Neuroprotection最新文献

{"title":"Downregulation of forkhead box O1 (FOXO1) acetylation ameliorates cognitive dysfunction by inhibiting endoplasmic reticulum stress-regulated neuronal apoptosis in APP/PS1 transgenic mice.","authors":"Nan Zhang, Zongyuan Zhao, Xiaoxiao Chen, Hanbing Yao, Min Zhu, Shuqing Ma, Hui Wang, Xianghong Yin, Ying Zhou, Chenfei Zheng, Jianmin Li, Jingye Pan, Kaicheng Wang, Bin Yang, Yunting Wang, Junming Fan, Yongsheng Gong, Rong Liu, Jing Zeng, Xiaofang Fan, Yangping Shentu","doi":"10.1002/nep3.66","DOIUrl":"10.1002/nep3.66","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a neurodegenerative disorder that affects the central nervous system. Silent information regulator sirtuin 1 (SIRT1) may deacetylate and suppress forkhead box O (FOXO) activities to promote neuronal survival. FOXO1 is involved in the regulation of metabolism, senescence, stress response, and apoptosis. Moreover, endoplasmic reticulum stress (ERS) mediates cell apoptosis. Therefore, this study aimed to determine whether the downregulation of SIRT1 expression exacerbates cognitive dysfunction by activating FOXO1 acetylation and promoting ERS-mediated apoptosis in amyloid precursor protein/presenilin 1 (APP/PS1) transgenic mice.</p><p><strong>Methods: </strong>We used APP/PS1 transgenic mice to construct an in vivo AD model. Additionally, we used β-amyloid (Aβ)-incubated HT22 cells and primary neurons (PNs) for in vitro analyses. Cognitive function was assessed using novel object recognition, the Morris water maze, and fear conditioning. Discrepancies between wild-type (WT) and APP/PS1 transgenic mice were evaluated using an unpaired <i>t</i> test. In addition, one-way analysis of variance was conducted for behavioral assessments and other tests involving four distinct groups, followed by a Tukey's honestly significant difference test for post hoc pairwise comparisons.</p><p><strong>Results: </strong>The expression of SIRT1 was downregulated (in animal experiments, WT mice vs. APP/PS1 mice, <i>n</i> = 3, <i>p</i> = 0.002; in cell experiments, HT22 cells vs. HT22 cells + Aβ<sub>1-42</sub>, <i>n</i> = 3, <i>p</i> = 0.001; primary neurons vs. primary neurons + Aβ<sub>1-42</sub>, <i>n</i> = 3, <i>p</i> < 0.001), whereas FOXO1 acetylation was upregulated both in vivo and in vitro (in animal experiments, WT mice vs. APP/PS1 mice, <i>n</i> = 3, <i>p</i> < 0.001; in cell experiments, HT22 cells vs. HT22 cells + Aβ<sub>1-42</sub>, <i>n</i> = 3, <i>p</i> = 0.004; primary neurons vs. primary neurons + Aβ<sub>1-42,</sub> <i>n</i> = 3, <i>p</i> < 0.001), leading to cognitive dysfunction, Aβ plaque deposition, and neuronal apoptosis. Quercetin, a SIRT1 agonist, reversed these changes (For SIRT1, APP/PS1 mice vs. Quercetin-treated APP/PS1 mice, <i>n</i> = 3, <i>p</i> = 0.014; HT22 cells + Aβ<sub>1-42</sub> vs. HT22 cells + Aβ<sub>1-</sub> <sub>42</sub> + Quercetin, <i>n</i> = 3, <i>p</i> = 0.003; primary neurons + Aβ<sub>1-42</sub> vs. primary neurons + Aβ<sub>1-42</sub> + Quercetin, <i>n</i> = 3, <i>p</i> = 0.014. For ac-FOXO1, APP/PS1 mice vs. Quercetin-treated APP/PS1 mice, <i>n</i> = 3, <i>p</i> < 0.001; HT22 cells+ Aβ<sub>1-42</sub> vs. HT22 cells + Aβ<sub>1-42</sub> + Quercetin, <i>n</i> = 3, <i>p</i> = 0.023; primary neurons + Aβ<sub>1-</sub> <sub>42</sub> vs. primary neurons + Aβ<sub>1-42</sub> + Quercetin, <i>n</i> = 3, <i>p</i> = 0.003). However, the FOXO1 antagonist AS1842856 invalidated the positive effects of quercetin in APP/PS1 transgenic mice (ac-FOXO1: Quercetin-treated APP/PS1 mice vs. A","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 2","pages":"183-201"},"PeriodicalIF":4.1,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746038","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 dynamic relationship of brain-derived neurotrophic factor and oxytocin: Introducing the concept of neurosocial plasticity.","authors":"Jamshid Faraji, Gerlinde A S Metz","doi":"10.1002/nep3.73","DOIUrl":"10.1002/nep3.73","url":null,"abstract":"<p><p>The human brain functions as a highly integrated system. Interconnected cellular and molecular networks within this system process sensory information, cognitive functions, and motor responses. The brain also exhibits a remarkable potential for plasticity-driven adaptive learning and memory. Importantly, neuroplasticity serves as a key mechanism of neuroprotection while also enabling the brain to compensate for injury through adaptive structural remodeling. Understanding the brain as a dynamic system requires examining how its components interact to produce adaptive physiological responses and complex behaviors, such as social interactions. Key molecules, such as brain-derived neurotrophic factor (BDNF) and oxytocin (OT), play pivotal roles in maintaining the brain's dynamic complexity and integrative functioning. In this review, we introduce the concept of \"neurosocial plasticity\", which refers to the brain's ability to adapt both neural circuitry and social behavior through the dynamic interaction between BDNF and OT. This concept highlights how BDNF-OT interactions may support both neural plasticity and the capacity for adaptive social functioning. We then explore how their co-localization, co-expression, and co-regulation may regulate neural and social plasticity, ultimately shaping the brain's adaptability and the development of social behaviors across various contexts.