Neuropathology and Applied Neurobiology最新文献

{"title":"Lewy Bodies Are Not Associated With Neuronal or Synaptic Loss in Dementia With Lewy Bodies.","authors":"Jade I Hawksworth, Eddie Kirkby-Geddes, Searlait Thom, Joe O'Neill, Amelia Ikwue, Lucy Wood, Tiago F Outeiro, Daniel Erskine","doi":"10.1111/nan.70085","DOIUrl":"10.1111/nan.70085","url":null,"abstract":"<p><strong>Aims: </strong>The misfolding and accumulation of the protein α-synuclein (αSyn) into cytoplasmic inclusions termed Lewy bodies (LBs) and Lewy neurites is the defining neuropathological feature of LB diseases, such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB). The loss of neurons and/or synapses has been postulated to underlie the clinical syndrome of DLB. The present study sought to elucidate the relationship between LB burden and neuronal and synaptic loss in DLB.</p><p><strong>Methods: </strong>Post-mortem brain tissue from the cingulate gyrus and inferior temporal gyrus, two regions vulnerable to LB pathology, was obtained from DLB (N = 20) and control cases (N = 20). Formalin-fixed paraffin-embedded tissue was stained to quantify LB, Alzheimer-type pathology and a neuronal marker. Frozen tissue from the contralateral hemisphere was processed for immunoblotting to compare the abundance of synaptic markers across cases.</p><p><strong>Results: </strong>Across both regions, no evidence of reduced total neuronal density was observed, but a modest reduction in parvalbumin interneurons was observed in the cingulate gyrus, and there were only modest reductions in some synaptic markers in DLB. LB burden was markedly variable across DLB cases but was not associated with any synaptic marker abundance or neuronal density.</p><p><strong>Conclusions: </strong>Taken together, these findings do not support an association between LB density and neuronal or synaptic loss in DLB, even in regions with particularly high burdens of LBs, such as the cingulate gyrus. These findings suggest that the link between αSyn proteinopathy and disease requires further investigation.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 3","pages":"e70085"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13253057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148218915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glioneuronal Tumour With Neurocytic Differentiation (GNTN): a Molecularly Defined Tumour Type Formerly Referred to as Extraventricular Neurocytoma.","authors":"Alice Métais, Myriam Edjlali, Farah Sassi, Guillaume Chotard, Emmanuelle Uro-Coste, Benoit Lhermitte, Romain Appay, Giuseppe Pinto, Christian Thomas, Luca Bertero, Miriam Ratliff, Sandro M Krieg, Andreas von Deimling, Felix Sahm, Pascale Varlet, Philipp Sievers","doi":"10.1111/nan.70080","DOIUrl":"10.1111/nan.70080","url":null,"abstract":"<p><p>Tumours historically classified as extraventricular neurocytoma (EVN), initially in comparison with central neurocytoma, are defined by location and morphology; however, emerging molecular data demonstrate that this term is outdated. We report 14 previously unpublished tumours with a robust EVN DNA methylation profile, independent of original histopathologic diagnosis or anatomic location. Integrated molecular analyses identified FGFR1 alterations, particularly FGFR1::TACC1 fusions, as the predominant molecular driver of this tumour class. A smaller number of tumours harboured FGFR1 hotspot mutations (p.N546K and p.K656E). Among these, two cases additionally showed NF1 variants, and one tumour carried a PIK3CA mutation (p.H1047L). In addition, a single case exhibited an NTRK2 fusion. Histologically, tumours exhibited neurocytic differentiation with neuropil islands and a minor glial component, while immunohistochemistry showed frequent OLIG2 expression, contrasting with the typical immunophenotype of central neurocytoma. Notably, tumours with an EVN DNA methylation profile were identified in both extraventricular and intraventricular locations, demonstrating that anatomy-based definitions are inadequate for this tumour type. Clinical follow-up (median 33.2 months) showed predominantly lower grade behaviour, with occasional recurrence. Collectively, these findings support the view that tumours previously labelled as EVN do not represent a direct counterpart of central neurocytoma but instead constitute a molecularly and epigenetically distinct glioneuronal tumour type. We propose the designation glioneuronal tumour with neurocytic differentiation (GNTN) to reflect its biological identity and to align the terminology with contemporary molecular neuropathology, and recommend DNA methylation profiling as an essential diagnostic criterion.