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Background: This research aims to determine the probable protective effect of nano-curcumin (N-CUR) on caffeine (1,3,7-trimethylxanthine)-induced neurotoxicity in cerebral rats. Methods: Twenty-four male Wistar rats were divided into three groups: control, caffeine (150 mg kg−1), and caffeine (150 mg kg−1) treated with N-CUR (300 mg kg−1). All treatments were administrated by gavage every day for a month. Results: Administration of caffeine significantly elevated the levels of serum interleukins 6 (IL-6), tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and cyclooxygenase2 (COX-2). Also, there was a significant increase in levels of cerebral malondialdehyde (MDA), significantly diminished glutathione (GSH), and superoxide dismutase (SOD) activity. Caffeine administration significantly downregulated the gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulated the expression of nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB). Administration of N-CUR caused a significant amelioration in TNF-α and IL-6 levels and a significant rise in SOD activity, while it caused a significant downregulation in NF-κB mRNA expression. Additionally, N-CUR has exerted insignificant amelioration of COX-2 and MDA contents and Nrf2 mRNA expression compared to the caffeine-treated group. Conclusion: N-CUR may have a mild to moderate ameliorative effect on caffeine-induced apoptosis, oxidative stress, and inflammatory response in the cerebrum. Highlights: Caffeine induced oxidative stress, apoptosis, and inflammation in the cerebrum. Caffeine resulted in significantly increased COX-2 and VEGF levels. Caffeine increased the expression of NF-ĸB and inhibited Nrf2 in cerebrum. N-CUR may have a mild to moderate ameliorative effect on caffeine exposure. Humans could confine caffeine intake to evade any alterations in the cerebrum. [ABSTRACT FROM AUTHOR]

Abstract Background This research aims to determine the probable protective effect of nano-curcumin (N-CUR) on caffeine (1,3,7-trimethylxanthine)-induced neurotoxicity in cerebral rats. Methods Twenty-four male Wistar rats were divided into three groups: control, caffeine (150 mg kg−1), and caffeine (150 mg kg−1) treated with N-CUR (300 mg kg−1). All treatments were administrated by gavage every day for a month. Results Administration of caffeine significantly elevated the levels of serum interleukins 6 (IL-6), tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and cyclooxygenase2 (COX-2). Also, there was a significant increase in levels of cerebral malondialdehyde (MDA), significantly diminished glutathione (GSH), and superoxide dismutase (SOD) activity. Caffeine administration significantly downregulated the gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulated the expression of nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB). Administration of N-CUR caused a significant amelioration in TNF-α and IL-6 levels and a significant rise in SOD activity, while it caused a significant downregulation in NF-κB mRNA expression. Additionally, N-CUR has exerted insignificant amelioration of COX-2 and MDA contents and Nrf2 mRNA expression compared to the caffeine-treated group. Conclusion N-CUR may have a mild to moderate ameliorative effect on caffeine-induced apoptosis, oxidative stress, and inflammatory response in the cerebrum.

Sustained attention is important for maintaining cognitive function and autonomy during ageing, yet older people often show reductions in this domain. The role of the underlying neurobiology is not yet well understood, with most neuroimaging studies primarily focused on fMRI. Here, we utilise sMRI to investigate the relationships between age, structural brain volumes and sustained attention performance. Eighty-nine healthy older adults (50–84 years, M age 65.5 (SD=8.4) years, 74 f) underwent MRI brain scanning and completed two sustained attention tasks: a rapid visual information processing (RVP) task and sustained attention to response task (SART). Independent hierarchical linear regressions demonstrated that greater volumes of white matter hyperintensities (WMH) were associated with worse RVP_ A' performance, whereas greater grey matter volumes were associated with better RVP_ A' performance. Further, greater cerebral white matter volumes were associated with better SART_ d' performance. Importantly, mediation analyses revealed that both grey and white matter volumes completely mediated the relationship between ageing and sustained attention. These results explain disparate attentional findings in older adults, highlighting the intervening role of brain structure. • White matter hyperintensities are significant predictors of sustained attention. • Cerebral grey matter volumes are significant predictors of sustained attention. • Cerebral white matter volumes are significant predictors of sustained attention. • Structural brain volumes completely mediate age effects on sustained attention. • These sMRI findings explain the attentional variability prevailing in older adults. [ABSTRACT FROM AUTHOR]

