Basic and Clinical Neuroscience最新文献

{"title":"Cortical Activity During Postural Recovery Under Dual-task Conditions: A Quantitative EEG Study.","authors":"Ehsan Sinaei, Mohammad Nami, Zahra Saadat","doi":"10.32598/bcn.2025.7028.1","DOIUrl":"10.32598/bcn.2025.7028.1","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the cortical activity differences between healthy older adults and younger individuals during postural adjustments in response to external perturbations under both single-task (ST) and dual-task (DT) conditions.</p><p><strong>Methods: </strong>Nineteen young adults (mean age: 24.25±3.15) and 20 older adults (mean age: 65.55±4.67 years) were recruited. Participants stood barefoot while a load (3% body weight) was unpredictably released, inducing postural perturbations. In DT trials, participants performed a cognitive task (counting backward) while maintaining balance. Quantitative electroencephalography was recorded from 32 channels, focusing on cortical regions involved in postural control (e.g. motor and sensorimotor cortices). Alpha (8-12 Hz) and beta (12.5-25 Hz) absolute power in specific brain regions (C3, C4, Fz, Cz, Pz) were analyzed using a 3-way mixed-design analysis of variance.</p><p><strong>Results: </strong>Older adults exhibited significantly higher alpha power in sensorimotor areas (C4, Pz) during DT conditions, compared to younger adults. Group×condition interactions revealed greater beta power in the frontal and central regions (F4, C4) in older adults under DT conditions. Post hoc analysis indicated significantly greater beta power in older adults during DT than in younger individuals.</p><p><strong>Conclusion: </strong>These findings suggest that older adults rely more on cortical resources for postural recovery, particularly under cognitively demanding DT conditions. The increased alpha and beta power in cortical regions reflects a shift towards compensatory cortical strategies, likely due to age-related declines in automatic postural control mechanisms. Understanding these neural changes can inform fall prevention strategies targeting both cognitive and motor functions in older adults.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 4","pages":"777-786"},"PeriodicalIF":1.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136887","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":"Brain Mapping of Behavior Contagion Based on Visibility Graph Analysis of ERP Signals.","authors":"Mohammad Hossein Sorayani, Abdol-Hossein Vahabie, Javad Hatami, Reza Khosrowabadi","doi":"10.32598/bcn.2025.7653.1","DOIUrl":"10.32598/bcn.2025.7653.1","url":null,"abstract":"<p><strong>Introduction: </strong>Behavior contagion in social decision-making refers to the alignment of an individual's behavior and decisions with those of others in social interactions. Despite previous studies in the field, it remains necessary to understand how brain activities are spatiotemporally organized during contagion. Since brain activities include both positive and negative fluctuations, monitoring these occurrences in a polar space using a visibility graph (VG) can aid in a better understanding of this phenomenon.</p><p><strong>Methods: </strong>We subjected a healthy group to a psycho-economic task while their EEG was simultaneously recorded. The participants' performances were compared before and after observation of others' preferences in a dictator game task. Subsequently, two groups were differentiated based on their behavior contagion rate. Then, the VGs of event-related potentials (ERPs) in both contagion and non-contagion groups were compared before and after observation.</p><p><strong>Results: </strong>Our results indicated that the VG features differentially change in various EEG channels. For instance, changes in clustering coefficient, modularity, and efficiency of VGs suggested that the number of ERP components varies after contagion, specifically at the frontal, frontocentral, centroparietal, and parietal regions.</p><p><strong>Conclusion: </strong>This result may raise questions about the ERP analysis of contagion, particularly when using the same number and length of components (e.g. P300) for comparing ERPs before and after contagion.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 4","pages":"833-844"},"PeriodicalIF":1.