Journal of Neuropathology and Experimental Neurology最新文献_第9页

GSK126 mitigates oxidative stress in Alzheimer disease models via an enhancer of Zeste homolog 2-H3 lysine 27 trimethylation-superoxide dismutase 1 axis. GSK126通过Zeste同源物2-H3赖氨酸27三甲基化-超氧化物歧化酶1轴增强子减轻阿尔茨海默病模型中的氧化应激。

IF 3.3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-05-01 DOI: 10.1093/jnen/nlag008

Yonghui Zhong, Lanying Wei, Rongliang Xue

{"title":"GSK126 mitigates oxidative stress in Alzheimer disease models via an enhancer of Zeste homolog 2-H3 lysine 27 trimethylation-superoxide dismutase 1 axis.","authors":"Yonghui Zhong, Lanying Wei, Rongliang Xue","doi":"10.1093/jnen/nlag008","DOIUrl":"10.1093/jnen/nlag008","url":null,"abstract":"Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and neuronal loss and with limited effective therapies. Oxidative stress, driven by disrupted redox balance and excessive reactive oxygen species (ROS), is believed to be a key pathogenic driver. This study aimed to explore the role and mechanism of the selective enhancer of Zeste homolog 2 (EZH2) methyltransferase inhibitor GSK126 in alleviating AD-related OS in AD models. Using Aβ1-42-induced AD model rats, we conducted Morris water maze tests, histologic and immunohistochemical staining, CCK-8/Annexin V-PI assays, Western blot, quantitative Reverse Transcription PCR (qRT-PCR), and Chromatin Immunoprecipitation quantitative Real-Time PCR (ChIP-qPCR). GSK126 shortened escape latency, reduced hippocampal pathology/apoptosis, upregulated Superoxide dismutase 1 (SOD1), and lowered ROS/malondialdehyde/protein carbonyls, thereby increasing antioxidant capacity in the AD model rats. In okadaic acid-treated SH-SY5Y cells, GSK126 enhanced viability, reduced apoptosis by downregulating Bax/c-Cas3 and upregulating Bcl-2 and upregulated SOD1 by inhibiting EZH2-mediated H3 lysine 27 trimethylation (H3K27me3) enrichment at the SOD1 promoter. SOD1 overexpression antagonized EZH2-induced damage. These results suggest that GSK126 could alleviate AD-related pathologic alterations in these models via the EZH2-H3K27me3-SOD1 axis, thereby suggesting a potential therapeutic target for AD.","PeriodicalId":16682,"journal":{"name":"Journal of Neuropathology and Experimental Neurology","volume":" ","pages":"464-474"},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Occult prostatic adenocarcinoma metastasis to the sphenoid sinus: A case report and literature review. 隐匿性前列腺腺癌向蝶窦转移1例并文献复习。

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-05-01 DOI: 10.1093/jnen/nlaf113

Thomas Auen, Michael Punsoni

引用次数: 0

A case series of calcium pyrophosphate deposition in the spine: An underrecognized debilitating disease. 脊柱焦磷酸钙沉积系列病例：一种未被充分认识的衰弱性疾病。

IF 3.3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-05-01 DOI: 10.1093/jnen/nlaf151