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"63-78"},"PeriodicalIF":4.1,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745994","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":"Oral microbiota and central nervous system diseases: A review.","authors":"Xiaoxuan Zhang, Mengmeng Zhong, Yang Li, Hui Wang, Guangjun Xi, Feng Wang, Chao Cheng, Yachen Shi","doi":"10.1002/nep3.75","DOIUrl":"10.1002/nep3.75","url":null,"abstract":"<p><p>Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"79-94"},"PeriodicalIF":4.1,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745999","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":"Stroke and associated comorbidities in Southeast Asian countries.","authors":"Aishika Datta, Soumya Akundi, Kaveri Wagh, Gangadhar Bhurle, Deepaneeta Sarmah, Arvind Sharma, Sudhir Shah, Anupom Borah, Shailendra Saraf, Pallab Bhattacharya","doi":"10.1002/nep3.71","DOIUrl":"10.1002/nep3.71","url":null,"abstract":"<p><p>Stroke, a leading cause of mortality and morbidity worldwide, is a complex cerebrovascular disease. Stroke risk factors are diverse, encompassing age, sex, and ethnicity. Comorbid conditions, including hypertension, hyperglycemia, hyperlipidemia, and atrial fibrillation, exacerbate stroke outcomes, contributing to the overall stroke burden within populations. In addition to these factors, lifestyle-related diseases can impact individuals across all age groups, and often include as comorbidities linked to stroke. Socioeconomic conditions, healthcare access, and the quality of clinical data significantly influence the prevalence of comorbidities. Asia, the largest continent and home to 60% of the world's population, includes many developing nations undergoing diverse economic transitions. In Southeast Asian countries, stroke prevalence is high, imposing a substantial burden on healthcare systems and economies. Research disparities in stroke are often attributed to insufficient demographic data on comorbidities. Hence, the review discusses all previously published results of hospital-based studies and data from national registries. It has been noticed that due to insufficient documentation on stroke-related comorbidities in various developing countries of Southeast Asia, stroke management becomes difficult. Therefore, this review aims to discuss the association between various comorbidities and stroke, with special emphasis on the incidence and prevalence of stroke burden in Southeast Asian countries.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"29-47"},"PeriodicalIF":4.1,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745968","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":"Decoding the role of large heat shock proteins in the progression of neuroinflammation-mediated neurodegenerative disorders.","authors":"Shailendra K Saxena, Deepak Sharma, Swatantra Kumar, Vimal K Maurya, Saniya Ansari, Hardeep S Malhotra, Amit Singh","doi":"10.1002/nep3.68","DOIUrl":"10.1002/nep3.68","url":null,"abstract":"<p><p>Chronic neuroinflammation and protein aggregation are the fundamental events mainly responsible for the progression of neurodegenerative diseases (NDs). Potential neurotoxic changes in the intra- and extracellular environment are typical hallmarks of many NDs. Treatment of ND is challenging, as the symptoms in these patients arises when a significant numbers of neurons have already been destroyed. Heat shock proteins (HSPs) can bind to recipient cells that are susceptible to stress, such as neurons, in the extracellular environment, therefore enhancing stress resistance. Among all, HSP60, HSP70, and HSP90 are highly conserved molecular chaperones involved in protein folding and assembly, maintaining cellular homeostasis in the central nervous system. Notably, α-synuclein accumulation is a major pathophysiology in Parkinson's disease, where HSP90 modulates the assembly of α-synuclein in vesicles to prevent its accumulation. Moreover, HSP90 regulates the activity of the glycogen synthase kinase-3β protein, which is crucial in diabetes mellitus-associated neurocognitive disorder. Therefore, understanding the molecular mechanism by which HSPs facilitate protein aggregation and respond to inflammatory stimuli, including metabolic disease such as diabetes, is essential for understanding the significance of HSPs in NDs. This review emphasizes the role of various HSPs in the progression of NDs such as Alzheimer's, Parkinson's, multiple sclerosis, and Huntington's disease, including diabetes, which is one of the major risk factors for neurodegeneration.