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136884","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":"Effects of <i>Nigella sativa</i> Nano-hydroalcoholic Extract on Neuronal Damages in the Hippocampus of Male Rats After Cerebral Ischemia/Reperfusion.","authors":"Mahsa Golmohammadi, Atarodalsadat Mostavafinia, Mohammad Mahdi Nazarnejad, Zahra Nadia Sharifi","doi":"10.32598/bcn.2025.7517.1","DOIUrl":"10.32598/bcn.2025.7517.1","url":null,"abstract":"<p><strong>Introduction: </strong>Cerebral ischemia is one of the leading causes of global mortality and disability in many countries. Damage caused by reperfusion is due to the inflammatory function of the injured tissue. Ischemia-reperfusion causes the formation of oxygen free radicals and other oxidants. The CA1 region of the hippocampus is one of the highly sensitive parts of the brain in ischemia and hypoxia. The <i>Nigella sativa</i> plant, with its antioxidant properties, can remove free radicals and cell-damaging compounds to prevent cell death and damage to viable cells. To determine the effects of hydroalcoholic extract and nano-hydroalcoholic extract containing <i>N. sativa</i> on the CA1 region of the hippocampus in male Wistar rats following transient global ischemia/reperfusion.</p><p><strong>Methods: </strong>Four groups of 32 male Wistar rats were randomly formed: Control, ischemia, hydroalcoholic extract of black recipient seed, and nano-extract of hydroalcoholic black seed recipient. Ligation of bilateral common carotid arteries induced an ischemia model. Following the behavioral test, brain removal was completed and prepared for Nissl staining and stereological evaluations, along with the expression levels of <i>Bax</i> and <i>Bcl2</i>, using the real-time PCR technique.</p><p><strong>Results: </strong>A considerable rise in the number of viable pyramidal cells was observed in the hydroalcoholic extract and nano-hydroalcoholic extract groups compared to the ischemia group. <i>Bax</i> expression was elevated, and the expression of <i>Bcl-2</i> declined after transient global I/R in the CA1 region. The effects of transient global ischemia/reperfusion (I/R) on gene expression were reversed by the injection of hydroalcoholic and nano-hydroalcoholic extracts containing <i>N. Sativa</i>.</p><p><strong>Conclusion: </strong>Transient global I/R remarkably promotes cell death and morphological changes. It appears that the hydroalcoholic extract of <i>N. sativa</i>, particularly the nanohydroalcoholic extract, at a dose of 400 mg/kg, may be a suitable solution for treating ischemia-induced brain damage.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 4","pages":"819-832"},"PeriodicalIF":1.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136872","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":"The Impact of Small Molecule on the Astrocyte's Viability Derived From Epileptic Brain Tissues.","authors":"Javad Momeni, Elham Hosseini, Maryam Khaleghi Ghadiri, Fariborz Samini, Alireza Tabibkhooei, Ali Gorji, Sajad Sahab Negah","doi":"10.32598/bcn.2025.5446.3","DOIUrl":"10.32598/bcn.2025.5446.3","url":null,"abstract":"<p><strong>Introduction: </strong>Astrocyte dysfunction plays a crucial role in epileptogenesis by impacting neuronal excitability and synaptic transmission. This study investigates how specific small molecules (SMs) affect the survival of astrocytes derived from various brain regions (the neocortex, hippocampus, or amygdala) of patients with medically refractory epilepsy.</p><p><strong>Methods: </strong>This study evaluated astrocyte responses to three distinct SMs (valproate, forskolin, and GSK3 inhibitor/WNT activator CHIR99021), individually or in combined forms, to determine their differential effects on astrocyte survival.</p><p><strong>Results: </strong>The effects of SMs on astrocyte survival varied based on the brain tissue source and individual patient differences. Astrocytes from the amygdala of two patients showed heightened sensitivity to the SMs, while astrocytes from the neocortex of one patient exhibited decreased viability following treatment with CHIR99021 and valproate. Moreover, astrocytes from the hippocampus exhibited a significant decrease in viability in one patient, whereas no significant changes were observed in other patients.</p><p><strong>Conclusion: </strong>Variability in astrocyte responses to SMs, influenced by brain region and patient differences, may highlight their role in shaping diverse therapeutic outcomes in individuals. Further studies are required to clarify the factors involved in the different behaviors of astrocytes in response to SMs in epilepsy.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 4","pages":"751-762"},"PeriodicalIF":1.