Serica J Hallstead, Jennifer M Dailey, Michael Punsoni

{"title":"A case series of calcium pyrophosphate deposition in the spine: An underrecognized debilitating disease.","authors":"Serica J Hallstead, Jennifer M Dailey, Michael Punsoni","doi":"10.1093/jnen/nlaf151","DOIUrl":"10.1093/jnen/nlaf151","url":null,"abstract":"Calcium pyrophosphate deposition (CPPD) disease is an inflammatory arthritis prevalent in elderly individuals. Spinal CPPD is uncommon, and presentation can vary widely with common clinical and radiographic mimics. We identified 9 cases of lumbar and 1 case of thoracic spinal CPPD (age range: 63-85 years; 5 male, 5 female) at our institution over a 10-year period. All presented with pain (90% chronic, 10% acute); 4 had prior instrumentation and 1 had prior trauma. CPPD was not clinically suspected in any case. Preoperative imaging diagnoses include central canal stenosis, neuroforaminal narrowing, septic arthropathy, synovial cyst, degeneration, and epidural mass/abscess. Intraoperatively, a spinal cyst was most often described. All pathologic examinations revealed purple granular calcified material with positively birefringent rhomboid crystals embedded within fibrocartilage. Following a neuropathologic diagnosis, only 2 patients received CPPD treatment. This study aims to highlight that spinal CPPD is underdiagnosed and undertreated. Although clinical presentations are variable, wider recognition of this rare disease among neuropathologists receiving spinal specimens may provide earlier diagnosis. Accurate pathologic diagnosis can improve identification, refine clinical suspicion, and facilitate management. Improved identification, particularly in elderly patients and those with prior trauma/instrumentation, will promote appropriate therapy and management.","PeriodicalId":16682,"journal":{"name":"Journal of Neuropathology and Experimental Neurology","volume":" ","pages":"446-454"},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13127886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Methyltransferase-like protein 16 suppresses spinal cord injury by regulating microglia polarization via N6-methyladenosine-modified downregulation of MCEMP1. 甲基转移酶样蛋白16通过n6 -甲基腺苷修饰的MCEMP1下调来调节小胶质细胞极化，从而抑制脊髓损伤。

IF 3.3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-05-01 DOI: 10.1093/jnen/nlaf164

Lei Zhang, Haijun Chang, Guangming Jiang, Chao Zhu, Shan Zhou, Yanling Wang, Hui Chang

{"title":"Methyltransferase-like protein 16 suppresses spinal cord injury by regulating microglia polarization via N6-methyladenosine-modified downregulation of MCEMP1.","authors":"Lei Zhang, Haijun Chang, Guangming Jiang, Chao Zhu, Shan Zhou, Yanling Wang, Hui Chang","doi":"10.1093/jnen/nlaf164","DOIUrl":"10.1093/jnen/nlaf164","url":null,"abstract":"N6-methyladenosine (m6A) modification is a prevalent epigenetic mechanism influencing spinal cord injury (SCI) progression. Methyltransferase-like protein 16 (METTL16) plays crucial roles in various diseases. However, its specific function and mechanism in SCI remain undefined. After establishment of an SCI model mice, pathological alterations in spinal cord tissue were assessed using hematoxylin and eosin, Nissl, and TUNEL staining. Datasets from Gene Expression Omnibus were acquired to identify METTL16-regulated core target genes, MCEMP1, associated with SCI. Methylation sites in MCEMP1 were predicted using the SRAMP database, and METTL16 m6A modification of MCEMP1 by METTL16 was validated utilizing methylated RNA immunoprecipitation and RNA pull-down. mRNA levels of METTL16 and MCEMP1 were quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Western blot was used to assess protein expression of METTL16, MCEMP1, polarization markers, and apoptosis proteins. Inflammatory cytokine secretion was measured via enzyme-linked immunosorbent assay (ELISA). Neuronal apoptosis in mouse BV2-hippocampal neuron cocultures was evaluated using flow cytometry. The results showed that METTL16 was downregulated in SC tissue following SCI. MCEMP1 suppression resulted from METTL16-mediated m6A methylation modification of MCEMP1. METTL16 promoted M2 polarization of microglia in vitro and inhibited neuronal apoptosis by repressing MCEMP1 expression, thereby mitigating SCI.","PeriodicalId":16682,"journal":{"name":"Journal of Neuropathology and Experimental Neurology","volume":" ","pages":"487-495"},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transthyretin immunohistochemistry on muscle and nerve biopsies detects hereditary and wild-type transthyretin amyloidosis with high sensitivity and specificity. 肌肉和神经活检的甲状腺素免疫组化检测遗传性和野生型甲状腺素淀粉样变性具有高敏感性和特异性。

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-05-01 DOI: 10.1093/jnen/nlaf111

Mohamed Elnagdy, Chunyu Cai

引用次数: 0

Chronic traumatic encephalopathy neuropathologic change is associated with highest stage limbic-predominant age-related TDP-43 encephalopathy. 慢性创伤性脑病神经病理改变与最高阶段边缘显性年龄相关性TDP-43脑病相关。