This document presents three case studies of patients who experienced severe brain injuries, specifically from gunshot wounds. The first case study focuses on a 29-year-old man who suffered extensive damage to the left cerebral and cerebellar hemispheres, resulting in various neurological symptoms. Despite these challenges, the patient showed progress in their recovery, highlighting the potential for cognitive and emotional abilities to be sustained by the right hemisphere. The second case study discusses a patient who underwent cranioplasty and a gastrostomy procedure after a gunshot brain injury, and despite the development of hemiplegia and severe aphasia, they showed improvement over time. The third case study explores a patient who underwent a hemispherectomy to treat Rasmussen encephalitis, and the study suggests that the brain can reorganize itself in response to chronic disease, leading to improvements in function. The article emphasizes the importance of early and aggressive treatment for severe brain injuries and acknowledges the need for further research in this area. [Extracted from the article]

Microglia colonize the brain starting on embryonic day (E) 9.5 in mice, and their population increases with development. We have previously demonstrated that some microglia are derived from intraventricular macrophages, which frequently infiltrate the pallium at E12.5. To address how the infiltration of intraventricular macrophages is spatiotemporally regulated, histological analyses detecting how these cells associate with the surrounding cells at the site of infiltration into the pallial surface are essential. Using two‐photon microscopy‐based in vivo imaging, we demonstrated that most intraventricular macrophages adhere to the ventricular surface. This is a useful tool for imaging intraventricular macrophages maintaining their original position, but this method cannot be used for observing deeper brain regions. Meanwhile, we found that conventional cryosection‐based and naked pallial slice‐based observation resulted in unexpected detachment from the ventricular surface of intraventricular macrophages and their mislocation, suggesting that previous histological analyses might have failed to determine their physiological number and location in the ventricular space. To address this, we sought to establish a methodological preparation that enables us to delineate the structure and cellular interactions when intraventricular macrophages infiltrate the pallium. Here, we report that brain slices pretreated with agarose‐embedding maintained adequate density and proper positioning of intraventricular macrophages on the ventricular surface. This method also enabled us to perform the immunostaining. We believe that this is helpful for conducting histological analyses to elucidate the mechanisms underlying intraventricular macrophage infiltration into the pallium and their cellular properties, leading to further understanding of the process of microglial colonization into the developing brain. [ABSTRACT FROM AUTHOR]

Purpose/Aim: Cardiovascular function is controlled and regulated by a functional brain-heart axis. Although the exact mechanism is not fully understood, several studies suggest a hemispheric asymmetry in the neural control of cardiovascular function. Thus, the purpose of this study was to examine whether endothelial function and arterial compliance differ between individuals with left- and right-sided strokes.Materials and Methods: This was a cross-sectional exploratory study. Thirty individuals more than 6 months after stroke participated in the study. The endothelial function was assessed by ultrasound-measured flow-mediated dilation of the nonparetic arm brachial artery (baFMD). The arterial stiffness was assessed by measuring carotid-femoral pulse wave velocity (cfPWV) and central aortic pulse wave analysis [augmentation index (AIx), augmentation index normalized to a heart rate of 75 bpm (AIx@75) and reflection magnitude (RM)] using applanation tonometry. Results: Participants with right-sided stroke had worse endothelial function than those with left-sided stroke. This difference (baFMD = 2.51%) was significant (p = 0.037), and it represented a medium effect size (r = 0.38). Likewise, they had higher arterial stiffness than those with left-sided stroke. This difference (AIx = 10%; RM = 7%) was significant (p = 0.011; p = 0.012), and it represented a medium effect size (r = 0.48; r = 0.47).Conclusions: Our findings suggest that individuals with right-sided stroke have reduced endothelial function and arterial compliance compared to those with left-sided stroke. These data may indicate that those with right-sided strokes are more susceptible to cardiovascular events. [ABSTRACT FROM AUTHOR]

The human cerebrum contains a large amount of cortico-cortical association fibers. Among them, U-fibers are short-range association fibers located in white matter immediately deep to gray matter. Although U-fibers are thought to be crucial for higher cognitive functions, the organization within U-fiber regions are still unclear. Here we investigated the properties of U-fiber regions in the ferret cerebrum using neurochemical, neuronal tracing, immunohistochemical and electron microscopic techniques. We found that U-fiber regions can be subdivided into two regions, which we named outer and inner U-fiber regions. We further uncovered that outer U-fiber regions have smaller-diameter axons with thinner myelin compared with inner U-fiber regions. These findings may indicate functional complexity within U-fiber regions in the cerebrum. • Features within U-fiber regions were investigated using the ferret cerebrum. • U-fiber regions can be subdivided into two regions: outer and inner U-fiber regions. • Both outer and inner U-fiber regions contain cortical association fibers. • Inner U-fiber regions mainly have larger-diameter axons with thicker myelin. • Our findings reveal novel organizations within U-fiber regions in the cerebrum. [ABSTRACT FROM AUTHOR]

