Free neuropathology最新文献

{"title":"A malignant choroid plexus tumor with heterologous differentiation and BAP1 deletion suggesting choroid plexus blastoma.","authors":"Arnault Tauziède-Espariat, Alice Métais, Léa Guerrini-Rousseau, Farah Sassi, Lauren Hasty, Raphaël Saffroy, Volodia Dangouloff-Ros, Kévin Beccaria, Euphrasie Servant, Pascale Varlet","doi":"10.17879/freeneuropathology-2025-8899","DOIUrl":"10.17879/freeneuropathology-2025-8899","url":null,"abstract":"","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"18"},"PeriodicalIF":0.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234478","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":"69th Annual Meeting of the German Society of Neuropathology and Neuroanatomy (DGNN) - Meeting Abstracts: September 25-27, 2025 Frankfurt am Main, Germany.","authors":"","doi":"10.17879/freeneuropathology-2025-8974","DOIUrl":"https://doi.org/10.17879/freeneuropathology-2025-8974","url":null,"abstract":"<p><p>Sehr geehrte Damen und Herren, liebe Kolleginnen und Kollegen, im Namen der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie heiße ich Sie herzlich willkommen zur 69. Jahrestagung unserer Fachgesellschaft, die in diesem Jahr zudem das 75-jährige Jubiläum der DGNN feiert. Dieses besondere Jubiläum gibt uns Anlass, auf die Wurzeln und die beeindruckende Entwicklung unserer Fachgesellschaft zurückzublicken. Die Frankfurter Schule mit Persönlichkeiten wie Carl Weigert und Ludwig Edinger legte wesentliche Grundlagen für die Neurowissenschaften, deren Bedeutung bis heute kaum zu überschätzen ist. Ein entscheidender Schritt in der Geschichte unseres Faches war der Zusammenschluss der Neuropathologen in der \"Arbeitsgemeinschaft morphologisch arbeitender Neurologen und Psychiater\". Unterstützt durch den Pathologen Prof. Lauche und die Frankfurter Edinger-Stiftung fanden im Mai 1950 Vorgespräche statt, die schließlich am 7. Oktober 1950 zur Gründungsversammlung der \"Vereinigung Deutscher Neuropathologen\" führten. Diese Gründung legte den Grundstein für die heutige DGNN, die seit 75 Jahren als wissenschaftliche Plattform für Austausch und Fortschritt im Bereich der neuropathologischen Forschung dient. Besonders hervorheben möchte ich den hohen Stellenwert der Nachwuchsförderung in unserer Gesellschaft. Seit jeher ist es ein zentrales Anliegen der DGNN, junge Wissenschaftlerinnen und Wissenschaftler zu unterstützen, zu fördern und ihnen eine Plattform für ihre wissenschaftliche Entwicklung zu bieten. Nur durch die gezielte Förderung des wissenschaftlichen Nachwuchses können wir die Zukunft unseres Fachgebiets sichern und kontinuierlich neue Impulse für die Neuropathologie setzen. Der Kongress 2025 in Frankfurt am Main bietet uns erneut die Gelegenheit, in Vorträgen und Diskussionen die neuesten wissenschaftlichen Erkenntnisse zu erörtern sowie den kollegialen Austausch zu pflegen. Besonders freue ich mich auf das breite Spektrum an Themen und den angeregten Dialog, der unsere Fachgesellschaft lebendig hält. Mein Dank gilt allen Mitgliedern und Unterstützern, die die DGNN mit ihrem Engagement und ihrer Leidenschaft prägen und voranbringen. Ich wünsche uns allen einen erfolgreichen und inspirierenden Kongress sowie ein bedeutungsvolles Jubiläumsjahr. Mit herzlichen Grüßen Karl Heinz Plate Frankfurt am Main, im August 2025.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"17"},"PeriodicalIF":0.0,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139758","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":"Histopathologic evidence of intimal hyperplasia in carotid artery webs associated with stroke.","authors":"Farhan Khan, Alisa Nobee, Skylar Lewis, John E Donahue, Shadi Yaghi","doi":"10.17879/freeneuropathology-2025-7139","DOIUrl":"10.17879/freeneuropathology-2025-7139","url":null,"abstract":"<p><p><b>Background:</b> Carotid artery webs (CWs) are an underrecognized cause of ischemic stroke, particularly in younger patients who lack conventional vascular risk factors. CWs are thought to represent an intimal variant of fibromuscular dysplasia (FMD); however, histopathologic data supporting this hypothesis remain limited. We report a case series of three patients with CW-related ischemic stroke who underwent carotid endarterectomy (CEA), allowing for histological analysis of the resected specimens. <b>Methods:</b> We retrospectively reviewed patients admitted to a Comprehensive Stroke Center between January 2015 and April 2025 with ischemic