Image segmentation and registration of carp brain tissue slices oriented to brain atlas construction.

In order to prepare specimens to clarify the anatomical localization of intracerebral hematomas (ICHs), we examined 18 autopsy cases ranging from 1 day to 2.5 months after onset: Five cases of hypertensive ICH (two cases of putaminal hematoma, one case of thalamic hematoma, one case of mixed-type hematoma, and one case of cerebellar hematoma), two cases of subarachnoid hemorrhage with ICH, three cases of cerebral amyloid angiopathy-related hemorrhage, two cases of ICH associated with blood coagulation abnormalities, and six cases of brain death with ICH (brain death period: 10 h to 13 days). Paraffin blocks containing hematomas that have hardened and have poor formalin penetration can be easily sectioned at 6 μm thickness by using Histoheme, an ammonia-based softening reagent. By mounting the sections on MAS-coated glass slides or New Silan III-coated glass slides, we were able to minimize the peeling of hematomas from the slides. Conventional staining (Klüver-Barrera staining, Elastica-Masson Goldner staining) showed decreased staining of the brain tissue surrounding the hematoma due to the effects of edema, making the localization of the hematoma unclear. Synaptophysin (SYP) immunostaining was visualized with 3,3'-diaminobenzidine tetrahydrochloride (DAB)-CoCl2 and double stained with eosin azur 50 (EA50) (DAB-CoCl2 SYP + EA50). This method revealed gray matter as black and fresh to relatively recent hematoma as red, and clearly demonstrated the anatomical localization of the hematoma without any reduction in staining due to edema. In contrast, hematomas in cases more than 29 days after onset showed heterogeneous staining in red or green, and the boundary between the brain tissue and the hematoma was unclear. However, with double staining using DAB-CoCl2 SYP and Masson Goldner staining, the hematoma stained dark red, and the boundary with the brain tissue was more clearly visible than with DAB-CoCl2 SYP + EA50.

Exosomes derived from neural stem cells contribute to cerebral ischemia/reperfusion injury via inhibiting autophagy in rats.

Da-Bu-Yin-Wan rescues cognitive deficits in aging and Alzheimer's disease models by Wnt/β-catenin-dependent restoration of lysosomal acidification.

Therapeutic potential of Oxalis corniculata in circumventing Alzheimer's disease through in vitro and in silico investigations.

Cerebrospinal fluid HOMER1 and NPTX2 as candidate signatures in early-stage multiple system atrophy-parkinsonism.

Brain aging mediates region-specific transcriptomic alterations.

Intracortical microstimulation induces rapid microglia process convergence.

Sleep deprivation attenuates acute ischemic stroke-induced hippocampal neuronal injury via the IL-38/NF-κB axis.

Bionic design based on liposome-exosome hybrid nanoparticles for synergistic delivery of paeonol to achieve neuroprotection and improvement of motor function in Parkinson's disease model mice.

Introduction: Medial sulci are key intraoperative landmarks and radiologic boundaries that determine safe interhemispheric approaches and accurate Magnetic Resonance Imaging (MRI) interpretations. The cingulate, paracingulate, calcarine, parietooccipital, callosal, rostral, supra-rostral, and subparietal sulci are the principal surgical corridors and radiologic boundaries on the medial surface. These structures serve as essential neuroanatomical landmarks and surgical corridors in micro neurosurgical procedures; however, they exhibit considerable morphological variability. This scoping review consolidates cadaveric morphology and morphometry to define reliable versus variable medial sulcal features that guide surgical corridors and radiologic localisation. Aim: To synthesise cadaveric morphological and morphometric data on the medial cerebral sulci and determine which sulci demonstrate consistent versus variable anatomical patterns. Materials and Methods: In the present scoping review, the comprehensive literature search identified 4,440 records in total. After applying the eligibility criteria of the original cadaveric anatomical studies that described the morphology and/or morphometry of the cingulate, paracingulate, calcarine, parietooccipital, and subparietal sulci in the human brain, a total of eight cadaveric studies were included. Data were extracted on sample characteristics, morphological classification, and quantitative morphometry of the medial cerebral sulci. Results: A total of 8 cadeveric studies met the inclusion criteria collectively examining 422 hemispheres.Across 422 hemispheres, the cingulate sulcus was consistent, whereas the paracingulate sulcus was variable in shape. The present study mapped sulcal configurations to interhemispheric approach planning. The calcarine sulcus demonstrated relatively stable morphometry, with mean anterior and posterior segment lengths of 23-35 mm. The parieto-occipital sulcus was a reliable boundary between the cuneus and precuneus, with mean lengths of approximately 40 mm. The subparietal sulcus was described less frequently, highlighting a gap in the detailed morphometric literature. Conclusion: Cadaveric evidence confirms both consistent and highly variable features of the medial cerebral sulci. The paucity of detailed morphometric descriptions for certain sulci, especially the subparietal, callosal, rostral and supra-rostral sulci, underscores the need for further targeted anatomical research.