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"48-62"},"PeriodicalIF":4.1,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745984","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":"Pilot functional magnetic resonance imaging study of clemastine-aided functional recovery on a mouse model of demyelination.","authors":"Ander Egimendia, Irati L de la Pisa, Daniel Padro, Lorena Colás, Sandra Plaza-García, David Otaegui, Pedro Ramos-Cabrer","doi":"10.1002/nep3.70","DOIUrl":"10.1002/nep3.70","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS) is a chronic demyelinating disease characterized by autoimmune attacks on myelin sheaths. Its deleterious effects may be reversed by remyelination, a process that restores the integrity of myelin sheaths and, consequently, neuronal function. However, the functional implications of demyelination and remyelination in MS, as well as the potential impact of therapeutic interventions, remain incompletely understood. We used noninvasive longitudinal resting-state functional magnetic resonance imaging in a cuprizone murine model of demyelination to investigate these unsolved questions.</p><p><strong>Methods: </strong>Three groups of (<i>n</i> = 6) animals were studied. A control group was fed with standard food for 5 weeks while two treatment groups (cuprizone and clemastine) suffered progressive demyelination by feeding them with 2% cuprizone. At Week 5 (W5), all animals returned to the standard diet and studied for another 5-week period to compare controls vs spontaneous (cuprizone group) vs clemastine-aided (clemastine group) remyelination group. Group clemastine was treated with this antihistaminic (oral gavage) during the remyelination period (Weeks 5-10). Anatomical magnetic resonance imaging (T2w-MRI) and resting state functional MRI (rs-FMRI) studies were conducted on weeks W0, W2, W5 (maximal demyelination) W7 and W10 (remyelination). MRI images were processed with the FMRIB Software Library, involving seed-free functional imaging and seed-based correlation. This study uses the <i>t</i>-test and the D'Agostino-Pearson normality test to make an assessment.</p><p><strong>Results: </strong>The principal findings of our research include: (1) cuprizone-treated animals suffer an initial phase of elevated connectivity at Week 2 with respect to controls, transitioning to reduced connectivity at Week 5; (2) different temporal trajectories across brain regions, reflecting varying susceptibility to demyelination; (3) while spontaneous remyelination normalizes connectivity in most networks at Week 10 (5 weeks after ceasing cuprizone intoxication), the thalamocortical axis exhibits lasting disruption even 6 months after normalization of diet; and (4) on the contrary, clemastine-aided remyelination re-establishes normal thalamocortical connectivity at 6 months after demyelination.</p><p><strong>Conclusion: </strong>This approach provides insights into the dynamic processes of demyelination and remyelination, informing the development of more effective interventions for MS.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"104-115"},"PeriodicalIF":4.1,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745976","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":"A multicenter single-arm objective performance criteria trial evaluating the efficacy and safety of a dedicated venous sinus thrombectomy device for severe cerebral venous sinus thrombosis.","authors":"Shadamu Yusuying, Yan Wu, Ming Li, Jiangang Duan, Jian Chen, Yujiao Chen, Chen Zhou, Hetao Bian, Chuanhui Li, Chuanjie Wu, Ran Meng, Xunming Ji","doi":"10.1002/nep3.63","DOIUrl":"10.1002/nep3.63","url":null,"abstract":"<p><strong>Aim: </strong>Approximately 21% of patients with cerebral venous sinus thrombosis (CVST) are refractory to anticoagulation treatment and face poor prognosis. These patients may benefit from endovascular therapy. Although numerous studies have reported promising results with endovascular therapy, it remains challenging to obtain convincing evidence of its efficacy and safety due to the unique challenges posed by CVST, such as larger vessel diameters, distinct pathophysiology, and substantial clot burden. Therefore, dedicated endovascular therapy tools should be developed specifically for CVST. This study aimed to evaluate the efficacy and safety of a dedicated venous sinus thrombectomy device in patients with acute or subacute CVST.