Folia neuropathologica最新文献

{"title":"Intracerebral ifenprodil enhances autophagy function in 6-OHDA-lesioned rats to provide synaptic plasticity.","authors":"Xinyu Zhao, Fugang Tian, Zhicong Yin, Xin Yu","doi":"10.5114/fn.2026.160642","DOIUrl":"https://doi.org/10.5114/fn.2026.160642","url":null,"abstract":"<p><p>Progressive degeneration of dopamine neurons in the substantia nigra is the primary pathological abnormality in Parkinson's disease (PD). It has been demonstrated that overactivation of glutamatergic neurons leads to excessive accumulation of intracellular calcium and impairs autophagy. To assess the neuroprotective effects of ifenprodil, rats with 6-hydroxydopamine (6-OHDA)-induced injuries were administered ifenprodil either intraperitoneally (I.P.) or directly into the caudate-putamen (CPU) and substantia nigra pars reticulata (SNr). The results indicate that ifenprodil increases motor function in 6-OHDA-lesioned rats. Furthermore, ifenprodil enhances tyrosine hydroxylase (TH) neuron expression and promotes neuronal autophagy by upregulating beclin-1 and LC3-2 while downregulating P62 and PARP expression. Additionally, ifenprodil may enhance synaptic plasticity by downregulating NR2B-CaMKII and PSD95 expression. A notable improvement was observed in the CPU group. Our study showed that direct delivery of ifenprodil to specific brain regions produced superior therapeutic effects compared to systemic administration in 6-OHDA-lesioned rat models.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"150-159"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship of early-onset sepsis and neonatal encephalopathy: early-onset sepsis can increase short-term adverse outcomes of neonatal encephalopathy.","authors":"Li Yang, Shirui Zhu, Mei Xue, Jianping Zhang, Ling Li, Beibei Wang, Jun Zhang","doi":"10.5114/fn.2026.159243","DOIUrl":"10.5114/fn.2026.159243","url":null,"abstract":"<p><strong>Introduction: </strong>It has been reported that neonatal encephalopathy (NE) with early-onset sepsis (EOS) may have worse outcomes in comparison to non-septic NE. The aim of this study was to evaluate the association of EOS and short-term adverse outcomes of NE.</p><p><strong>Material and methods: </strong>This retrospective observational study evaluated the short-term outcomes of NE patients with and without EOS at the The Affiliated Hospital of Yangzhou University Medical College Hospital between July 2021 and July 2024. Eighty-seven patients with mild NE were included in the study, 21 of whom also had EOS (EOSNE group) and 66 of whom did not have EOS (NE group), and these two groups were used to compare the short-term outcomes.</p><p><strong>Results: </strong>Abnormal neurological examinations were found in 42.9% of the EOSNE group vs. 19.7% of the NE group, which was significantly higher in the EOSNE group (p = 0.03). The seizure rate until discharge day in the EOSNE group was 38.1% vs. 15.2% in the NE group, which was significantly higher in the EOSNE group (p = 0.02). Abnormal electroencephalogram (EEG) findings were observed in 47.6% of the EOSNE group vs. 15.2% of the NE group (p = 0.004). Also, 47.6% of the EOSNE group vs. 15.2% in the NE group used antiplatelet medications until discharge day, which was significantly higher in the EOSNE group (p = 0.004). The proportion of patients receiving blood products was significantly higher in the EOSNE group (57.1% vs. 15.2% p = 0.001).</p><p><strong>Conclusions: </strong>The rate of hospitalization in EOSNE patients was higher than in NE patients. Abnormal neurological examinations, abnormal EEG, seizures, receipt of blood products, and use of antiepileptic drugs were more common in these patients.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"173-177"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREM2/DAP12 complex promotes proliferation and invasion of glioma cells via the PI3K-AKT signaling pathway.","authors":"Zhitong Deng, Xingming Zhong, Yong Cai, Jianguo Yang, Yiqi Wang, Zhenhai Fei, Hua Gu, Tao Yang, Zhaohui Zhao","doi":"10.5114/fn.2025.156003","DOIUrl":"10.5114/fn.2025.156003","url":null,"abstract":"<p><strong>Introduction: </strong>Triggering receptor expressed on myeloid cells 2 (TREM2), part of the immunoglobulin superfamily, is implicated in various malignancies. However, its role in glioma formation remains unclear. Our study uncovered a potential mechanism involving TREM2.