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 3","pages":"e70080"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Regional Microglial Remodelling in the Hippocampus of the App^NL-G-F Alzheimer's Model.","authors":"Ryan J Bevan, Jessica F Minett, Alice L Smith, Ana Cardus Figueras, Philip R Taylor","doi":"10.1111/nan.70082","DOIUrl":"10.1111/nan.70082","url":null,"abstract":"<p><strong>Aims: </strong>Microglia undergo profound structural and functional changes during Alzheimer's disease, yet the earliest stages of morphological remodelling that occur prior to amyloid deposition remain poorly defined. We hypothesised that microglia in the hippocampus of App^NL-G-F mice would exhibit early, region-specific structural adaptations before local plaque formation, reflecting an initial phase of disease-associated structural remodelling.</p><p><strong>Methods: </strong>Two-month-old App^NL-G-F and wildtype mice were examined using high-resolution confocal microscopy of Iba1-labelled microglia in the dorsal CA1 apical field. Automated three-dimensional reconstructions were generated in Imaris, and quantitative morphometric analyses quantified cell density, Iba1 coverage, process topology and Sholl-based arbor complexity. Statistical analyses were performed using linear mixed-effects models incorporating sex as a fixed factor in all analyses.</p><p><strong>Results: </strong>Microglial density and total Iba1 coverage were unaffected in App^NL-G-F mice at this age. In contrast, Sholl analysis revealed significant genotype-dependent reductions in process intersections and total process length, accompanied by reduced individual-cell territorial coverage, indicating an early contraction of the surveillance arbor independent of cell number.</p><p><strong>Conclusions: </strong>These findings demonstrate that hippocampal microglia in App^NL-G-F mice undergo an early, coordinated structural remodelling before local amyloid deposition becomes apparent. This preplaque adaptation defines an early structural remodelling of hippocampal microglia prior to evident local amyloid deposition, providing new insight into the earliest structural adaptations associated with neuroimmune engagement in AD pathogenesis.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 3","pages":"e70082"},"PeriodicalIF":3.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148033467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Widespread hnRNP K Mislocalisation Suggests Differential Neuronal Vulnerability in the Neurodegenerative and Ageing Human Brain.","authors":"Xinwa Jiang, Christina E Toomey, Tammaryn Lashley, Ariana Gatt","doi":"10.1111/nan.70072","DOIUrl":"10.1111/nan.70072","url":null,"abstract":"<p><p>Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is a widely distributed RNA-binding protein in the human brain, playing a crucial role in post-transcriptional regulation, including mRNA metabolism and neuroplasticity. We have previously identified an increase in neuronal hnRNP K mislocalisation in cases of frontotemporal lobar degeneration (FTLD) compared to controls, where loss of nuclear hnRNP K was linked to alternative splicing events. However, the broader distribution of hnRNP K mislocalisation across different brain regions, other diseases and its pathological significance remains unclear. This study systematically examined hnRNP K mislocalisation across 13 brain regions from 19 cases, including different pathological subtypes of FTLD, Parkinson's disease (PD), Alzheimer's disease (AD) and age-matched neurologically normal controls, using immunohistochemistry and quantitative image analysis. The results of the study show that hnRNP K mislocalisation is observed throughout the brain, characterised by nuclear depletion and cytoplasmic aggregation. In the cerebral cortex, mislocalisation was most pronounced in the frontal lobe and least in the occipital lobe, with significant predominance in the depth of sulci compared to gyri. Notably, the basal ganglia, thalamus, medulla and cerebellum exhibited particular vulnerability to hnRNP K pathology. In contrast, Purkinje cells within the cerebellum and CA1-CA2 pyramidal neurons within the hippocampus showed lower levels of mislocalisation. Furthermore, levels of hnRNP K mislocalisation within the putamen correlated significantly with motor symptoms, suggesting a potential link between hnRNP K pathology and motor dysfunction. These findings highlight the propensity of hnRNP K mislocalisation in neurodegenerative diseases and the aged brain and underscore the need for further investigation into its functional consequences.