</p><p><strong>Methods: </strong>This prospective, multicenter, single-arm trial utilized an objective performance criterion design. Enrolled patients received treatment with a dedicated venous sinus thrombectomy device to recanalize occluded sinuses or veins. The primary objective was to compare the immediate postoperative recanalization rate with a preset target value to determine whether the device met the clinical application needs. The trial plans to enroll 146 patients from 11 tertiary medical centers in China.</p><p><strong>Discussion: </strong>This trial is expected to fill a critical gap in endovascular treatments for CVST and support the development of reliable, dedicated thrombectomy devices for future studies.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"2 4","pages":"318-328"},"PeriodicalIF":4.1,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745979","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":"Liver enzyme and risk of vascular dementia: A univariable and multivariable Mendelian randomization of European descent.","authors":"Jieyu Chen, Jianzhun Chen, Chunyu Liang, Chenxi Liu, Liu Jie, Bin Liu, Xinglong Yang","doi":"10.1002/nep3.67","DOIUrl":"10.1002/nep3.67","url":null,"abstract":"<p><strong>Background: </strong>Observational studies have indicated a link between liver enzymes and dementia, but the causal relationship remains uncertain. We conducted a two-sample Mendelian randomization (MR) study to investigate potential causal links between liver function markers (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], and γ-glutamyltransferase [GGT]) and various forms of dementia (all-cause dementia, Alzheimer's disease [AD], vascular dementia [VaD], and frontotemporal dementia [FTD]).</p><p><strong>Methods: </strong>Genome-wide association study (GWAS) data of liver enzyme levels with 517 single nucleotide polymorphisms from 315,572 individuals of European descent were considered as exposures. Additional GWAS data on dementia from the FinnGen consortium and the UK Biobank were used as outcomes. The causal relationship was evaluated using univariable MR (UVMR) and multivariable MR (MVMR) methods. UVMR approaches such as inverse variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode were used, with IVW as primary. MVMR techniques, such as extended versions of IVW, MR-Egger, and Q-minimization methods, were used to assess causal effects. The robustness of the MR analysis findings was verified through heterogeneity, horizontal pleiotropy, and leave-one-out analyses.</p><p><strong>Results: </strong>MVMR analysis demonstrated that a genetically determined one standard deviation rise in blood GGT levels was associated with an increased risk of VaD (IVW: odds ratio = 1.007, 95% confidence interval = 1.002-1.011, <i>p</i> = 0.010). These findings remained consistent after adjusting for confounding variables in MVMR analysis. Sensitivity analyses further supported the causal relationship. However, no significant links were observed between ALT, AST, ALP, and all-cause dementia, VaD, AD, or FTD.</p><p><strong>Conclusions: </strong>Our study suggests clinical implications, demonstrating that high blood GGT concentrations are potential causal risk factors for VaD in European populations. Further research is needed to uncover the underlying biological mechanisms between GGT and VaD and validate the clinical relevance of early prevention and intervention strategies.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"2 4","pages":"310-317"},"PeriodicalIF":4.1,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745958","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":"Neurodegeneration in acute and chronic central nervous system disorders: Novel ideas and approaches.","authors":"Piotr Walczak, Xunming Ji, Shen Li, Johannes Boltze","doi":"10.1002/nep3.69","DOIUrl":"10.1002/nep3.69","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"2 4","pages":"243-245"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12020453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065336","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":"Correction to \"Tolerability and first hints for potential efficacy of motor-cognitive training under inspiratory hypoxia in health and neuropsychiatric disorders: A translational viewpoint\".","authors":"","doi":"10.1002/nep3.64","DOIUrl":"https://doi.org/10.1002/nep3.64","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1002/nep3.47.].</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"2 4","pages":"329"},"PeriodicalIF":0.0,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745963","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}