AIMS Neuroscience最新文献

{"title":"Serum hypomagnesemia is associated with febrile seizures in young children.","authors":"Zakaria Ahmed Mohamed,&nbsp;Chunjiao Tang,&nbsp;Erick Thokerunga,&nbsp;Ali Omar Jimale,&nbsp;Jingyi Fan","doi":"10.3934/Neuroscience.2022032","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022032","url":null,"abstract":"<p><strong>Background: </strong>Febrile seizures (FS) frequently manifest in children below 5 years of age. Although the exact etiology is still unknown, genetic predisposition, changes in neurotransmitter levels, and serum electrolyte imbalance are some of the known risk factors. This study examined the possible association between serum magnesium levels in children with FS compared to febrile children without seizures.</p><p><strong>Methods: </strong>A retrospective case-control study was conducted from February 2019 to January 2021, recruiting 230 age and gender-matched cases and controls (115 each). Extracted data were analyzed using SPSS using an independent student's t-test, Chi-square test, and Pearson's correlation analysis.</p><p><strong>Results: </strong>The mean serum magnesium levels were 0.93 ± 0.129 vs 0.97 ± 0.0961; p < 0.001, between cases and controls respectively. Similarly, hypomagnesemia (<0.85 mmol/L) was detected in 26.1% and 8.7% of the cases and controls, respectively; p < 0.001. A significant negative correlation was found between serum magnesium levels and the occurrence of febrile seizures; r = [-0.169], p < 0.05.</p><p><strong>Conclusion: </strong>Serum magnesium was significantly low in febrile children with seizures compared to those without, and hypomagnesemia was associated with the occurrence of febrile seizures. These results portray hypomagnesemia as a possible risk factor for febrile seizure, and so should be validated in future large cohort studies so that guidelines are set for proper management of these children.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"551-558"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10550931","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}

{"title":"Impaired spatial memory in adult vitamin D deficient BALB/c mice is associated with reductions in spine density, nitric oxide, and neural nitric oxide synthase in the hippocampus.","authors":"Md Mamun Al-Amin,&nbsp;Robert K P Sullivan,&nbsp;Suzy Alexander,&nbsp;David A Carter,&nbsp;DanaKai Bradford,&nbsp;Thomas H J Burne","doi":"10.3934/Neuroscience.2022004","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022004","url":null,"abstract":"<p><p>Vitamin D deficiency is prevalent in adults and is associated with cognitive impairment. However, the mechanism by which adult vitamin D (AVD) deficiency affects cognitive function remains unclear. We examined spatial memory impairment in AVD-deficient BALB/c mice and its underlying mechanism by measuring spine density, long term potentiation (LTP), nitric oxide (NO), neuronal nitric oxide synthase (nNOS), and endothelial NOS (eNOS) in the hippocampus. Adult male BALB/c mice were fed a control or vitamin D deficient diet for 20 weeks. Spatial memory performance was measured using an active place avoidance (APA) task, where AVD-deficient mice had reduced latency entering the shock zone compared to controls. We characterised hippocampal spine morphology in the CA1 and dentate gyrus (DG) and made electrophysiological recordings in the hippocampus of behaviourally naïve mice to measure LTP. We next measured NO, as well as glutathione, lipid peroxidation and oxidation of protein products and quantified hippocampal immunoreactivity for nNOS and eNOS. Spine morphology analysis revealed a significant reduction in the number of mushroom spines in the CA1 dendrites but not in the DG. There was no effect of diet on LTP. However, hippocampal NO levels were depleted whereas other oxidation markers were unaltered by AVD deficiency. We also showed a reduced nNOS, but not eNOS, immunoreactivity. Finally, vitamin D supplementation for 10 weeks to AVD-deficient mice restored nNOS immunoreactivity to that seen in in control mice. Our results suggest that lower levels of NO and reduced nNOS immunostaining contribute to hippocampal-dependent spatial learning deficits in AVD-deficient mice.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 1","pages":"31-56"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8941191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10627131","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}

{"title":"Depression and Parkinson's disease: a Chicken-Egg story.","authors":"Ashok Chakraborty,&nbsp;Anil Diwan","doi":"10.3934/Neuroscience.2022027","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022027","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a neurodegenerative disease, however, besides the motor symptoms, such as rest tremor, hypokinesia, postural instability and rigidity, PD patients have also non-motor symptoms, namely neuropsychiatric disorders. Apart from the required motor symptoms, psychopathological symptoms are very common and include mood disorders, anxiety disorders, hallucinations, psychosis, cognitive deterioration and dementia. The underlying pathophysiological process in PD is mainly due to the loss of dopaminergic neural cells and thereby causes the shortage of nigrostriatal dopamine content in them. In addition, it may involve other neurotransmitter systems such as the noradrenergic, serotonergic, cholinergic and noradrenergic systems as well. Depression can result from any unhealthy conditions making the diagnosis a challenging task. The manifestation of depression associated with or without PD is inadequate. The co-occurrence of depression and PD often leads to the conceptual discussion on whether depressive symptoms appear before or after PD develops. This paper will discuss the conceptual mechanism of PD and depression. Keep in mind both conditions belong to two separate entities but share some similar aspects in their pathophysiology.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"479-490"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10551705","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}

