JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY神经病理学与实验神经病学杂志
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY(英文缩写 J NEUROPATH EXP NEUR),ISSN 0022-3069,eISSN 1554-6578,中文译名:神经病理学与实验神经病学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.148 | Q3 |
| 2022 | 3.200 | Q2 |
| 2023 | 3.200 | Q2 |
| 2024 | 3.000 | Q2 |
| 2025 | 3.300 | Q2 |
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY 最新收录文献
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2. Mitochondrial alterations in pellagra-associated central chromatolysis: Comparison with ballooned achromatic neurons of other etiologies.
PMID:日期:2026-10-01Neuronal central chromatolysis (CC) is the histopathological hallmark of pellagra encephalopathy, a neurological deficit resulting from vitamin deficiencies. Pellagrous CC neurons are morphologically similar to ballooned achromatic neurons in other conditions but the distinct pathomechanisms remain unclear. We performed a clinico-neuropathological analysis of 10 autopsy cases of pellagra encephalopathy. The pellagra encephalopathy cases were immunohistochemically compared with disease controls, including cases of axonal injury and neurodegenerative diseases. Electron microscopic evaluation and immunohistochemical examinations targeting mitochondrial fragmentation were performed for a representative case. Four of 10 pellagra encephalopathy patients exhibited prolonged impairment of consciousness distinguishable from alcohol withdrawal delirium. Pellagrous CC neurons were negative for cytoskeletal markers whereas ballooned achromatic neurons in the disease control cases were positive. Immunohistochemical analysis of mitochondrial markers revealed that CC neurons exhibited more intense immunoreactivity for COX-IV and mitochondrial fissure factor compared to the disease controls. Transmission electron microscopy of these CC neurons revealed a marked increase in the mitochondria with amorphous densities. These findings indicate that the pathomechanism of pellagrous CC is distinct from that of the ballooned achromatic neurons of other etiologies. Mitochondrial alterations in pellagrous CC neurons suggest that neuronal energy deficits resulting from nicotinamide adenine dinucleotide deficiency induce mitochondrial fragmentation.
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3. Keratan sulfate proteoglycan is not expressed in human fetal cerebellar system except pontine nuclei and transitory vermal septa or in fasciculi caudal to the internal capsule.
PMID:日期:2026-10-01We determined spatial/temporal expression of keratan sulfate proteoglycan (KS) in the developing cerebellar system, fasciculi, and dysgeneses. KS is an extracellular molecule secreted by astrocytes that forms a template for neuroblastic migration and axonal fascicles and creates perineural nets. We studied KS immunoreactivity in cerebellar cortex, deep cerebellar, inferior olivary, red and pontine nuclei, and white matter of 25 control human fetuses 12-41 weeks gestation and 16 cerebellar dysgeneses. Dentate, inferior olivary, and red nuclei were nonreactive at all ages. Pontine nuclei were positive from the early second trimester. Bergmann glia and cerebellar white matter pathways were nonreactive throughout fetal and postnatal life. Transitory KS septa demarcated the vermal/hemispheric boundary. KS was not expressed in Dandy-Walker or Chiari malformations, cerebellar hypoplasia, heterotopia, pontocerebellar hypoplasia, or rhombencephalosynapsis. Axonal fascicles caudal to the internal capsule did not exhibit KS. The absence of hindbrain KS contrasts with strong forebrain immunoreactivity. Lack of KS expression in typically developing cerebellum and associated brainstem nuclei (except pontine), or in dysgeneses, implies that KS does not contribute to cerebellar system malformation pathogenesis. Transitory KS septa define early vermal margins similar to neuromeric segmentation septa. The intense KS template of the internal capsule does not extend caudally into brainstem fascicles.
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4. Somatic PIK3CA and PTEN mutations with endothelial PI3K/AKT/mTOR activation in RAS-negative brain arteriovenous malformations.