stroke or transient ischemic attack attributed to an ipsilateral carotid web who subsequently underwent carotid endarterectomy. Clinical data, imaging findings, and histopathologic features were analyzed. All cases met criteria for embolic stroke of undetermined source (ESUS) prior to surgery. <b>Results:</b> Three patients with CW-related stroke underwent carotid endarterectomy following recurrent events or high embolic risk. In two cases, superimposed thrombi led to initial misdiagnoses such as soft plaque or dissection. Histopathologic analysis consistently demonstrated fibrovascular tissue with intimal fibroid hyperplasia and myxoid degeneration, without lipid-rich plaques or inflammatory infiltrates. No patients experienced recurrent stroke or TIA by the time of their last documented follow-up. <b>Conclusions:</b> CWs represent a distinct non-atherosclerotic pathology characterized by intimal hyperplasia and myxoid degeneration. Superimposed thrombus may complicate diagnosis, often mimicking plaque or dissection. Advanced imaging, including MR vessel wall imaging and intravascular optical coherence tomography (OCT), can aid in accurate identification. Carotid revascularization may be effective in selected patients, particularly those with recurrence or ESUS. Prospective studies are needed to inform standardized diagnostic and therapeutic strategies.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"16"},"PeriodicalIF":0.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980948","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":"Neuroinflammatory mechanisms may help identify candidate biomarkers in chronic traumatic encephalopathy (CTE).","authors":"Guneet S Bindra, Shaheryar Asad, Jean Shanaa, Forshing Lui, Andrew E Budson, Katherine W Turk, Jonathan D Cherry","doi":"10.17879/freeneuropathology-2025-6382","DOIUrl":"10.17879/freeneuropathology-2025-6382","url":null,"abstract":"<p><p>Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that can only be diagnosed post-mortem via pathological autopsy. The primary risk factor for CTE is a history of repetitive head impacts (RHI) received through contact sports including American football, hockey or soccer, military-related head injuries, or intimate partner violence. Recent findings have demonstrated that neuroinflammation is a critical compo-nent of early CTE pathogenesis and is likely part of the mechanism driving disease onset and progression. Additionally, the innate specificity, or 'signature', of a neuroinflammatory response may function as a dis-ease-specific marker for various neurodegenerative conditions. This would suggest an enormous repository of novel CTE biomarker candidates to be added to ongoing clinical trials, helping bolster diagnosis. However, few studies have truly leveraged immune mediators as candidate CTE markers. In this review, we argue and provide support that inflammatory mechanisms could serve as a viable source for novel biomarkers that are specific to CTE pathol-ogy. This includes an evaluation of inflammatory or damage-related markers such as CCL11 (C-C Motif Chem-okine Ligand 11, also known as Eotaxin-1), CCL21 (C-C Motif Chemokine Ligand 21) and GFAP (Glial Fibrillary Acidic Protein). We discuss the neuroinflammatory responses that give rise to these biomarkers in addition to the advantages and limitations of using each to diagnose CTE with particular attention to sensitivity and specifici-ty. Although further research is necessary to validate immune mediators, the latter show promise as diagnos-tic biomarkers for CTE and may also eventually serve as therapeutic targets for mitigating chronic inflamma-tion in at-risk populations.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"15"},"PeriodicalIF":0.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644284","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":"Multiple sclerosis: 2024 update.","authors":"Luisa Klotz, Maija Saraste, Laura Airas, Tanja Kuhlmann","doi":"10.17879/freeneuropathology-2025-6762","DOIUrl":"10.17879/freeneuropathology-2025-6762","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a complex immune-mediated disease that leads to neurological disability, with ongoing challenges in understanding its initiation, predicting progression, and optimizing personalized treatment. This review article summarizes key research findings from 2024, covering advances in diagnostic criteria, understanding of pathophysiology, and treatment