{"title":"Naringin ameliorates motor dysfunction and exerts neuroprotective role against vanadium-induced neurotoxicity.","authors":"Adeshina O Adekeye,&nbsp;Adedamola A Fafure,&nbsp;Ayoola E Ogunsemowo,&nbsp;Linus A Enye,&nbsp;Olusola S Saka,&nbsp;Oluwatosin O Ogedengbe","doi":"10.3934/Neuroscience.2022031","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022031","url":null,"abstract":"<p><p>Exposure to vanadium has been known to lead to a progressive neurodegenerative disorder like Parkinson's disease. Naringin is a known flavonoid glycoside that is mostly seen in the flesh of grapefruit and orange and is believed to have protective effects for the treatment of neurodegenerative disorders. This study sought to investigate the role of Naringin in the treatment of vanadium-induced neurotoxicity. Vanadium (10 mg/kg BW) was injected intraperitoneally to induce motor dysfunction, followed by treatment with Naringin (30 mg/kg BW) intraperitoneally for 14 days. Oxidative stress imbalance was monitored by checking Glutathione Peroxidase (GPX) and Catalase levels. Histological and immunohistochemical alterations were observed using RBFOX3 polyclonal antibody to determine neuronal cell distribution and NLRP3 inflammasome antibody as a marker of inflammation. Exposure to vanadium induces neurotoxicity by significantly increasing the Catalase and Glutathione Peroxidase (GPX) levels. Vanadium administration also led to increased inflammatory cells and a significant reduction of the viable neuronal cells in the SNc and CPu. Treatment with Naringin showed a neuroprotective role by dependently restoring the Catalase and Glutathione Peroxidase (GPX) levels, inflammasome activation, and neuronal damage in the SNc and CPu. Naringin demonstrated anti-oxidative, and anti-inflammatory responses by inhibiting oxidative stress, and inflammation and exerts neuroprotective effects by inhibiting apoptosis following vanadium-induced neurotoxicity in adult Wistar rats.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"536-550"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10551704","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}

{"title":"Pharmacological evidence for the possible involvement of the NMDA receptor pathway in the anticonvulsant effect of tramadol in mice.","authors":"Mazyar Zahir,&nbsp;Amir Rashidian,&nbsp;Mohsen Hoseini,&nbsp;Reyhaneh Akbarian,&nbsp;Mohsen Chamanara","doi":"10.3934/Neuroscience.2022024","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022024","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have shown controversial results regarding the pro- or anticonvulsant effects of tramadol. Additionally, the underlying mechanism of seizure induction or alleviation by tramadol has not been fully understood. In the current study, the effects of tramadol on pentylenetetrazole (PTZ)-induced seizure and the possible involvement of the N-methyl-D-aspartate (NMDA) pathway were assessed in mice.</p><p><strong>Methods: </strong>Male Naval Medical Research Institute (NMRI) mice were treated with intravenous infusion of PTZ in order to induce clonic seizures and determine seizure threshold. Tramadol was injected intraperitoneally (0.1-150 mg/kg) 30 minutes prior to elicitation of seizures. The possible effects of intraperitoneal injections of NMDA receptor antagonists, ketamine (0.5 mg/kg) and MK-801 (0.5 mg/kg) on the anticonvulsant property of tramadol were investigated subsequently.</p><p><strong>Results: </strong>Tramadol (1-100 mg/kg) increased PTZ-induced seizure threshold in a dose-dependent, time-independent manner, with optimal anticonvulsant effect at a dose of 100 mg/kg. Acute administration of either ketamine (0.5 mg/kg) or MK-801 (0.5 mg/kg) potentiated the anticonvulsant effect of a subeffective dose of tramadol (0.3 mg/kg).</p><p><strong>Conclusion: </strong>These results suggest a possible role of the NMDA pathway in the anticonvulsant effect of tramadol.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"444-453"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10558630","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}