PMID:日期:2026-10-01Somatic mutations affecting endothelial signaling pathways have emerged as important contributors to brain arteriovenous malformations (bAVMs). Although activating mutations in the RAS/MAPK pathway have been frequently reported, alternative molecular mechanisms remain incompletely understood. We describe 2 autopsy-confirmed bAVMs harboring somatic PIK3CA mutations, including one case with a concurrent PTEN alteration. Histologically, both lesions demonstrated typical bAVM architecture without unusual structural features. Immunohistochemical analysis revealed lesion-restricted activation of the PI3K/AKT/mTOR pathway in endothelial cells; adjacent normal vessels were negative. In contrast, ERK phosphorylation was focal and limited; targeted sequencing did not identify pathogenic RAS/MAPK mutations. These findings suggest dominant PI3K pathway activation with secondary or limited MAPK engagement. Variant allele frequencies were interpreted cautiously owing to whole-genome amplification from autopsy-derived tissue. In one case, prior Gamma Knife radiosurgery was considered to have contributed to the findings but histological features of radiation-associated vascular injury were not observed. Together, these findings support molecular heterogeneity in bAVMs and suggest that PIK3CA-driven PI3K pathway activation may contribute to vascular remodeling in RAS-negative lesions. Correlation of molecular alterations with pathway-specific endothelial activation highlights the value of integrated genetic and pathological assessment in bAVMs.
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5. Mechanism of TRIM32 regulation of synaptic protein expression in the development of epilepsy in a rat model.
PMID:日期:2026-10-01Accumulating evidence indicates that tripartite motif-containing protein 32 (TRIM32) has important functions in brain physiology and disease. This study investigated the role of TRIM32 in the development of epilepsy and its impact on synaptic remodeling. A rat model of epilepsy was established using pilocarpine with lithium chloride pretreatment and TRIM32 expression was examined by Western blotting and immunohistochemistry. The interaction between TRIM32 and BDNF was assessed by co-immunoprecipitation and immunofluorescence colocalization. TRIM32 knockdown in epileptic rats was achieved by shRNA transfection. Cognitive and anxiety-like behaviors were evaluated using the Y-maze and open-field tests; Western blotting was used to quantify the synaptic proteins PSD-95 and SYN and to assess activity of the BDNF/TrkB/CREB signaling pathway. TRIM32 expression was significantly reduced in epileptic rats. Moreover, TRIM32 knockdown aggravated epilepsy-associated cognitive deficits, impaired open-field performance, and exacerbated synaptic loss. Mechanistically, TRIM32 deficiency intensified these abnormalities through dysregulation of the BDNF/TrkB/CREB pathway. These data suggest that TRIM32 regulates synaptic protein expression in epilepsy and that its deficiency worsens anxiety-like behavior, cognitive impairment, and synaptic loss by perturbing BDNF/TrkB/CREB signaling, thereby providing insights that may inform future therapeutic strategies targeting this signaling pathway.
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6. Multiparameter flow cytometry of CSF identifies elevated CD8+ effector memory and TEMRA T-cells in immune-mediated neurologic disorders.
PMID:日期:2026-10-01Conventional CSF markers often fail to distinguish immune-mediated neurologic disorders (IMNDs) from non-immune-mediated neurologic disorders (N-IMNDs). We performed multiparametric flow cytometric profiling of CSF T-cell developmental subsets in 37 IMND patients and 10 N-IMND controls to identify IMND-associated T-cell signatures. CSF CD8+ T-cells were detectable in 86% (32/37) of IMND patients versus 0% (0/10) of N-IMND controls (Padj < .001). Among CD8+ T-cell-positive IMND cases, effector memory (CD45RA-CCR7-, median, 65.0%; IQR, 45.5%-73.5%) and terminally differentiated effector memory T-cells (TEMRA, CD45RA+CCR7-, median, 35.0%; IQR, 0%-49.5%) predominated. Hierarchical clustering demonstrated significant separation between IMND and N-IMND driven by CD8+ T-cell subset profiles (R2 = 0.165, P = .001), whereas CD4+ T-cell subsets showed no disease-associated clustering. Paired blood-CSF analysis in 6 treatment-naïve IMND patients revealed compartmentalized enrichment of CD8+ effector memory (blood median 19.2%; IQR, 6.4%-26.9%; CSF median 47.3%; IQR, 42.2%-53.7%; P = .031), confirming CNS-restricted CD8+ T-cell activation. These findings identify CSF CD8+ effector memory profiles as a potential biomarker distinguishing IMNDs from N-IMNDs that may complement conventional biomarkers for CNS autoimmunity.