strategies. New studies reinforce the strong link between Epstein-Barr virus (EBV) and MS, while recent data point towards a role of genetics in MS disease progression. The 2024 McDonald criteria revision enhances diagnostic specificity and includes novel MRI markers and facilitates measurement of cerebrospinal fluid biomarkers. Additionally, recent genetic discoveries, advanced imaging techniques, and emerging biomarkers are refining disease monitoring and prognosis. Finally, we highlight promising therapeutic developments, including Bruton Tyrosine Kinase (BTK) inhibitors and CAR T-cell therapies, with the former representing a paradigm shift in the potential of targeting MS progression beyond focal inflammation.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602357","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":"Evaluating ultrastructural preservation quality in banked brain tissue.","authors":"Macy Garrood, Alicia Keberle, Allison Sowa, William Janssen, Emma L Thorn, Claudia De Sanctis, Kurt Farrell, John F Crary, Andrew T McKenzie","doi":"10.17879/freeneuropathology-2025-6763","DOIUrl":"10.17879/freeneuropathology-2025-6763","url":null,"abstract":"<p><p>The ultrastructural analysis of postmortem brain tissue can provide important insights into cellular architecture and disease-related changes. For example, connectomics studies offer a powerful emerging approach for understanding neural circuit organization. However, electron microscopy (EM) data is difficult to interpret when the preservation quality is imperfect, which is common in brain banking and may render it unsuitable for certain research applications. One common issue is that EM images of postmortem brain tissue can have an expansion of regions that appear to be made up of extracellular space and / or degraded cellular material, which we call ambiguous interstitial zones. In this study, we report a method to assess whether EM images have ambiguous interstitial zone artifacts in a cohort of 10 postmortem brains with samples from each of the cortex and thalamus. Next, in matched samples from the contralateral hemisphere of the same brains, we evaluate the structural preservation quality of light microscopy images, including immunostaining for cytoskeletal proteins. Through this analysis, we show that on light microscopy, cell membrane morphology can be largely maintained, and neurite trajectory visualized over micrometer distances, even in specimens for which there are ambiguous interstitial zone artifacts on EM. Additionally, we demonstrate that synaptic structures can be successfully traced across serial EM sections in some postmortem samples, indicating the potential for connectivity studies in banked human brain tissue when appropriate preservation and visualization protocols are employed. Taken together, our analysis may assist in maximizing the usefulness of donated brain tissue by informing tissue selection and preparation protocols for various research goals.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"13"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12189018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144499693","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":"Applying machine learning to assist in the morphometric assessment of brain arteriolosclerosis through automation.","authors":"Jerry J Lou, Peter Chang, Kiana D Nava, Chanon Chantaduly, Hsin-Pei Wang, William H Yong, Viharkumar Patel, Ajinkya J Chaudhari, La Rissa Vasquez, Edwin Monuki, Elizabeth Head, Harry V Vinters, Shino Magaki, Danielle J Harvey, Chen-Nee Chuah, Charles S DeCarli, Christopher K Williams, Michael Keiser, Brittany N Dugger","doi":"10.17879/freeneuropathology-2025-6387","DOIUrl":"10.17879/freeneuropathology-2025-6387","url":null,"abstract":"<p><p>Objective quantification of brain arteriolosclerosis remains an area of ongoing refinement in neuropathology, with current methods primarily utilizing semi-quantitative scales completed through manual histological examination. These approaches offer modest inter-rater reliability and do not provide precise quantitative metrics. To address this gap, we present a prototype end-to-end machine learning (ML)-based algorithm, Arteriolosclerosis Segmentation (ArtSeg), followed by Vascular Morphometry (VasMorph) - to assist persons in the morphometric analysis of arteriolosclerotic vessels on whole slide images (WSIs). We digitized hematoxylin and eosin-stained glass slides (13 