</p><p><strong>Material and methods: </strong>The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) datasets were utilized to assess the expression levels of TREM2 and DNAX-activating protein of 12 kDa (DAP12), explore their relationship, and evaluate their impact on patient prognosis. Western blotting was used to measure TREM2 expression in different glioma grades. Co-immunoprecipitation (Co-IP) was used to examine TREM2 and DAP12 interaction. Cell proliferation, invasion, and apoptosis were assessed via the cell proliferation test, cell invasion assay, and flow cytometry. An intracranial xenograft model was created by injecting tumor cells into nude mice. Mice injected with si-DAP12-transfected or non-transfected glioma cells were treated with 740Y-P, followed by survival analysis and immunohistochemistry.</p><p><strong>Results: </strong>TREM2 and DAP12 were overexpressed in gliomas, with high levels associated with lower overall survival (p < 0.05 and p < 0.01). There was a strong positive correlation between TREM2 and DAP12 expression (p < 0.0001). TREM2 positively regulated DAP12, forming a complex that influenced glioma cell proliferation, apoptosis, and invasion (p < 0.05, p < 0.01, and p < 0.001). DAP12 knockdown significantly inhibited proliferation and invasion while promoting apoptosis of glioma cells, linked to the PI3K/AKT signaling pathway (p < 0.05 and p < 0.01). 740Y-P treatment counteracted the effects of DAP12 knockdown (p < 0.05, p < 0.01, p < 0.001, and p < 0.0001). In vivo, DAP12 knockdown inhibited glioma tumorigenicity (p < 0.001).</p><p><strong>Conclusions: </strong>TREM2 positively regulates DAP12 and forms a complex that impacts glioma development via the PI3K/AKT pathway. Targeting the TREM2/DAP12 complex presents a potential therapeutic approach for gliomas.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":" ","pages":"31-49"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic effect and mechanism of bone marrow mesenchymal stem cell-derived exosomes on traumatic brain injury through the ERK signaling pathway.","authors":"Yun Zhang, Qingli Wang, Yunlong Wang, Fengquan Gao, Weidong Wu, Qingyu Meng","doi":"10.5114/fn.2026.158520","DOIUrl":"https://doi.org/10.5114/fn.2026.158520","url":null,"abstract":"<p><strong>Introduction: </strong>The aim of this study was to investigate the effect and possible mechanism of bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exo) on traumatic brain injury (TBI) in order to provide new strategies for clinical treatment of TBI.</p><p><strong>Material and methods: </strong>Thirty-two healthy male rats were randomly divided into the control group, model group, model control group, and mesenchymal stem cell (MSC) exosome group, with 8 rats in each group. TBI model rats were established using Feeney's free-falling method. Bone marrow mesenchymal stem cells were isolated and cultured, their exosomes were extracted, and MSC exosomes were injected into the bilateral medial hippocampus of rats in the model control group and MSC exosome group. A Morris water maze was used to detect behavioral indicators in each group; hematoxylin-eosin (HE) staining was used to observe the morphological changes of rat hippocampal neurons; an immunohistochemical method was used to detect the expression of the protein Erk/P-Erk in the Erk signaling pathway of rat hippocampal cells; RT-PCR and Western blot were used to detect the mRNA and protein expression levels of b-catenin and cyclin D1.</p><p><strong>Results: </strong>Compared with the model control group, the MSC exosome group showed a reduced escape latency, as well as an increased number of platform crossings and longer time spent in the platform quadrant. Compared with the model group and the model control group, the lateral compartments of brain tissue in rats in the MSC exosome group did not widen significantly. The arrangement gradually became orderly and compact, with some local areas of looseness remaining, but overall structural improvement was observed. The Erk/P-Erk, and b-catenin levels in the MSC exosome group increased, and the cyclin D1 level decreased.</p><p><strong>Conclusions: </strong>BMSC-Exo have a significant therapeutic effect on TBI by upregulating the expression of proteins related to the ERK signaling pathway and regulating neuron-related proteins and cell proliferation, which provides a potential new strategy for the treatment of TBI.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"178-185"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radial extracorporeal shock wave therapy in patients with spasticity after stroke based on randomized clinical trials: a systematic review and meta-analysis, and trial sequential analysis.","authors":"Yi Liu, Ran Ma, Jing Mao, Na Liu","doi":"10.5114/fn.2026.161801","DOIUrl":"10.5114/fn.2026.161801","url":null,"abstract":"<p><strong>Introduction: </strong>Extracorporeal shock wave therapy (ESWT) was first used to treat kidney stones with lithotripsy. The present meta-analysis aims to evaluate radial ESWT (rESWT) in patients with spasticity after stroke in randomized controlled trials (RCTs) comparing the timing of Modified Ashworth Scale (MAS) measurement as a primary outcome in these patients.