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136845","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":"Intranasal Autologous Conditioned Serum Attenuates Memory Impairment After mPFC Ischemia in Mice.","authors":"Sareh Kazmi, Neda Yazdanfar, Fatemehsadat Seyedaghamiri, Alireza Pishgahi, Mehdi Yousefi, Tahereh Ghadiri, Saeed Sadigh-Eteghad, Mehdi Farhoudi","doi":"10.32598/bcn.2025.7486.1","DOIUrl":"10.32598/bcn.2025.7486.1","url":null,"abstract":"<p><strong>Introduction: </strong>Globally, stroke ranks as the second most prevalent cause of death, contributing significantly to worldwide mortality burdens, imposing a significant economic and emotional challenge on societies. This study was designed to investigate the effect of autologous conditioned serum (ACS) on memory and associated molecular factors in a mouse model of photothrombotic ischemic stroke.</p><p><strong>Methods: </strong>The photothrombotic model was used to induce medial prefrontal cortex (mPFC) ischemia. ACS were prepared by intracardiac puncture of C57BL/6 mice using special ACS syringes. After blood incubation, the sample was centrifuged, and the serum was analyzed with ELISA kits to quantify the levels of interleukin-1 receptor antagonist (IL-1RA) and insulin-like growth factor (IGF-I). The ischemic animals received 48 μL intranasal ACS two times a day, once a day, or once every other day for one week. Behavioral tests, including the Lashley-III maze and social interaction test, were conducted following treatment administration. Additionally, IGF-1, IL-1β, IL-1RA levels, and phospho-tau/total-tau ratio were measured in the mPFC area by western blot. Histological analysis was performed to assess ischemic volume.</p><p><strong>Results: </strong>The results indicated that once-daily administration of ACS significantly improved spatial memory in the Lashley-III maze and showed a notable enhancement in social memory as measured by the social interaction test. In terms of molecular analysis, ACS increased the levels of IGF-1 and IL-1RA, whilst decreasing the levels of IL-1β and p-tau/total-tau ratio.</p><p><strong>Conclusion: </strong>In conclusion, post-stroke intranasal ACS administration enhances memory, possibly by increasing the level of IGF-1 and attenuating inflammation through the inhibition of IL-1β signal by IL-1RA, and regulation of tau levels.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 4","pages":"805-818"},"PeriodicalIF":1.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136850","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":"Pathways Mediating Blindsight After V1 Injury: A Systematic Review of Human and Monkey Studies.","authors":"Mohammad Reza Balali, Mohaddeseh Hosseini, Maryam Khanboloki, Mohammad Mohammadi, Amir Mohammad Khorshidvand, Mohammad Taghi Joghataei","doi":"10.32598/bcn.2025.7005.1","DOIUrl":"10.32598/bcn.2025.7005.1","url":null,"abstract":"<p><strong>Introduction: </strong>Although damage to the visual area (V1) leads to visual impairment, some patients retain the ability to process visual information unconsciously, a phenomenon known as blindsight. This study aims to systematically review and compare the proposed neural pathways mediating blindsight in humans and monkeys, providing a structured framework for future investigations in this field.</p><p><strong>Methods: </strong>This is a systematic review of related articles retrieved from online databases. Following the screening process, we employed the JBI critical appraisal checklist as well as the SYRCLE tool to assess the risk of bias in human and animal studies. We selected 25 articles focusing on the mediating pathways of blindsight.</p><p><strong>Results: </strong>In humans, the pathways from the lateral geniculate nucleus (LGN) to V5, from the superior colliculus (SC) to higher brain areas, and to the remaining segments of V1 are crucial. The pathway that connects the SC, pulvinar, and amygdala is essential for processing emotional visual information. Studies conducted on monkeys emphasized the importance of the SC-pulvinar pathway and the connections between the LGN and extrastriate visual areas for developing blindsight.</p><p><strong>Conclusion: </strong>Rather than a single consistent pathway, blindsight appears to involve multiple parallel routes whose engagement depends on factors such as lesion extent, individual neuroanatomy, and time since injury. Future studies should explore the therapeutic potential of these pathways by integrating.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 3","pages":"533-550"},"PeriodicalIF":1.