participants, total 42 WSIs) of human brain frontal or occipital lobe cortical and/or periventricular white matter collected from three brain banks (University of California, Davis, Irvine, and Los Angeles Alzheimer's Disease Research Centers). ArtSeg comprises three ML models for blood vessel detection, arteriolosclerosis classification, and segmentation of arteriolosclerotic vessel walls and lumens. For blood vessel detection, ArtSeg achieved area under the receiver operating characteristic curve (AUC-ROC) values of 0.79 (internal hold-out testing) and 0.77 (external testing), Dice scores of 0.56 (internal hold-out) and 0.74 (external), and Hausdorff distances of 2.53 (internal hold-out) and 2.15 (external). Arteriolosclerosis classification demonstrated accuracies of 0.94 (mean, 3-fold cross-validation), 0.86 (internal hold-out), and 0.77 (external), alongside AUC-ROC values of 0.69 (mean, 3-fold cross-validation), 0.87 (internal hold-out), and 0.83 (external). For arteriolosclerotic vessel segmentation, ArtSeg yielded Dice scores of 0.68 (mean, 3-fold cross-validation), 0.73 (internal hold-out), and 0.71 (external); Hausdorff distances of 7.63 (mean, 3-fold cross-validation), 6.93 (internal hold-out), and 7.80 (external); and AUC-ROC values of 0.90 (mean, 3-fold cross-validation), 0.92 (internal hold-out), and 0.87 (external). VasMorph successfully derived sclerotic indices, vessel wall thicknesses, and vessel wall to lumen area ratios from ArtSeg-segmented vessels, producing results comparable to expert assessment. This integrated approach shows promise as an assistive tool to enhance current neuropathological evaluation of brain arteriolosclerosis, offering potential for improved inter-rater reliability and quantification.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"12"},"PeriodicalIF":0.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144287431","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":"Selective cellular and regional vulnerability in frontotemporal lobar degeneration: a scoping review.","authors":"Kashif Ravasia, Veronica Hirsch-Reinshagen","doi":"10.17879/freeneuropathology-2025-5812","DOIUrl":"https://doi.org/10.17879/freeneuropathology-2025-5812","url":null,"abstract":"<p><p>The three main types of frontotemporal lobar degeneration (FTLD) are characterized by the accumulation of abnormal proteins, namely tau, TDP-43 and FUS. The distribution of these proteins within different human brain regions is well known, as is the range of morphological variability of the cellular inclusions they form. Compared to the extensive knowledge that exists about distinct protein aggregates in FTLD, surprisingly little is known about the specific cell (sub)types that these inclusions affect. Even less is known about disease-specific abnormalities other than protein inclusions in affected and unaffected areas. These are non-trivial knowledge gaps. First, knowing which cell subtypes are vulnerable or resilient to the development of pathological protein inclusions is crucial to understand the cellular disease mechanisms. Second, mounting evidence suggests that non-cell autonomous mechanisms may play important roles in neurodegenerative conditions. For example, astrocytic tau pathology is associated with synaptic loss in corticobasal degeneration but not in progressive supranuclear palsy. Furthermore, changes that are more difficult and time-consuming to quantify, for example loss of a specific neuronal subtype that does not develop pathological inclusions, remain virtually unexplored and their relevance for disease progression are unknown. This scoping review is an attempt to collate all histological evidence from human studies that address the question of cell-specific vulnerability in the most common FTLD subtypes. By taking a systematic approach including various brain cell types such as neurons and their subtypes as well as astrocytes, microglia and oligodendrocytes and the entire central nervous system with its affected and unaffected regions, this review summarizes the current status in the field and highlights important knowledge gaps.