Free neuropathology最新文献

We report a central nervous system schwannoma, VGLL-fused in a young man's frontal lobe. Somatic abnormalities included an EWSR1::VGLL1 fusion, which incorporated the entire translated region of VGLL1, but excluded most domains of EWSR1. The tumor histologically merged with the brain, and showed both schwannoma-like and neuroblastoma-like areas. A germline LZTR1 mutation was subsequently identified, implying the patient suffered from schwannomatosis.

The mechanical perfusion of solutions through the cerebrovascular system is critical for several types of postmortem research. However, achieving consistently high-quality perfusion in this setting is challenging. Several previous studies have reported that longer postmortem intervals are associated with decreased perfusion quality, but the mechanisms and temporal progression of perfusion impairment are poorly understood. In this study, we describe our experience in developing a protocol for in situ perfusion of the postmortem brain in human whole-body donors (n = 77). Through the evaluation of different approaches, we found that cannulation of the internal carotid arteries combined with clamping of the vertebral arteries allows targeted perfusion of the brain. We evaluated perfusion quality through three complementary methods: gross anatomical appearance, CT imaging, and histology. These quality assessment measures were partially correlated across donors, indicating that they offer complementary perspectives on perfusion quality. Correlational analysis of our cohort of banked brains confirms that perfusion quality decreases as the postmortem interval increases, with a heterogenous pattern across brain regions. Our findings provide data for optimizing brain banking protocols and suggest future directions for investigating the mechanisms of postmortem perfusion impairment.

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.

Background: 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. Methods: 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. Results: 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. Conclusions: 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.

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.