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390102","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":"Vismodegib Improved Therapy of Medulloblastoma by Targeting Sonic Hedgehog Signaling Pathway on DAOY Medulloblastoma Cell Line.","authors":"Masume Behruzi, Mehrdad Ghorbanlou, Ronak Shabani, Auob Rustamzadeh, Enam Alhagh Gorgich, Elham Seidkhani, Farnoosh Usefi, Mehdi Mehdizadeh, Fatemeh Moradi","doi":"10.32598/bcn.2024.6423.1","DOIUrl":"10.32598/bcn.2024.6423.1","url":null,"abstract":"<p><strong>Introduction: </strong>Targeting smoothened (SMO) has been a remarkable strategy for treating sonic hedgehog (Shh)-dependent cancers, especially medulloblastoma. GDC-0449, also known as vismodegib, is a potent SMO inhibitor with mild toxicity and high affinity. Thus, this study aimed to investigate the anti-medulloblastoma efficacy of vismodegib in the DAOY medulloblastoma cell line.</p><p><strong>Methods: </strong>Human DAOY medulloblastoma cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM). 50, 80, 100, and 150 μM doses of vismodegib were used to treat cells. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), scratch, and trypan blue assays, as well as real-time polymerase chain reaction (RT-PCR) and immunofluorescence studies, were performed 24 and 48 h post-treatment.</p><p><strong>Results: </strong>The MTT and trypan blue assays showed a significant difference in viability between the control and treatment groups. The results of the scratch assay showed that in the control group, the cells were able to repair the lesion, while the scratch disintegrated at higher doses of vismodegib. The expression of <i>SMO</i>, <i>Gli1</i>, and <i>MYCN</i> genes, the main components of the SHH signalling pathway, was significantly reduced in the vismodegib-treated groups compared to the control group. Also, a notable increase in the activation of metastasis-promoting genes (<i>Bax</i> and <i>p53</i>) and a reduction in the activation of the metastasis-inhibiting gene (<i>Bcl2</i>) were observed.</p><p><strong>Conclusion: </strong>The results of the current study confirm that vismodegib is a potent inhibitor of the Shh pathway and may be used in combination with new therapeutic methods to treat medulloblastoma.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 3","pages":"609-618"},"PeriodicalIF":1.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148389432","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":"<i>Vitis Vinifera</i> L. Flavones Preserve Mitophagy in the Amyloid-beta 1-42-induced Model of Alzheimer's Disease Neurodegeneration.","authors":"Peng Zhang, Hui Xiao","doi":"10.32598/bcn.2025.6592.1","DOIUrl":"10.32598/bcn.2025.6592.1","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by amyloid-beta (Aβ) accumulation, leading to inflammation, oxidative stress, and impaired synaptic function. This study aimed to investigate the neuroprotective mechanisms of <i>Vitis vinifera</i> L. flavones (VTF) against Aβ-induced neurodegeneration and their potential as AD therapeutics.</p><p><strong>Methods: </strong>In an in vitro analysis, Aβ1-42 oligomers were used to induce mitophagy in SHSY5Y neuroblastoma cells. Cells were treated with VTF alone and in combination with chloroquine (CQ), a lysosomal inhibitor, to assess Aβ1-42-induced mitophagy. Transmission electron microscopy (TEM) and immunofluorescence (IFC) were used to investigate the effects of Aβ1-42 on autophagosomes and deposition. Cellular protection against Aβ-induced damage was assessed using the Cell Counting Kit-8 (CCK-8) assay. Western blotting (WB) was used to determine the expression of autophagy-lysosomal pathway proteins (Beclin-1, Atg7, p62, and BACE1) and the LC3-II/LC3-I ratio, which serves as a marker of autophagy.</p><p><strong>Results: </strong>CQ and VTF demonstrated significant neuroprotection against Aβ1-42-induced neurodegeneration (P<0.05). VTF, alone or with CQ, increased viable cell count (~1.2-fold; P<0.05), indicating reparative capabilities. TEM and IFC showed robust protection by VTF and CQ against Aβ protein deposition, as well as preservation of mitochondrial and autophagosomal structures. VTF and CQ treatments reduced Beclin-1, Atg7, and BACE1 levels, indicating the modulation of mitophagy and autophagy-lysosomal suppression. VTF+CQ maintained LC3-II/LC3-I balance, confirming VTF's role in preserving autophagy (P<0.01).</p><p><strong>Conclusion: </strong>This study reveals the novel neuroprotective role of VTF, emphasizing its potential as an AD therapeutic. Future research should extend investigations to in vivo models and clinical settings to enhance our understanding of VTF's neuroprotective efficacy.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 3","pages":"641-656"},"PeriodicalIF":1.