AIMS Neuroscience最新文献

{"title":"Chronic traumatic encephalopathy: Diagnostic updates and advances.","authors":"Kevin Pierre,&nbsp;Vanessa Molina,&nbsp;Shil Shukla,&nbsp;Anthony Avila,&nbsp;Nicholas Fong,&nbsp;Jessica Nguyen,&nbsp;Brandon Lucke-Wold","doi":"10.3934/Neuroscience.2022030","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022030","url":null,"abstract":"<p><p>Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs secondary to repetitive mild traumatic brain injury. Current clinical diagnosis relies on symptomatology and structural imaging findings which often vary widely among those with the disease. The gold standard of diagnosis is post-mortem pathological examination. In this review article, we provide a brief introduction to CTE, current diagnostic workup and the promising research on imaging and fluid biomarker diagnostic techniques. For imaging, we discuss quantitative structural analyses, DTI, fMRI, MRS, SWI and PET CT. For fluid biomarkers, we discuss p-tau, TREM2, CCL11, NfL and GFAP.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"519-535"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10551706","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":"Biomarkers and molecular mechanisms of Amyotrophic Lateral Sclerosis.","authors":"Ashok Chakraborty,&nbsp;Anil Diwan","doi":"10.3934/Neuroscience.2022023","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022023","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in adults involving non-demyelinating motor disorders. About 90% of ALS cases are sporadic, while 10-12% of cases are due to some genetic reasons. Mutations in superoxide dismutase 1 (<i>SOD1</i>), <i>TAR</i>, <i>c9orf72</i> (chromosome 9 open reading frame 72) and <i>VAPB</i> genes are commonly found in ALS patients. Therefore, the mechanism of ALS development involves oxidative stress, endoplasmic reticulum stress, glutamate excitotoxicity and aggregation of proteins, neuro-inflammation and defective RNA function. Cholesterol and LDL/HDL levels are also associated with ALS development. As a result, sterols could be a suitable biomarker for this ailment. The main mechanisms of ALS development are reticulum stress, neuroinflammation and RNA metabolism. The multi-nature development of ALS makes it more challenging to pinpoint a treatment.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"423-443"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10550930","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":"Recognition of letters displayed as successive contour fragments.","authors":"Sherry Zhang,&nbsp;Jack Morrison,&nbsp;Wei Wang,&nbsp;Ernest Greene","doi":"10.3934/Neuroscience.2022028","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022028","url":null,"abstract":"<p><p>Shapes can be displayed as parts but perceived as a whole through feedforward and feedback mechanisms in the visual system, though the exact spatiotemporal relationships for this process are still unclear. Our experiments examined the integration of letter fragments that were displayed as a rapid sequence. We examined the effects of timing and masking on integration, hypothesizing that increasing the timing interval between frames would impair recognition by disrupting contour linkage. We further used different mask types, a full-field pattern mask and a smaller strip mask, to examine the effects of global vs local masking on integration. We found that varying mask types and contrast produced a greater decline in recognition than was found when persistence or mask density was manipulated. The study supports prior work on letter recognition and provides greater insight into the spatiotemporal factors that contribute to the identification of shapes.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"491-515"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10558626","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":"Neuromodulatory roles of <i>PIPER GUINEENSE</i> and honey against Lead-Induced neurotoxicity in social interactive behaviors and motor activities in rat models.","authors":"Uchewa O Obinna,&nbsp;Emecheta S Shallom,&nbsp;Egwu A Ogugua,&nbsp;Ede C Joy,&nbsp;Ibegbu O Augustine","doi":"10.3934/Neuroscience.2022026","DOIUrl":"https://doi.org/10.3934/Neuroscience.2022026","url":null,"abstract":"<p><strong>Background: </strong><i>Piper guineense</i> and honey contain antioxidative, anti-inflammatory, and antimicrobial properties that can help restore neuronal and other cell damage. To investigate the neuromodulatory roles of <i>p. guineense</i> and honey against lead toxicity on the hippocampus and cerebellum, impairing social behaviors and motor activities.</p><p><strong>Methodology: </strong>Thirty Wistar rats were separated into six groups of five rats each, marked with dye. Group A served as control; B was untreated lead; C was a medium dose of the extract (50 mg/kg) and honey (1000 mg/kg); D was a high dose of the extract (80 mg/kg) and honey (1500 mg/kg); E received extract (80 mg/kg), and F received honey (1500 mg/kg). All groups received 110 mg/kg of lead orally, except the control. Social interaction, antidepressant effects, and motor activities were studied using a sociability chamber (SC), Forced Swim Test (FST), and String methods. A blood sample was used to evaluate glutathione peroxidase (GPx) and glutathione oxide transaminase (GOT), while the lipid level was estimated using cerebellar homogenate. Neuronal damage, vacuolation, necrosis, cell degeneration, and alterations in both hippocampus and cerebellum marked untreated group, with decreased GPx and GOT activities followed by impaired motor activities, social behavior, memory, and motivation. Using SCT, group B spent significantly lesser time (47.60 ± 47.60) with stranger 1 compared to A (138.20 ± 34.05), while group C spent considerably more time with stranger 1 (86.80 ± 30.32) than group B at P ≥ 0.05. The treatment increased the enzyme level and restored histoarchitecture (Figures 1-12), improving motor activities, social behavior, memory, motivation, and social affiliation (Tables 3, 4, 2, and 6). The extract and honey may be helpful as neuromodulators in lead toxicity in a dose-dependent manner.</p>","PeriodicalId":7732,"journal":{"name":"AIMS Neuroscience","volume":"9 4","pages":"460-478"},"PeriodicalIF":2.7,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9826751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10558628","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":"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}