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11980436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059740","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":"Neurooncology: 2025 update.","authors":"Michel Mittelbronn","doi":"10.17879/freeneuropathology-2025-6316","DOIUrl":"10.17879/freeneuropathology-2025-6316","url":null,"abstract":"<p><p>This collection of studies highlights groundbreaking advancements in brain tumor research, particularly primary CNS tumors and brain metastasis. One major focus is the tumor microenvironment, where alterations in cerebral microcirculation and hypoxic-ischemic conditions have been shown to influence metastatic progression. In glioblastoma, recurrent tumors exhibit distinct DNA methylation profiles, and global DNA methylation has emerged as an independent diagnostic marker for IDH-wildtype glioblastoma. A whole-tumor perspective further emphasizes the extensive intratumoral heterogeneity driving glioblastoma evolution. The immune landscape of glioblastoma is another key area of research. Cranioencephalic functional lymphoid units have been implicated in tumor progression, while time-dependent single-cell phenotyping offers novel insights into immune cell dynamics within glioblastoma. Additionally, histone serotonylation has been identified as a critical epigenetic regulator in ependymoma tumorigenesis. Diagnostic and prognostic innovations are paving the way for improved patient care. Histomorphological features provide enhanced prognosis prediction for glioblastoma patients. Confocal laser microscopy enables real-time intraoperative histopathological diagnostics, and sequencing of cerebrospinal fluid-derived cell-free DNA presents a promising non-invasive diagnostic approach. Together, these top studies of 2024 underscore the complexity of brain tumor biology and the integration of epigenetics, immune interactions, and advanced diagnostics into clinical practice. These insights mark significant progress toward personalized treatment strategies and improved outcomes in neurooncology.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11960715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766058","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":"Morphological substrate of chronic schizophrenia in elderly patients: a clinicopathological study.","authors":"Kurt A Jellinger","doi":"10.17879/freeneuropathology-2025-6135","DOIUrl":"10.17879/freeneuropathology-2025-6135","url":null,"abstract":"<p><p><b>Objective:</b> Patients with schizophrenia are at a higher risk of developing dementia, but the basis of cognitive impairment is a matter of discussion. Conflicting results regarding the association of schizophrenia with Alzheimer disease (AD) may partly be attributable to the inclusion of non-AD lesions, which few clinicopathological studies have considered. Therefore, a re-evaluation of an autopsy cohort of elderly schizophrenics published previously [1] was performed. <b>Material & methods:</b> Among 99 consecutive autopsy cases of patients who met the DSM-5 and ICD.10 criteria for schizophrenia (mean age 69.5 ± 8.25 years), 56 showed moderate to severe dementia. All brains were blindly examined using the current criteria for AD and looking for concomitant lesions. They were compared with the frequency of AD in an autopsy series of 1.750 aged demented individuals <b>Results:</b> Four cases revealed the features of definite AD, five probable AD, and three aged 82-89 years were classified as primary age-related tauopathy (PART). Two cases were a cortical type of dementia with Lewy bodies (DLB), one Lewy body disease of brainstem type; six showed hippocampal sclerosis, 14 argyrophilic grain disease (AGD), and one progressive supranuclear palsy (PSP). Other co-pathologies were frequent lacunes in basal ganglia, moderate cerebral amyloid angiopathy, minor development anomalies in the entorhinal cortex, Fahr's disease, metastatic tumors, and acute or old cerebral infarctions (n = 4 each). Definite AD was seen in 48 % of the age-matched demented control group. <b>Conclusions:</b> In this cohort of elderly schizophrenic patients, only 7.6 % fulfilled the neuropathological criteria of definite or probable AD and 3.6 % of PART compared to 6 % to 13.7 % typical and atypical AD in the literature, whereas a considerable number of cases showed non-AD co-pathologies. This is in line with other studies showing that the frequency of AD in elderly schizophrenics may be equal to or less than in age-matched controls. Further studies are needed to elucidate the mechanisms of cognitive decline in schizophrenia.</p>","PeriodicalId":73056,"journal":{"name":"Free neuropathology","volume":"6 ","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652471","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}