Potassium bromate is used in cheese production, beer making and is also used in pharmaceutical and cosmetic. It is a proven carcinogen as it is a strong oxidizing agent that generates free radicals during xenobiotic metabolism. Urtica dioica (Ud) (from the plants' family of Urticaceae) is a plant that has long been used as a medicinal plant in many parts of the world. It has been shown to have anti-inflammatory, antioxidant and immunosuppressive properties. So, this study aimed to clarify the effect of Potassium bromate on the histological structure of cerebral cortex of adult male albino rats, evaluate the possible protective role of Urtica dioica. Thirty adult healthy male albino rats were divided into three groups; group I (Control group), group II (KBrO3 treated group). Group III (KBrO3 and Urtica dioica treated group).At the end of the experiment, rats in all groups were anesthetized and specimens were processed for light and electron microscope. Morphometric and statistical analyses were also performed. Nerve cells of the treated group showed irregular contours, dark nuclei, irregular nuclear envelopes, dilated RER cisternae, and mitochondria with ruptured cristae. Vacuolated neuropil was also observed. Immunohistochemically, stained sections for GFAP showed strong positive reaction in the processes of astrocytes. Recovery group showed revealed nearly the same as the histological picture as the control group. In conclusion, potassium bromate induces degenerative effects on neurons of cerebral cortex and urtica dioica provide an important neuroprotective effects against these damaging impacts through their antioxidant properties. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the present study was to compare the features of the structural complexity of the cerebral hemispheres in men and women using fractal analysis of outlined and skeletonized images, as well as quantitative analysis of digital skeletons of the cerebral hemispheres. Material and Methods: Magnetic resonance imaging brain scans of 100 individuals aged 18-86 years (44 males and 56 females) were investigated. Five tomographic sections of each brain were selected for morphometric study (4 coronal and 1 axial sections). The sections were preprocessed, and outlined and skeletonized images were obtained. Fractal analysis was conducted using the two-dimensional box counting method, and fractal dimensions of outlined and skeletonized images were determined. Additionally, quantitative analysis of skeletonized images was performed, determining the following parameters: branches, junctions, end-point voxels, junction voxels, slab voxels, triple points, quadruple points, average branch length, and maximum branch length. Results: We observed that both variants of fractal dimension in males and females did not show significant differences, although most quantitative parameters in males were larger than those in females. Conclusions: The spatial and structural complexity of the cerebral hemispheres, as characterized by fractal dimensions, is almost indistinguishable between males and females. However, in some individual tomographic sections, the male brain may exhibit a slightly higher number of end-point voxels, corresponding to the gyri of the cerebral hemispheres. The obtained data can be used in clinical practice for diagnostic purposes (e.g., for detecting malformations) and for theoretical studies in neuroanatomy.

Patients with COVID-19 have been reported to experience neurological complications, although the main cause of death in these patients was determined to be lung damage. Notably, SARS-CoV-2-induced pathological injuries in brains with a viral presence were also found in all fatal animal cases. Thus, an appropriate animal model that mimics severe infections in the lungs and brain needs to be developed. In this paper, we compared SARS-CoV-2 infection dynamics and pathological injuries between C57BL/6Smoc-Ace2em3(hACE2-flag-Wpre-pA)Smoc transgenic hACE2-C57 mice and Syrian hamsters. Importantly, the greatest viral distribution in mice occurred in the cerebral cortex neuron area, where pathological injuries and cell death were observed. In contrast, in hamsters, viral replication and distribution occurred mainly in the lungs but not in the cerebrum, although obvious ACE2 expression was validated in the cerebrum. Consistent with the spread of the virus, significant increases in IL-1β and IFN-γ were observed in the lungs of both animals. However, in hACE2-C57 mice, the cerebrum showed noticeable increases in IL-1β but only mild increases in IFN-γ. Notably, our findings revealed that both the cerebrum and the lungs were prominent infection sites in hACE2 mice infected with SARS-CoV-2 with obvious pathological damage. Furthermore, hamsters exhibited severe interstitial pneumonia from 3 dpi to 5 dpi, followed by gradual recovery. Conversely, all the hACE2-C57 mice experienced severe pathological injuries in the cerebrum and lungs, leading to mortality before 5 dpi. According to these results, transgenic hACE2-C57 mice may be valuable for studying SARS-CoV-2 pathogenesis and clearance in the cerebrum. Additionally, a hamster model could serve as a crucial resource for exploring the mechanisms of recovery from infection at different dosage levels. [ABSTRACT FROM AUTHOR]