{"title":"Gut neurotoxin p-cresol induces brain-derived neurotrophic factor secretion and increases the expression of neurofilament subunits in PC-12 cells","authors":"G. Tevzadze, T. Barbakadze, Elisabed Kvergelidze, E. Zhuravliova, L. Shanshiashvili, D. Mikeladze","doi":"10.3934/Neuroscience.2022002","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022002","url":null,"abstract":"Increased p-cresol levels reportedly alter brain dopamine metabolism and exacerbate neurological disorders in experimental animals. In contrast to toxic concentrations, low doses of p-cresol may have distinct effects on neuronal metabolism. However, the role of p-cresol in synapse remodeling, neurite outgrowth, and other anabolic processes in neurons remains elusive. We propose that low doses of p-cresol affect neuronal cell structural remodeling compared with the high concentration-mediated harmful effects. Thus, the effects of p-cresol on the secretion of brain-derived neurotrophic factor (BDNF) and neurofilament subunit expression were examined using rat pheochromocytoma cells (PC-12 cells). We observed that low doses of p-cresol potentiated nerve growth factor-induced differentiation via secretion of BDNF in cultured PC-12 cells. Opioidergic compounds modulated these p-cresol effects, which were reversed by oxytocin. We propose that this effect of p-cresol has an adaptive and compensatory character and can be attributed to the induction of oxidative stress. Accordingly, we hypothesize that low doses of p-cresol induce mild oxidative stress, stimulating BDNF release by activating redox-sensitive genes. Given that the intestinal microbiome is the primary source of endogenous p-cresol, the balance between gut microbiome strains (especially Clostridium species) and opioidergic compounds may directly influence neuroplasticity.","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"11 1","pages":"12 - 23"},"PeriodicalIF":2.7,"publicationDate":"2021-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70227471","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}

{"title":"Cognitive and linguistic dysfunction after thalamic stroke and recovery process: possible mechanism","authors":"S. Obayashi","doi":"10.3934/Neuroscience.2022001","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022001","url":null,"abstract":"Thalamic stroke may result in cognitive and linguistic problems, but the underlying mechanism remains unknown. Especially, it is still a matter of debate why thalamic aphasia occasionally occurs and then mostly recovers to some degree. We begin with a brief overview of the cognitive dysfunction and aphasia, and then review previous hypotheses of the underlying mechanism. We introduced a unique characteristic of relatively transient “word retrieval difficulty” of patients in acute phase of thalamic stroke. Word retrieval ability involves both executive function and speech production. Furthermore, SMA aphasia and thalamic aphasia may resemble in terms of the rapid recovery, thus suggesting a shared neural system. This ability is attributable to the supplementary motor area (SMA) and inferior frontal cortex (IFG) via the frontal aslant tract (FAT). To explore the possible mechanism, we applied unique hybrid neuroimaging techniques: single-photon emission computed tomography (SPECT) and functional near-infrared spectroscopy (f-NIRS). SPECT can visualize the brain distribution associated with word retrieval difficulty, cognitive disability or aphasia after thalamic stroke, and f-NIRS focuses on SMA and monitors long-term changes in hemodynamic SMA responses during phonemic verbal task. SPECT yielded common perfusion abnormalities not only in the fronto–parieto–cerebellar–thalamic loop, but also in bilateral brain regions such as SMA, IFG and language-relevant regions. f-NIRS demonstrated that thalamic stroke developed significant word retrieval decline, which was intimately linked to posterior SMA responses. Word retrieval difficulty was rapidly recovered with increased bilateral SMA responses at follow-up NIRS. Together, we propose that the cognitive domain affected by thalamic stroke may be related to the fronto–parieto–cerebellar–thalamic loop, while the linguistic region may be attributable to SMA, IFG and language-related brain areas. Especially, bilateral SMA may play a crucial role in the recovery of word retrieval, and right language-related region, including IFG, angular gyrus and supramarginal gyrus may determine recovery from thalamic aphasia.","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 1","pages":"1 - 11"},"PeriodicalIF":2.7,"publicationDate":"2021-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44251907","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}