</p><p><strong>Material and methods: </strong>A comprehensive literature search was conducted across multiple databases, such as PubMed/Medline, Web of Science, Scopus, and Cochrane Library, until January 16, 2024, without any limitations to find relevant RCTs. The Review Manager 5.3 software was used to compute the effect sizes, which were expressed as the standardized mean difference (SMD) along with a 95% confidence interval (CI). A total of 25 RCT articles were included in the meta-analysis. The estimate of effect size showed statistically significant MAS grade reduction immediately after treatment, 1 week after, 2 weeks after, 3 weeks after, 4 weeks after, 6 weeks after, 8 weeks after, and 12 weeks after.</p><p><strong>Results: </strong>Twenty-five RCTs were entered into the meta-analysis. The pooled SMDs of MAS score for spasticity in post-stroke patients before compared to after rESWT were as follows: 1.82 (95% CI: 1.32, 2.32, p < 0.00001) immediately after, 1.25 (95% CI: 0.85, 1.66, p < 0.00001) one week after, 2.30 (95% CI: 1.07, 3.53, p = 0.0002) after two weeks, 1.19 (95% CI: 0.88, 1.49, p < 0.00001) after four weeks, 1.21 (95% CI: 0.88, 1.54, p < 0.00001) after eight weeks, and 1.83 (95% CI: 1.94, 2.73, p < 0.0001) twelve weeks after rESWT.</p><p><strong>Conclusions: </strong>The research revealed that rESWT was associated with a notable decrease in the MAS score in patients who had suffered a stroke at all observed time points. Both upper and lower limbs showed significant improvement, especially in the upper limb. All ethnic groups, particularly Arabs, showed significant improvement in MAS scores after treatment.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"113-124"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Region-specific tau phosphorylation and microtubule pathology following α-synuclein exposure in the mouse brain: biochemical and ultrastructural evidence.","authors":"Magdalena Gąssowska-Dobrowolska, Gabriela Olech-Kochańczyk, Magdalena Gewartowska, Lidia Babiec, Ewelina Bielska, Grzegorz Czapski, Anna Wilkaniec, Elżbieta Gawinek, Agata Adamczyk","doi":"10.5114/fn.2026.163699","DOIUrl":"https://doi.org/10.5114/fn.2026.163699","url":null,"abstract":"<p><p>Accumulating evidence indicates that pathological interactions between  -synuclein (ASN) and tau contribute to the progression of  -synucleinopathies; however, the mechanisms linking ASN exposure to tau dysregulation and neuronal cytoskeletal pathology remain incompletely understood. In the present study, we investigated whether bilateral intrastriatal injection of ASN oligomers induces alterations in tau phosphorylation associated with microtubule (MT) abnormalities in the mouse brain. Western blot analyses were performed in the striatum, midbrain, and cortex at 180 days post-injection to assess tau phosphorylation at disease-associated epitopes (Ser199/202, Ser404, and Ser416) together with  /  -tubulin levels. Ultrastructural changes in neuronal cytoskeletal organisation were evaluated qualitatively using transmission electron microscopy (TEM). ASN exposure induced selective, bidirectional, site- and region-specific changes in tau phosphorylation rather than uniform hyperphosphorylation. Increased p-tau(Ser199/202) levels were observed in the striatum and cortex, whereas p-tau(Ser404) was elevated in the midbrain but decreased in the cortex. No significant changes in p-tau(Ser416) or  /  -tubulin levels were detected in any analysed brain region. TEM analyses further revealed disrupted neuronal MT organisation, characterised by fragmented and loosely packed MT networks, reduced MT abundance, and occasional loss of cytoskeletal elements accompanied by axonal or synaptic swelling, despite preserved total  /  -tubulin levels. Collectively, our findings indicate that ASN oligomers induce selective, region-specific dysregulation of tau phosphorylation that co-occurs with neuronal MT disorganisation and cytoskeletal abnormalities. Together, these findings support a link between ASN-induced, site- and region-specific tau dysregulation and neuronal cytoskeletal pathology in  -synucleinopathies.