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390025","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":"Short-term Efficacy of Commercial Curcumin Nanomicelle on Cognition, Oxidative Stress and Choline Esterase in Alzheimer's Disease.","authors":"Samira Kazemi, Narges Hesni Langroudi, Peyman Hasani Abharian, Kamran Tavakol, Mohammad Taghi Joghataei, Shima Tavakol, Sepide Arbabi Bidgoli","doi":"10.32598/bcn.2024.4970.1","DOIUrl":"10.32598/bcn.2024.4970.1","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disease accompanied by cognitive dysfunction. Preclinical changes can precede the onset of clinical symptoms by decades, highlighting the need for preventative and therapeutic strategies to mitigate or delay disease progression. This pilot clinical trial aimed to investigate the effects of commercially available curcumin nanomicelles on oxidative stress pathways and serum cholinesterase levels in patients with AD.</p><p><strong>Methods: </strong>Fifteen volunteers with mild-to-severe AD and 15 age-matched healthy controls were enrolled. Participants with AD received 80 mg of thermodynamically stable 10 nm curcumin nanomicelles on alternate days for two months. Cognitive function, as assessed by the mini-mental state examination (MMSE), did not exhibit significant changes in patients with AD following curcumin nanomicelle administration (19.8 versus 20.6). Serum levels of oxidative stress biomarkers, including catalase (CAT), superoxide dismutase (SOD) inhibition, malondialdehyde (MDA) concentration, and cholinesterase activity, were evaluated before and after intervention.</p><p><strong>Results: </strong>The results showed no significant differences in cognition improvement, CAT activity, SOD inhibition, MOD concentration, or cholinesterase activity between patients with AD and healthy controls or before and after curcumin nanomicelle administration.</p><p><strong>Conclusion: </strong>Although curcumin nanocarriers did not enhance antioxidant biomolecule levels, they did not provoke lipid peroxidation. Therefore, this study suggests that optimizing nanocarrier parameters, including concentration, particle size larger than 10 nm, and blood-brain barrier (BBB)targeting, warrants further investigation in a long-term study to explore their potential as supplemental therapies for AD.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 3","pages":"595-608"},"PeriodicalIF":1.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390111","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":"Alpha-mangostin Ameliorates Apoptosis, Inflammation and Oxidative Stress in Cuprizone-induced Demyelination in C57BL/6 Mice.","authors":"Sara Banaeeyeh, Bibi Marjan Razavi, Hossein Hosseinzadeh","doi":"10.32598/bcn.2024.799.3","DOIUrl":"10.32598/bcn.2024.799.3","url":null,"abstract":"<p><strong>Introduction: </strong>Alpha-mangostin (α-MG), the most abundant xanthone found in <i>Garcinia mangostana</i> Linn, has been reported to possess potent antioxidant and anti-inflammatory properties. This study aimed to investigate the neuroprotective effects of α-MG against cuprizone (CZ)-induced demyelination in the corpus callosum (CC) of mice, an established animal model for multiple sclerosis (MS).</p><p><strong>Methods: </strong>Adult female C57BL/6 mice were fed a chow containing 0.4% (w/w) CZ for 5 weeks. The animals were randomly assigned to six groups: (1) control group receiving a standard diet; (2) CZ group receiving the CZ-containing diet; (3-5) CZ diet plus α-MG at doses of 20, 40, and 80 mg/kg/day administered via gavage; (6) standard diet plus α-MG at 80 mg/kg/day. At the end of the treatment period, levels of malondialdehyde (MDA), proapoptotic and anti-apoptotic markers (Bax, Bcl-2, cleaved caspase-3), and the inflammatory cytokine tumor necrosis factor-alpha (TNF-α) were measured in the CC.</p><p><strong>Results: </strong>Compared with the control group, CZ-treated mice exhibited significant weight loss (P<0.0001), elevated MDA levels (P<0.01), an increased Bax/Bcl-2 ratio, enhanced cleaved caspase-3 expression (P<0.0001), and increased TNF-α levels (P<0.001). Treatment with α-MG at 80 mg/kg significantly mitigated weight loss (P<0.01). Furthermore, α-MG at all tested doses (20, 40, and 80 mg/kg) significantly reduced MDA levels (P<0.01, P<0.001, and P<0.0001, respectively). Administration of α-MG at 80 mg/kg also significantly reduced the Bax/Bcl-2 ratio, cleaved caspase-3 expression (P<0.0001), and TNF-α levels (P<0.0001) compared with the CZ group.</p><p><strong>Conclusion: </strong>These findings demonstrate that α-MG attenuates the detrimental effects of CZ-induced demyelination in the CC by reducing oxidative stress, inflammation, and apoptosis.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"16 3","pages":"569-582"},"PeriodicalIF":1.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390058","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}