A practical workflow for fixation and autofluorescence reduction in correlative light and electron microscopy of postmortem human brain tissue.

Identification of functional neural networks of human brains with fMRI.

Late-onset Alzheimer's disease (AD) arises in part from a complex genetic architecture dominated by common, low-penetrance variants, many of which are enriched in glial cells and remain mechanistically unresolved. Unlike the rare coding mutations that contribute to early-onset AD, these common variants often lie in noncoding regions, complicating efforts to link genetic risk to cellular function. Emerging evidence suggests that many glial-enriched risk genes contribute to disease by disrupting communication between glia and neurons. Such interactions are essential for preserving synaptic health and modulating immune responses to pathology. Understanding how polygenic variation perturbs these pathways requires integrative strategies that combine large-scale postmortem brain datasets with experimentally tractable human cellular models. In this review, we highlight recent progress in decoding the cellular impact of AD risk variants through the lens of glial-neuronal communication. We first illustrate how human brain studies have mapped cell-type-specific gene expression and intercellular networks associated with genetic risk. We then discuss how human stem cell-derived co-culture and 3D models are being used to test these hypotheses in controlled experimental systems. As a case study, we focus on CLU (Clusterin), a well-replicated risk locus that modulates glial inflammation, lipid exchange, and neuronal vulnerability. Together, these studies build a scalable, human-centric framework for linking genotype to function and point toward new opportunities for therapeutic discovery rooted in intercellular biology.

Prenatal exposure to antiseizure medications and risk of autism spectrum disorder in offspring: an integrated pharmacovigilance and two-sample mendelian randomization study.