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"125-141"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Feasibility of blood count-derived inflammatory ratios in predicting haemorrhagic transformation and early functional outcomes after intravenous thrombolysis for ischaemic stroke.","authors":"Jakub Radziwon, Kamil Andruszkiewicz, Małgorzata Lewalska, Sandra Malinowska, Dariusz Gąsecki, Mariusz Kwarciany","doi":"10.5114/fn.2026.160015","DOIUrl":"https://doi.org/10.5114/fn.2026.160015","url":null,"abstract":"<p><strong>Introduction: </strong>Accurately stratifying the risk of poor outcomes after acute ischaemic stroke remains a critical challenge. Complete blood count (CBC)-derived indices, such as the neutrophil-to-lymphocyte ratio (NLR), have been proposed as prognostic markers. However, their performance compared to other recently proposed CBC-based parameters, including the derived neutrophil-to-lymphocyte ratio (dNLR) and neutrophil-to-lymphocyte-and-platelet ratio (NLPR), remains unclear.</p><p><strong>Material and methods: </strong>A retrospective analysis of records from 202 patients with acute ischaemic stroke treated with intravenous thrombolysis (IVT) was performed. NLR, dNLR, NLPR and six other novel inflammatory indices - lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), mean platelet volume to platelet count ratio (MPR), systemic inflammatory index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI) - were calculated from the CBC acquired upon admission and one day after IVT. Differences in laboratory parameters and ratios between groups of diverse outcomes were tested, and diagnostic performance between ratios was compared using multivariate logistic regression models.</p><p><strong>Results: </strong>Three inflammatory ratios (NLR, dNLR, NLPR) measured the day after IVT were found to be independent risk factors for a poor functional outcome at discharge. The upper quartile of NLR and dNLR alone presented similar performance (OR = 4.04, 95% CI: 2.06-7.92, p < 0.001; sensitivity 40%, specificity 86%, AUC = 0.63). However, dNLR showed higher discrimination value in the combined model with pre-mRS and NIHSS (OR = 5.50, 95% CI: 2.02-14.93, p < 0.001; sensitivity 81%, specificity 93%, AUC = 0.929). This parameter, along with glucose levels, was also associated with the risk of early intracranial bleeding (OR = 4.74, 95% CI: 1.24-18.21, p = 0.023).</p><p><strong>Conclusions: </strong>In this exploratory study, dNLR measured on the day after IVT was superior to NLR and other parameters in prognosis of unfavourable outcomes and recognition of intracranial haemorrhage. Nevertheless, clinical data such as pre-mRS and NIHSS combined remain the most important predictors.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 2","pages":"198-204"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of apocynin in alleviation of oxidative stress and neuronal autophagy after traumatic brain injury by activating the PI3K/Akt/Nrf2 pathway in rats.","authors":"Yan Feng, Yaru Ju, Ming Yang, Qiang Wu, Guozhu Sun, Zhongjie Yan, Jingchen Li","doi":"10.5114/fn.2026.159127","DOIUrl":"10.5114/fn.2026.159127","url":null,"abstract":"<p><strong>Introduction: </strong>The study aimed to determine whether apocynin (APO) can protect neurons in rats with traumatic brain injury (TBI) by activating the PI3K/Akt/Nrf2 pathway, acting as an antioxidant, and suppressing autophagy.</p><p><strong>Material and methods: </strong>Ninety male Sprague-Dawley rats (220-260 g) were randomly assigned to three groups: a control group with a sham operation, a group with TBI, and a group that received APO following TBI. Saline and APO were intraperitoneally administered for three consecutive days based on the aforementioned groups. Ten rats from each group underwent behavioral assessment, and neuronal morphology was evaluated using HE staining. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) were measured using the xanthine oxidase method, barbiturate sulfate method, and dithiobenzoic acid condensation method, respectively. Rat hippocampal tissue was extracted, and Western blotting was performed to assess the expression of autophagy-related proteins as well as signaling pathway-related proteins.</p><p><strong>Results: </strong>Compared to the TBI group, those treated with APO showed reduced cognitive deficits and neural damage resulting from TBI. The degree of neuronal damage in the treatment group was statistically significantly reduced. Treatment with APO in rats with TBI significantly elevated the hippocampal levels of GSH and SOD and significantly reduced the production of MDA and reactive oxygen species (ROS). Additionally, APO alleviated hippocampal neuronal autophagy by reducing LC3II and Beclin-1 expression levels. Regarding of the signaling pathway, APO elevated the expression of p-PI3K, p-Akt, Nrf2, and HO-1 in the hippocampus of TBI rats.