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70072"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13062711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropathologic Characterisation of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) With Coexisting α-Synuclein and Tau Pathology in a Young Adult.","authors":"Laura Gomez-Isaza, Javier Redding-Ochoa, Maria Luongo, Russell Alexander, Anindita Ray, Sonja W Scholz, Juan C Troncoso","doi":"10.1111/nan.70074","DOIUrl":"10.1111/nan.70074","url":null,"abstract":"<p><p>Mitochondrial membrane protein associated neurodegeneration (MPAN) is a rare and genetically defined subtype of neurodegeneration with brain iron accumulation (NBIA) caused by pathogenic variants in C19orf12. We report an autopsy case in a young adult with a homozygous C19orf12 missense variant. Neuropathological examination demonstrated iron deposition within the globus pallidus, widespread neuroaxonal spheroids, and extensive α-synuclein pathology of the brainstem, limbic and neocortical regions. In addition, we identified focal tau pathology in hippocampus, and entorhinal cortex.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70074"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ACTA1-Related Adult-Onset Scapuloperoneal Myopathy With Cores and Rods.","authors":"Alexandru Caramizaru, Marion Onnée, Sergey Nikitin, Amelia Dobrescu, Gianmarco Severa, Aysylu Murtazina, Andoni Urtizberea, Jean-Pascal Lefaucheur, Robert-Yves Carlier, Corinne Metay, Edoardo Malfatti","doi":"10.1111/nan.70067","DOIUrl":"10.1111/nan.70067","url":null,"abstract":"<p><strong>Aims: </strong>Actinopathies are myopathies associated with pathogenic variants in ACTA1, a gene encoding the skeletal alpha-actin protein. Although patients most frequently have a severe congenital myopathy, an important clinical and myopathological variability has been described. Recently, a scapuloperoneal myopathy phenotype associated with ACTA1 has been reported. Here, we present a Russian woman with a late-onset, slowly progressive, scapuloperoneal actinopathy associated with an unpublished heterozygous pathogenic ACTA1 variant.</p><p><strong>Methods: </strong>We performed a thorough analysis of clinical, muscle imaging, muscle biopsy, genetic, protein and cardiac alpha-actin expression data from a 65-year-old woman with a scapuloperoneal myopathy phenotype.</p><p><strong>Results: </strong>Disease onset was at around 30 years with proximal lower limbs muscle weakness, which slowly progressed towards an upper and lower limb distal involvement with prominent weakness of the fourth and fifth finger extensors. A muscle MRI showed a symmetric axial involvement, while lower limbs sections evidenced a severe symmetric involvement of quadriceps and biceps femoris long head, and a symmetric involvement of medial gastrocnemius associated with a right tibialis anterior involvement. Muscle biopsy showed cores and rods. The patient harboured the unpublished NM_001100.4:c.1001C > T, p.(Pro334Leu) ACTA1 variant. Immunofluorescence and western blot studies showed an increased expression of cardiac alpha-actin, an actin isoform which is normally predominant in the prenatal skeletal muscles and adult heart muscle, suggesting a possible role of this isoform in milder actinopathy phenotypes.</p><p><strong>Conclusions: </strong>We report a milder, late-onset, slowly progressive scapuloperoneal myopathy phenotype with cores and rods and cardiac alpha-actin overexpression, thus expanding the spectrum of actinopathies.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70067"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147458864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of Copy-Number Variations in CNS Tumours From Off-Target Reads of Hybrid-Capture Sequencing.","authors":"Jan Schnorrenberg, Yannis Luca Adrian, Judith Schlathölter, Christian Ruckert, Judit Horvath, Werner Paulus, Martin Hasselblatt, Christian Thomas","doi":"10.1111/nan.70070","DOIUrl":"10.1111/nan.70070","url":null,"abstract":"<p><p>Copy number variations (CNVs) play a central role in the classification, grading and prognostication of central nervous system (CNS) tumours. While genome-wide methylation arrays are widely used for CNV profiling, next-generation sequencing (NGS) panels are increasingly implemented in routine diagnostics. We hypothesised that off-target sequencing reads from small hybrid-capture panels not specifically designed for copy-number detection can yield clinically actionable genome-wide CNV profiles. We analysed 60 CNS tumour samples, including glioblastomas, oligodendrogliomas, ependymal tumours, medulloblastomas and choroid plexus tumours using a small-scale custom hybrid-capture panel (< 0,2 Mb) and compared CNV profiles inferred from sequencing reads to those obtained with methylation arrays. Additionally, 58 meningiomas and 6 pilocytic astrocytomas with BRAF fusions were profiled with the same NGS panel. Across 527 chromosomal arm-level alterations, concordance between NGS- and methylation-derived profiles was 95%. All 19 focal amplifications (e.g., EGFR, MDM4 and MYCN) and the majority of homozygous CDKN2A/B deletions were correctly detected. In meningiomas, genome-wide CNV profiling from off-target reads identified WHO-relevant alterations, including CDKN2A/B deletions and 1p/22q co-deletions, supporting molecular upgrading in 9/58 (16%) of histologically lower grade tumours. Focal copy-number variations on Chr7q suggestive of BRAF fusions were observed in 5/6 fusion-positive pilocytic astrocytomas. These findings demonstrate that off-target reads from minimal targeted NGS panels can generate genome-wide CNV profiles, comparable to methylation array data, without the need for additional assays or specialised probe designs.