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7. Comprehensive identification of FoxO signaling as a promising prognostic and immunotherapeutic biomarker in glioma.
PMID:日期:2026-10-01Convincing evidence suggests that FoxO signaling (FS) dysfunction is associated with cancer progression and tumorigenesis but its effect on the tumor microenvironment (TME) and immunotherapy response remains unclear. Here, we retrieved FS-related genes from the KEGG database, first analyzing their differential expression in 31 TCGA cancer types with matched Genotype-Tissue Expression (GTEx) normal tissue data. We then calculated FS scores via ssGSEA for 33 TCGA cancer types, systematically exploring their prognostic value and correlations with TME characteristics and immunotherapy response. High FS scores were consistently associated with an immunosuppressive TME and poorer OS across multiple tumor types. Analysis of the IMvigor210 immunotherapy cohort further revealed elevated FS scores correlated with anti-PD-1 treatment resistance. Focusing on gliomas, we identified FS-based molecular subtypes and constructed a PCA score that robustly predicted glioma prognosis and immune checkpoint inhibitor response. External validation was achieved in independent CGGA and GEO cohorts. Our findings indicate that FS is a key modulator of the immunosuppressive TME and support FS and PCA scores as potential prognostic and immunotherapeutic biomarkers for gliomas with their clinical utility pending experimental validation.
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8. Effects of phytocannabinoids, synthetic and semi-synthetic cannabinoids on microglia and astrocytes: Review of neuroinflammatory mechanisms.
PMID:日期:2026-10-01Over 120 phytocannabinoids and 190 synthetic and semi-synthetic cannabinoids have been identified. Many of these currently circulate in recreational and illicit drug markets. Epidemiological evidence indicates a progressive increase in their use but long-term effects of cannabinoids on the CNS remain poorly understood. Exogenous cannabinoids can interact with cannabinoid receptor CB2, which is expressed on astrocytes and microglia, the key regulators of neuroinflammatory responses. Dysregulated or chronic microglial activation can sustain neuroinflammation, a central mechanism underlying neurodegenerative diseases. Clarifying cannabinoid-induced alterations in glia is therefore crucial both because their widespread consumption and the global burden of neurodegenerative disorders, for which cannabinoids might offer therapeutic potential. This review was conducted by a multidisciplinary team following JBI and PRISMA-ScR guidelines that systematically mapped available evidence across PubMed, Scopus and Web of Science. The findings are thematically organized and qualitatively summarized and indicate compound and time-dependent effects. Acute exposure appears to be neuroprotective whereas chronic effects remain unclear. Preliminary data suggest that some synthetic and semi-synthetic cannabinoids may retain protective actions while Δ9-tetrahydrocannabinol (THC) may promote glial activation and neuroinflammation, These results underscore the need for further in vivo and longitudinal studies to evaluate long-term impacts and inform safe therapeutic and regulatory strategies.
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9. The NORAD-Pumilio regulatory axis in the evolution of inclusion body myositis.
PMID:日期:2026-10-01Sporadic inclusion body myopathy (sIBM) is the most common progressive degenerative skeletal muscle disease of older people with poorly understood pathogenesis. We assessed the involvement and impact of the noncoding RNA activated by DNA damage (NORAD) and its binding partner Pumilio (PUM) proteins on the evolution of the disease process in muscle biopsies from sIBM patients with mild or severe histopathologic changes. A disease severity-dependent increase in NORAD and PUM2 expression was present along with subsarcolemmal formations of NORAD-PUM (NP) bodies in the sIBM muscles. Similarly, Norad, Pum1, and Pum2 expression levels were upregulated as disease severity increased with age in VCP-A232E mice, a model for hereditary IBM. Crossbreeding VCP-A232E mice with Norad-/- mice leading to generation of VCP mutants with either single copy or the absence of Norad showed that Norad suppresses disease progression in the VCP-A232E model in a dose-dependent manner. Norad expression in the muscle from Pum2 overexpressing mice revealed significantly increased Norad transcripts in response to high Pum2 expression and the presence of NP bodies coalescing around muscle nuclei. Collectively, these findings provide strong evidence that elevated NORAD expression is a protective, compensatory response to disease-related induction of PUM2 activity in muscle.