</p><p><strong>Conclusions: </strong>In conclusion, APO represents a potential treatment for TBI due to its antioxidative and autophagy-reducing properties via the PI3K/Akt/Nrf2 pathway, thereby preventing hippocampal injury after brain trauma.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 1","pages":"50-62"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of synaptic plasticity in Alzheimer's disease: from molecular mechanisms to therapeutic targets.","authors":"Yunyun Li, Sichong Li, Jing Ma, Jing Zhao, Ning Ning, Jianfang Sun","doi":"10.5114/fn.2025.156508","DOIUrl":"10.5114/fn.2025.156508","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is characterized by a complex pathophysiology, involving abnormal aggregation of amyloid b (Ab) and tau proteins, neuroinflammatory responses, and significant synaptic dysfunction, which collectively contribute to cognitive decline. This review offers a novel perspective by focusing on the pivotal role of synaptic plasticity in the pathogenesis of AD, underscoring its potential as a therapeutic target. The study uniquely synthesizes current molecular and clinical research to illustrate how Ab and tau pathologies disrupt synaptic signaling and structure, further exacerbated by neuroinflammation. We explore both pharmacological interventions, such as BACE1 inhibitors and tau stabilizers, and non-pharmacological strategies, including cognitive therapy and neuromodulation techniques, which have shown promise in modulating synaptic plasticity and slowing cognitive deterioration. Despite these advancements, the field faces significant challenges, including the complexity of AD's underlying mechanisms and limitations in early diagnosis. This review not only highlights the significance of synaptic plasticity in AD but also proposes future research directions that could lead to innovative therapeutic approaches, offering new hope for effective treatment strategies.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 1","pages":"1-11"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP22 overexpression mitigates spinal cord injury via NLRP3 pathway modulation.","authors":"Ming-Chen Yu, Xiao-Lin Li, Shuai-Jin Lu, Ming-Liang Ning, Zhenzhong Yan, Yadong Yang","doi":"10.5114/fn.2025.156809","DOIUrl":"10.5114/fn.2025.156809","url":null,"abstract":"<p><strong>Introduction: </strong>The purpose of this study was to explore the effect of ubiquitin-specific protease (USP) 22 overexpression on spinal cord injury (SCI) in rats and its potential mechanism, to assess its role in the recovery of neurological function.</p><p><strong>Material and methods: </strong>A rat model of SCI was established. The rats were divided into four groups: the Sham group, the SCI group, the SCI + USP22Ad-USP22 group, and the SCI + vector group. The Basso Mouse Scale for locomotion was used for motor function scores. Real-time quantitative polymerase chain reaction and western blot were applied to detect the expression levels of USP22, inducible nitric oxide synthase, cluster of differentiation (CD) 86, arginase 1, and CD206. Additionally, the expression of inflammatory markers and microglial activation were assessed using immunofluorescence and enzyme-linked immunosorbent assay. Furthermore, western blot was employed to measure the expression levels of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome pathway-related proteins.</p><p><strong>Results: </strong>USP22 overexpression significantly improved the motor function of SCI rats, reduced the levels of microglial activation, and inhibited the activation of the nuclear factor-kB pathway. Additionally, USP22 overexpression not only reduced the expression levels of pro-inflammatory mediators (inducible nitric oxide synthase, CD86, tumor necrosis factor a, interleukin (IL)-1b, and IL-6) but also increased the expression levels of anti-inflammatory markers (arginase 1 and CD206). Furthermore, USP22 overexpression inhibited the expression of NLRP3 inflammasome-related proteins, alleviated neuro- inflammatory responses and promoted neurological function recovery.</p><p><strong>Conclusions: </strong>USP22 overexpression can improve neuroinflammation and motor function in SCI model rats, which may be related to the inhibition of NLRP3 inflammasome pathway activation.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"64 1","pages":"12-22"},"PeriodicalIF":1.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}