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70070"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MR-Guided Laser Interstitial Thermal Therapy for Recurrent Glioblastoma: A Case Report With Novel Insights Into Histopathological Changes and Immunological Responses.","authors":"Silas Haahr Nielsen, Sara Blaabjerg Artzi, Jane Skjøth-Rasmussen, Carl Christian Larsen, Nadine Margaretha Hammouda, Karen Bonde Larsen, Rune Rasmussen, Adam Espe Hansen, Bjarne Winther Kristensen","doi":"10.1111/nan.70071","DOIUrl":"10.1111/nan.70071","url":null,"abstract":"<p><p>MR-guided laser interstitial thermal therapy (LITT) offers a minimally invasive option for recurrent glioblastoma, but human post-treatment tissue data are scarce. In this case report, post-LITT tissue exhibited distinct zonal changes, including central necrosis within the ablation zone and reduced tumour proliferation with increased CD8⁺ T-cell infiltration in the perilesional transition zone, suggesting that LITT may influence the local immune landscape in recurrent glioblastoma.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70071"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myofibre Density Reveals a Critical Threshold Around Age 6 in Steroid-Naïve Duchenne Muscular Dystrophy: A Retrospective Observational Study.","authors":"Tetsuhiro Yamakado, Yuka Ishikawa, Koki Ise, Lei Wang, Yoshitaka Oda, Masumi Tsuda, Taichi Kimura, Masayoshi Nagao, Manabu Ito, Shinya Tanaka, Zen-Ichi Tanei","doi":"10.1111/nan.70068","DOIUrl":"10.1111/nan.70068","url":null,"abstract":"<p><strong>Aims: </strong>In Duchenne muscular dystrophy (DMD), robust histological markers for assessing early disease progression remain elusive. We defined myofibre density (MFD) as the count of myofibres per square millimetre, which, in our preliminary survey of DMD muscle biopsies, steeply declined with age (Spearman's ρ: -0.85). We aimed to characterise age-dependent MFD dynamics in early-stage DMD.</p><p><strong>Methods: </strong>We retrospectively assessed 46 archival muscle-biopsy slides (steroid-naïve; collected > 40 years ago) using semi-quantitative image analysis with digital restoration. MFD and classical histological variables were quantified. Age-MFD dynamics were modelled with segmented regression and validated using weakly informative Bayesian modelling. The primary measure was the MFD age-breakpoint. Secondary measures included breakpoint-detection power, age-predictive MFD cut-offs and behaviour of conventional variables across breakpoint-defined age bands.</p><p><strong>Results: </strong>After quality and age-distribution screening, 35 slides (age 1-11 years) were analysed. Segmented regression identified a breakpoint at 6.25 years (95% confidence interval [CI]: 5.08-7.42); after which MFD plateaued at lower levels. Bayesian posterior estimate was 6.37 years (95% credible interval: 5.24-7.66). A 10,000-run Monte Carlo simulation (n = 35) showed approximately 80% power to recapture the breakpoint within ±1.25 years. MFD cut-offs > 596 and < 426 fibres/mm² corresponded to 80% and 20% probabilities of age < 6.25 years. Between the early (< 5 years) and late (≥ 7.5 years) age bands defined by the breakpoint-CI limits, myofibre-size parameters, myofibre area and fat replacement shifted significantly.</p><p><strong>Conclusions: </strong>MFD, a simple metric, reveals a previously unrecognised phase of rapid myofibre loss lasting up to around age 6 in early-stage DMD.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70068"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Four-Repeat Tauopathy With PSP-Like Features in Severe Intellectual Disability: Two Autopsy Cases.","authors":"Yukiko Hata, Hiroya Kaneko, Koji Yoshida, Ryo Tanaka, Shojiro Ichimata, Naoki Nishida","doi":"10.1111/nan.70075","DOIUrl":"10.1111/nan.70075","url":null,"abstract":"<p><p>Autopsy of two adults with lifelong severe intellectual disability revealed four-repeat tauopathy. One case showed typical progressive supranuclear palsy, whereas the other demonstrated a PSP-like phenotype with restricted basal ganglia-brainstem involvement. Molecular autopsy identified variants in SPG7 and CTSD, suggesting intracellular vulnerability. These findings expand the neuropathological spectrum of severe intellectual disability and indicate that primary four-repeat tauopathy may occur in this underrecognised population.</p>","PeriodicalId":19151,"journal":{"name":"Neuropathology and Applied Neurobiology","volume":"52 2","pages":"e70075"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}