Applying perfusion fixation in brain banking encounters several significant impediments: the brain's large size, pre-procedural vascular damage and blockage, and the need to freeze portions of the brain to meet differing investigator aims. Subsequently, the need for a flexible and scalable perfusion fixation protocol in brain banking is crucial. This technical report explores our method of designing an ex situ perfusion fixation protocol in detail. Implementing this procedure brought forth various difficulties and valuable lessons, which we explore in detail. The perfused brains, as evaluated by routine morphological staining and RNA in situ hybridization, display intact biomolecular signals and well-preserved tissue cytoarchitecture. However, the procedure's effect in yielding better histology, when measured against immersion fixation, is uncertain. In addition, ex vivo magnetic resonance imaging (MRI) findings propose that the perfusion fixation procedure may introduce imaging imperfections, manifesting as air bubbles within the vasculature. We propose further research endeavors focused on the deployment of perfusion fixation as a reliable and replicable alternative to immersion fixation for the preparation of human brains postmortem.

For refractory hematopoietic malignancies, chimeric antigen receptor (CAR) T-cell therapy stands as a promising, innovative immunotherapy. Neurotoxicity is a significant and frequently occurring adverse event. While the physiopathological explanations are currently unknown, neuropathological reports are few in number. From 2017 to 2022, post-mortem examinations were carried out on the brains of six patients who had received CAR T-cell therapy. In each instance, paraffin blocks underwent polymerase chain reaction (PCR) to detect the presence of CAR T cells. Sadly, two patients perished from hematologic progression, while their fellow patients were claimed by the devastating consequences of cytokine release syndrome, lung infections, encephalomyelitis, and severe acute liver failure. Among the six presented neurological symptoms, two exhibited distinct clinical presentations, one with the progression of extracranial malignancy, and the other with encephalomyelitis. Severe perivascular and interstitial lymphocytic infiltration, largely CD8+, was a key finding in the neuropathology of the latter sample. Concurrently, a diffuse interstitial histiocytic infiltration impacted the spinal cord, midbrain, and hippocampus, along with extensive gliosis in the basal ganglia, hippocampus, and brainstem. Concerning neurotropic viruses, microbiological analysis was negative, and polymerase chain reaction testing failed to detect CAR T-cells. Another instance, without evidence of neurological signs, showcased cortical and subcortical gliosis, directly attributable to acute hypoxic-ischemic damage. A mild, patchy gliosis and microglial activation were observed in the remaining four cases; PCR testing revealed CAR T cells in just one of these cases. Our analysis of fatalities following CAR T-cell treatment in this cohort principally showed nonspecific or limited neuropathological changes. Potential pathological findings, revealed through the autopsy, might indicate causes for neurological symptoms apart from CAR T-cell related toxicity.

It is unusual to find pigment in ependymomas, besides melanin, neuromelanin, lipofuscin, or a combination of those pigments. We present, in this case report, a pigmented ependymoma found in the fourth ventricle of a grown individual, and we also examine 16 additional documented cases of pigmented ependymoma from the published literature. Presenting with hearing loss, headaches, and nausea, a 46-year-old woman sought medical attention. Through magnetic resonance imaging, a 25-centimeter contrast-enhancing cystic mass was observed to reside in the fourth ventricle; this mass was resected. Intraoperatively, the cystic, grey-brown tumor demonstrated an adhesion to the brainstem. Routine histological analysis revealed an ependymoma-suggestive tumor featuring true rosettes, perivascular pseudorosettes, and ependymal canals; however, chronic inflammation and a significant number of distended, pigmented tumor cells resembling macrophages were also apparent in both frozen and permanent sections. chronobiological changes The pigmented cells' GFAP-positive and CD163-negative status supported their classification as glial tumor cells. The pigment, negative for Fontana-Masson but positive for Periodic-acid Schiff and autofluorescent, clearly displayed the characteristics of lipofuscin. A low value was shown by the proliferation indices, alongside a partial loss of H3K27me3. The histone H3 protein's lysine 27 undergoes tri-methylation, a process denoted as H3K27me3, representing an epigenetic modification impacting DNA organization. The methylation classification's findings indicated a posterior fossa group B ependymoma (EPN PFB). The patient's clinical condition, as assessed at the three-month post-operative follow-up appointment, demonstrated no recurrence and remained excellent. The 17 cases analyzed, encompassing the presented case, indicated that pigmented ependymomas are highly frequent in middle-aged individuals, with a median age of 42 years, and tend to have favorable clinical courses. In contrast, another patient who developed secondary leptomeningeal melanin accumulations passed away. The 4th ventricle is the primary site of origin in a considerable 588% of cases, whereas the spinal cord (176%) and supratentorial (176%) locations are less common. cardiac pathology The patient's age at presentation and generally favorable prognosis brings the question into focus: do most other posterior fossa pigmented ependymomas align with the EPN PFB group? Additional study is needed to clarify this.

