare resources and processes between nations, and even within a nation, and these have significantly influenced the treatment procedure throughout the pandemic. However, neurologists have been called to care for patients with neurological symptoms who have COVID-19, and to continue managing COVID-19-affected neurological comorbidities in patients as before. This study highlights how the treatment procedures for neurological diseases are rapidly changing due to the spread of the SARS-CoV-2 virus. It also focuses on the challenges healthcare professionals are facing while providing proper treatment to neurological patients during the pandemic situation. Lastly, it offers some useful recommendations regarding the effective management of neurological diseases during the COVID-19 pandemic period.
{"title":"Adapting patient treatment of neurological diseases during the COVID-19 pandemic.","authors":"Scott Mendoza","doi":"10.3934/Neuroscience.2023006","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023006","url":null,"abstract":"<p><p>Treating neurological patients during the pandemic period has become extremely challenging. At the same time, responding properly to these challenges has been diverse around the world, with varying levels of readiness, discipline, and approach. Additionally, there are significant differences in healthcare resources and processes between nations, and even within a nation, and these have significantly influenced the treatment procedure throughout the pandemic. However, neurologists have been called to care for patients with neurological symptoms who have COVID-19, and to continue managing COVID-19-affected neurological comorbidities in patients as before. This study highlights how the treatment procedures for neurological diseases are rapidly changing due to the spread of the SARS-CoV-2 virus. It also focuses on the challenges healthcare professionals are facing while providing proper treatment to neurological patients during the pandemic situation. Lastly, it offers some useful recommendations regarding the effective management of neurological diseases during the COVID-19 pandemic period.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10323254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10168757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.3934/Neuroscience.2023010
Nisha Shantakumari, Musaab Ahmed
Whole Body Vibration has been found to induce physiological changes in human subjects, improving their neuromuscular, respiratory and cardiovascular functions. Evidence from animal research prove that whole-body vibration appears to induce changes in molecular and cellular levels to alter cognitive functions in mice. There is evolving evidence for a potential value of whole body vibration in improving cognition and preventing the development of age-related cognitive disorders in humans. However, literature on the biological consequences of whole-body vibration on the human brain is scanty. If so, gathering the available evidences would help decide the possibility of designing appropriate whole-body vibration protocols to extend its application to induce neurocognitive enhancement and optimize its effects. Therefore, a systematic review of the literature was performed, consulting the ProQuest, MEDLINE and Scopus bibliographic databases, to summarize the available scientific evidence on the effects of whole-body vibration on cognitive functions in adults. Results of the review suggest that whole-body vibration therapy enhances a wide spectrum of cognitive functions in adults although there isn't enough evidence available yet to be able to design a standardized protocol to achieve optimum cognitive enhancement.
{"title":"Whole body vibration therapy and cognitive functions: a systematic review.","authors":"Nisha Shantakumari, Musaab Ahmed","doi":"10.3934/Neuroscience.2023010","DOIUrl":"https://doi.org/10.3934/Neuroscience.2023010","url":null,"abstract":"<p><p>Whole Body Vibration has been found to induce physiological changes in human subjects, improving their neuromuscular, respiratory and cardiovascular functions. Evidence from animal research prove that whole-body vibration appears to induce changes in molecular and cellular levels to alter cognitive functions in mice. There is evolving evidence for a potential value of whole body vibration in improving cognition and preventing the development of age-related cognitive disorders in humans. However, literature on the biological consequences of whole-body vibration on the human brain is scanty. If so, gathering the available evidences would help decide the possibility of designing appropriate whole-body vibration protocols to extend its application to induce neurocognitive enhancement and optimize its effects. Therefore, a systematic review of the literature was performed, consulting the ProQuest, MEDLINE and Scopus bibliographic databases, to summarize the available scientific evidence on the effects of whole-body vibration on cognitive functions in adults. Results of the review suggest that whole-body vibration therapy enhances a wide spectrum of cognitive functions in adults although there isn't enough evidence available yet to be able to design a standardized protocol to achieve optimum cognitive enhancement.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10323263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10187517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}