{"title":"Tumor necrosis factor (TNF) induces astrogliosis, microgliosis and promotes survival of cortical neurons.","authors":"Ebtesam M Abd-El-Basset,&nbsp;Muddanna Sakkattu Rao,&nbsp;Solaiman M Alshawaf,&nbsp;Hasan Kh Ashkanani,&nbsp;Abdulaziz H Kabli","doi":"10.3934/Neuroscience.2021031","DOIUrl":"https://doi.org/10.3934/Neuroscience.2021031","url":null,"abstract":"<p><strong>Objectives: </strong>Neuro-inflammation occurs as a sequence of brain injury and is associated with production of cytokines. Cytokines can modulate the function and survival of neurons, microglia and astrocytes. The objective of this study is to examine the effect of TNF on the neurons, microglia and astrocytes in normal brain and stab wound brain injury.</p><p><strong>Methods: </strong>Normal BALB/c male mice (N) without any injury were subdivided into NA and NB groups. Another set mouse was subjected to stab wound brain injury (I) and were subdivided into IA and IB. NA and IA groups received intraperitoneal injections of TNF (1 µg/kg body weight/day) for nine days, whereas NB and IB groups received intraperitoneal injections of PBS. Animals were killed on 1^st, 2^nd, 3^rd, 7^th, and 9^th day. Frozen brain sections through the injury site in IA and IB or corresponding region in NA and NB groups were stained for neurodegeneration, immunostained for astrocytes, microglia and neurons. Western blotting for GFAP and ELISA for BDNF were done from the tissues collected from all groups.</p><p><strong>Results: </strong>The number of degenerating neurons significantly decreased in TNF treated groups. There was a significant increase in the number of astrocytes and microglia in TNF treated groups compared to PBS treated groups. In addition, it was found that TNF stimulated the expression of GFAP and BDNF in NA and IA groups.</p><p><strong>Conclusions: </strong>TNF induces astrogliosis and microgliosis in normal and injured brain and promotes the survival of cortical neurons in stab wound brain injury, may be by upregulating the BDNF level.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"8 4","pages":"558-584"},"PeriodicalIF":2.7,"publicationDate":"2021-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8611192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39702583","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}

{"title":"Potential molecular link between the β-amyloid precursor protein (APP) and hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme in Lesch-Nyhan disease and cancer.","authors":"Khue Vu Nguyen","doi":"10.3934/Neuroscience.2021030","DOIUrl":"https://doi.org/10.3934/Neuroscience.2021030","url":null,"abstract":"<p><p>Lesch-Nyhan disease (LND) is a rare X-linked inherited neurogenetic disorders of purine metabolic in which the cytoplasmic enzyme, hypoxanthine-guanine phosphoribosyltransferase (HGprt) is defective. Despite having been characterized over 60 years ago, however, up to now, there is no satisfactory explanation of how deficits in enzyme HGprt can lead to LND with the development of the persistent and severe self-injurious behavior. Recently, a role for epistasis between the mutated hypoxanthine phosphoribosyltransferase 1 (<i>HPRT1</i>) and the β-amyloid precursor protein (APP) genes affecting the regulation of alternative APP pre-mRNA splicing in LND has been demonstrated. Furthermore, there were also some reported cases of LND developing thrombosis while APP is an important regulator of vein thrombosis and controls coagulation. Otherwise, the surface expression of HGprt enzyme was also observed in several somatic tissue cancers while APP and the APP-like protein-2 (APLP2) are deregulated in cancer cells and linked to increased tumor cell proliferation, migration, and invasion. The present review provides a discussion about these findings and suggests a potential molecular link between APP and HGprt via epistasis between <i>HPRT1</i> and <i>APP</i> genes affecting the regulation of alternative APP pre-mRNA splicing. As a perspective, expression vectors for HGprt enzyme and APP are constructed as described in Ref. # 24 (Nguyen KV, Naviaux RK, Nyhan WL (2020) Lesch-Nyhan disease: I. Construction of expression vectors for hypoxanthine-guanine phosphoribosyltransferase (HGprt) enzyme and amyloid precursor protein (APP). <i>Nucleosides Nucleotides Nucleic Acids</i> 39: 905-922), and they could be used as tools for clarification of these issues. In addition, these expression vectors, especially the one with the glycosyl-phosphatidylinositol (GPI) anchor can be used as a model for the construction of expression vectors for any protein targeting to the cell plasma membrane for studying intermolecular interactions and could be therefore useful in the vaccines as well as antiviral drugs development (studying intermolecular interactions between the spike glycoprotein of the severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, as well as its variants and the angiotensin-converting enzyme 2, ACE2, in coronavirus disease 2019 (COVID-19) [43],[44], for example).</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"8 4","pages":"548-557"},"PeriodicalIF":2.7,"publicationDate":"2021-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8611187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39702582","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}

{"title":"Neuroethics: what the study of brain disorders can tell about moral behavior.","authors":"Carmelo M Vicario, Chiara Lucifora","doi":"10.3934/Neuroscience.2021029","DOIUrl":"10.3934/Neuroscience.2021029","url":null,"abstract":"<p><p>The growing interest in the study of morality has led to the birth of a new discipline in the field of moral philosophy called Neuroethics, a multidisciplinary approach that aims to combine philosophy and neuroscience. In this editorial, we explored the relevance of clinical models affected by neurological/psychiatric disorders to learn more about mechanisms sub-serving ethical behaviour at neural and cognitive level.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"8 4","pages":"543-547"},"PeriodicalIF":2.7,"publicationDate":"2021-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8611188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39702581","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}