Papers showcased in this update cover a variety of significant topics in vascular disease that have evolved over the past year. Two papers are devoted to the underlying causes of vascular malformations, the initial paper focusing on brain arteriovenous malformations, and the subsequent paper investigating cerebral cavernous malformations. Intracerebral hemorrhage, if these disorders rupture, and other neurological complications, including seizures, can result in considerable brain damage. Future comprehension of brain-immune system collaboration, post-cerebral trauma, particularly stroke, is highlighted in documents 3 to 6. The initial finding demonstrates the participation of T cells in white matter restoration post-ischemic injury, a phenomenon reliant on microglia's action, illustrating the vital interplay between innate and adaptive immunity systems. The next two articles center on B cells, a subject relatively understudied in the context of cerebral trauma. Neuroinflammation research gains a significant boost by investigating the unique contribution of antigen-experienced B cells from the meninges and skull bone marrow, in comparison to blood-derived counterparts. The potential for antibody-secreting B cells to be involved in vascular dementia will certainly be a focus of future research. Similarly, the authors of paper six observed that myeloid cells, which permeate the central nervous system, originate from tissues situated at the brain's edges. The transcriptional profiles of these cells are distinctive, differing significantly from those found in their blood counterparts, and potentially driving the infiltration of myeloid cells from bone marrow niches near the brain. Subsequently analyzed is the contribution of microglia, the brain's primary innate immune cells, to the formation and progression of amyloid plaques, followed by an examination of the potential clearance mechanisms of perivascular A from cerebral vessels in patients with cerebral amyloid angiopathy. The final two papers center on the contribution of senescent endothelial cells and pericytes. In a study using Hutchinson-Gilford progeria syndrome (HGPS) as a model of accelerated senescence, the potential benefit of a method focused on reducing telomere shortening for slowing the aging process was demonstrated. The final paper elucidates the role of capillary pericytes in regulating basal cerebral blood flow resistance and the slow modulation of cerebral blood flow. It is noteworthy that several of the publications highlighted therapeutic methods with the possibility of implementation within clinical populations.

The virtual 5th Asian Oceanian Congress of Neuropathology, joined by the 5th Annual Conference of the Neuropathology Society of India (AOCN-NPSICON), was held at NIMHANS, Bangalore, India, from September 24th to 26th, 2021, and coordinated by the Department of Neuropathology. 361 attendees, hailing from 20 countries throughout Asia and Oceania, including India, attended the event. A diverse group of pathologists, clinicians, and neuroscientists, representing Asia and Oceania, came together at the event, alongside invited speakers from the USA, Germany, and Canada. A thorough program, emphasizing the forthcoming WHO 2021 CNS tumor classification, delved into neurooncology, neuromuscular disorders, epilepsy, and neurodegenerative diseases. Keynote addresses and symposia, featuring 78 distinguished international and national faculty, showcased their expertise. R-848 chemical structure In addition, the program offered case-based learning modules, along with venues for junior faculty and postgraduate students to present their papers and posters. Several awards were presented for the best young investigators, papers, and posters. The conference's highlight included a distinctive debate on the trending topic of the decade, Methylation-based classification of CNS tumors, coupled with a panel discussion on COVID-19. The participants held the academic content in high regard.

Confocal laser endomicroscopy (CLE) offers a novel non-invasive in vivo imaging approach with substantial applicability in neurosurgery and neuropathology.