IF 3.3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-04-27 DOI: 10.1093/jnen/nlag040

Hailong Song, Kamar E Ameen-Ali, Claire Kennedy-Dietrich, Jean-Pierre Dolle, Edward B Lee, Douglas H Smith, William Stewart

{"title":"Chronic traumatic encephalopathy neuropathologic change is associated with highest stage limbic-predominant age-related TDP-43 encephalopathy.","authors":"Hailong Song, Kamar E Ameen-Ali, Claire Kennedy-Dietrich, Jean-Pierre Dolle, Edward B Lee, Douglas H Smith, William Stewart","doi":"10.1093/jnen/nlag040","DOIUrl":"10.1093/jnen/nlag040","url":null,"abstract":"Traumatic brain injury (TBI) is recognized as a major risk factor for neurodegenerative disease (NDD). Autopsy studies frequently describe chronic traumatic encephalopathy neuropathologic change (CTE-NC) in individuals with histories of repetitive head impact (RHI) exposure, often with accompanying comorbid neurodegenerative proteinopathies. Of these, deposition of abnormally phosphorylated TDP-43 (pTDP-43) has been reported but the prevalence and distribution of pTDP-43 in CTE-NC and its distinction from that encountered in wider NDD are uncertain. Here, patients with a history of RHI and documented NDD (n = 30), and age-matched controls with no known TBI or RHI exposure, either with (n = 24) or without (n = 18) NDD, were identified within the CONNECT-TBI archive. Standardized brain tissue sections stained for pTDP-43 were assessed. pTDP-43 pathology prevalence was similar among RHI patients (40%) and controls with NDD (33%). pTDP-43 was typically localized (limbic-predominant age-related TDP-43 encephalopathy neuropathologic change [LATE-NC] stage 1 to 2) in amygdala and hippocampus in controls with NDD and following RHI exposure without CTE-NC. In contrast, this pathology was often widespread and of high stage (LATE-NC stage 3; P = .0045) in patients with CTE-NC. Thus, CTE-NC may be associated with more widespread pTDP-43 pathology than encountered in aging or those with NDD and no history of TBI/RHI.","PeriodicalId":16682,"journal":{"name":"Journal of Neuropathology and Experimental Neurology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Localization of mast cells in human brain tissue: Implications for neuropsychiatric symptoms in COVID-19. 肥大细胞在人脑组织中的定位：对COVID-19神经精神症状的影响

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-04-17 DOI: 10.1093/jnen/nlag036

Jennifer Nicoloro-SantaBarbara, Matthew P Giannetti, Isaac H Solomon, Matthew J Hamilton, Peter Novak, Arthi Ramkumar, Mariana Castells, Jason L Hornick

引用次数: 0

Sudden death from a clinically silent right insular infarct in a patient with prior left insular astrocytoma. 左岛星形细胞瘤患者临床无症状右岛梗死猝死1例。

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-04-17 DOI: 10.1093/jnen/nlag034

Beau Idler, Meagan Chambers

引用次数: 0

A pediatric case of YAP1::MAML2 fusion-positive supratentorial ependymoma: A potential subtype of YAP1-fused ependymoma. 1例YAP1::MAML2融合阳性的幕上室管膜瘤：YAP1融合室管膜瘤的潜在亚型。

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-04-17 DOI: 10.1093/jnen/nlag042

Kento Kawata, Ryuma Tanaka, Kohei Fukuoka, Yohei Masugi, Kenta Masui, Ryosuke Hayashi, Koichi Ichimura, Takako Yoshioka, Junko Hirato, Arnault Tauziède-Espariat, Jumpei Ito, Tomoru Miwa

引用次数: 0

Correction to: Mapping the expression of endothelial adhesion receptors for Plasmodium falciparum-infected erythrocytes in fatal cerebral malaria in Malawian children. 更正：绘制恶性疟原虫感染的红细胞在马拉维儿童致死性脑疟疾中的内皮粘附受体的表达。

IF 3 3区医学

Journal of Neuropathology and Experimental Neurology Pub Date : 2026-04-01 DOI: 10.1093/jnen/nlag003

引用次数: 0