Infants who are HIV-exposed uninfected (HEU) are at greater risk of death compared with infants who are HIV-unexposed, particularly in the first 6 months of life. We investigated the causes of death (CoD) of HEU and HIV-unexposed infants using postmortem minimally invasive tissue sampling. This prospective, observational study enrolled decedents less than 6 months of age at a secondary-tertiary level care hospital in Soweto, South Africa. The minimally invasive tissue sampling included needle core-biopsy sampling for histopathology of brain, lung and liver tissue. Microbiologic culture and/or molecular tests were performed on lungs, liver, blood and cerebrospinal fluid. Underlying, immediate and antecedent CoD were determined by a multidisciplinary team of medical experts. The median age (9 [interquartile range 3, 30] vs. 8 [interquartile range 3, 22] days) and sex distribution (female 58.5% vs. 47.9%) were similar between HEU (n = 65) and HIV-unexposed (n = 119) decedents. A larger proportion of HEU decedents (60%, 39/65) compared with HIV-unexposed decedents (44.5%, 53/119; P = 0.045) had preterm birth as an underlying CoD. Among HEU infants compared with HIV-unexposed infants, sepsis was attributed as an immediate or antecedent cause of death in 46.2% (30/65) versus 36.1% (43/119), respectively. Of the 30 HEU infants with sepsis, 76.7% (23/30) were classified as presumed hospital acquired, most commonly associated with Acinetobacter baumannii (56.5% [13/23]) and Klebsiella pneumoniae (13.0% [3/23]). Similarly, among HIV-unexposed infants with sepsis (n = 43), 72.3% (31/43) were classified as presumed hospital acquired, with A. baumannii (38.9% [12/31]) and K. pneumoniae (38.9% [12/31]) as the predominant pathogens. Pneumonia was attributed as an immediate or antecedent cause of death in 32.3% (21/65) of HEU and 36.1% (43/119) of HIV-unexposed infants. Among those with pneumonia, presumed hospital-acquired pneumonia was identified in 47.6% (10/21) of HEU and 72.1% (31/43) of HIV-unexposed infants (P = 0.035), most frequently due to A. baumannii (50.0% [5/10] HEU; 41.9% [13/31] HIV-unexposed) and K. pneumoniae (30.0% [3/10] HEU; 19.4% [6/31] HIV-unexposed). Presumed community-acquired pneumonia was identified in 52.4% (11/21) of HEU and 27.9% (12/43) of HIV-unexposed infants (P = 0.035). The predominant community-acquired pathogens were respiratory syncytial virus (36.4% [4/11] HEU; 25.0% [3/12] HIV-unexposed) and K. pneumoniae (36.4% [4/11] HEU; 8.3% [1/12] HIV-unexposed). Our study highlights preterm birth as an important underlying CoD among HEU and HIV-unexposed decedents. There was a larger proportion of presumed community-acquired pneumonia deaths in HEU compared with HIV-unexposed decedents. Further research is warranted to explore these differences and develop effective preventive strategies.

Beyond regulation of mRNAs by individual ncRNA types, like miRNAs, circRNAs or lncRNAs, their interplay as competitive endogenous RNAs (ceRNAs) appears pivotal in diseases. ceRNAs are promising biomarkers in diagnosing diseases as well as in understanding off-target drug mechanisms or developing specific therapeutics. Many diseases are influenced at different molecular levels and across multiple organs, making cross-organ multi-omics interaction studies necessary to holistically understand diseases and their regulation. In our study we applied this approach to the cognitive dysfunction caused by deficiency of functioning tRNA 2'-O-methyltransferase FTSJ1. We investigated the expression changes of mRNA and multiple ncRNA species (miRNAs, lncRNAs, circRNAs) in Ftsj1-deficient versus wild-type C57BL/6J mice and constructed organ-specific ceRNA networks for the brain, heart, kidney, liver, spleen. Validation of potential ncRNA biomarkers was performed using degradome sequencing as well as qRT-PCR. The strongest effects of differential expression due to Ftsj1 deficiency were observed in liver and kidney, where especially genes involved in fatty acid metabolism showed altered expression. We reveal a prominent ceRNA network induced by Ftsj1 deficiency in liver and kidney, mediated by four hub-miRNAs (miR-378d, miR-3076-5p, miR-3474, miR-296-3p) enriched with acyl-CoA-related genes, including Acly, Acss2, and Mvk. In contrast, brain tissues showed minimal changes in gene expression, hinting at cross-organ interactions for cognitive dysfunction also supported by previously described phenotypes like muscle weakness in mice with Ftsj1 deficiency. Our results suggest the involvement of multiple cross-organ regulatory mechanisms for single gene-associated intellectual disability. For FTSJ1 deficiency, this indicates that the cognitive impairment presented by affected human individuals can be associated with metabolic impairment and ceRNA crosstalk along the liver-brain and kidney-brain axes. Our findings provide a new perspective on the development of cognitive impairments caused by mutations of individual genes and underline the importance of multi-omics cross-organ analyses for the development of therapeutics and identification of biomarkers based on ceRNA-mediated networks.

Detection of La Crosse virus RNA in clinical specimens obtained from children with La Crosse infection.

The effects of Kai-Xin-San in alleviating chronic social defeat stress-induced depression-like behaviors are associated with CD4+ T cells.

Decoding schizophrenia through postmortem human brain transcriptomics.