The present study evaluated the effect of PM2.5 exposure on the cerebral tissue of neonatal rats. Twenty-four female Wistar albino rats were classified into three groups including "control," "Exposure1," and "Exposure2" after mating and pregnancy. The control group used air with a clean standard condition, and the other two groups were exposed to gaseous pollutants and gaseous pollutants plus PM2.5 respectively for 40 days. The cerebral tissues were removed. Gene expression analysis was conducted for S100 and GFAP genes using quantitative real-time PCR and also western blot assay to indicate GFAP and S100 proteins level in the control, Exposure1, and Exposure2 groups. The histopathology, immunohistochemical staining, and oxidative stress (OS) activity were conducted for all groups. The results showed the significant expression of S100 and GFAP genes in Exposure1 and Exposure2 groups compared with the control group. The western blot analysis showed the significant increase of S100 and GFAP protein level in Exposure2 group. Based on the analysis of the involved enzymes in OS, superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) decreased, while malondialdehyde (MDA) increased in the Exposure1 and Exposure2 groups. According to the results of pathology and immunohistochemistry, severe tissue damage was observed in neonatal cerebral tissues in the Exposure2 group. These findings may help provide insight to identifying therapeutic targets for reducing human cerebral disorders caused by exposure to PM2.5 or other air pollutants. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the present study was to compare the features of the structural complexity of the cerebral hemispheres in men and women using fractal analysis of outlined and skeletonized images, as well as quantitative analysis of digital skeletons of the cerebral hemispheres. Material and Methods: Magnetic resonance imaging brain scans of 100 individuals aged 18-86 years (44 males and 56 females) were investigated. Five sections of each brain were selected for morphometric study (4 coronal and 1 axial sections). The sections were preprocessed, and outlined and skeletonized images were obtained. Fractal analysis was conducted using the twodimensional box counting method, and fractal dimensions of outlined and skeletonized images were determined. Additionally, quantitative analysis of skeletonized images was performed, determining the following parameters: branches, junctions, end-point voxels, junction voxels, slab voxels, triple points, quadruple points, average branch length, and maximum branch length. Results: We observed that both variants of fractal dimension in males and females did not show significant differences, although most quantitative parameters in males were larger than those in females. Conclusions: The spatial and structural complexity of the cerebral hemispheres, as characterized by fractal dimensions, is almost indistinguishable between males and females. However, in some individual brain sections, the male brain may exhibit a slightly higher number of end-point voxels, corresponding to the gyri of the cerebral hemispheres. The obtained data can be used in clinical practice for diagnostic purposes (e.g., for detecting malformations) and for theoretical studies in neuroanatomy. [ABSTRACT FROM AUTHOR]

Rabies, one of the earliest known diseases reported in the history of mankind, is a fatal acute viral disease of the central nervous system. Despite numerous studies on etiology of rabies, its exact mechanism of neuropathogenesis remains unidentified. Glutamate ammonia ligase (GLUL) is a protein present in brain which play an important role in the pathogenesis of many neurological conditions. GLUL was identified to be over expressed in brain of human rabies. Cerebral cortex is the part of brain primarily responsible for coordination of movements and behaviour in animals and humans. Hence the work was designed to study the immunohistochemical localisation of GLUL in cerebrum in rabid carcasses in order to elucidate its role in the pathology of this deadly viral infection. The carcasses of 219 rabies suspected dogs that were brought to the Department of Veterinary Pathology, CVAS, Mannuthy, for necropsy between January 2021 and August 2022 formed the materials for the study. One hundred and thirty-three cases were found positive for rabies using the gold standard test for rabies - Direct Fluorescent Antibody Test (dFAT) which was further confirmed by polymerase chain reaction targeting N gene with amplicon size 533 bp. Among these 133 confirmed cases, 30 selected samples (frontal, occipital, temporal, parietal lobes of cerebrum) were further processed for histopathological and immunohistochemical (IHC) studies. The IHC signals of GLUL obtained were compared with the clinical form of rabies. Immunohistochemical staining revealed localisation of GLUL in glial cells with different staining intensity in encephalitic and paralytic form of rabies. The study concluded that the IHC signals for GLUL were stronger for furious form of rabies and weak for dumb form of the disease.

Background and Aim: Magnetic resonance imaging (MRI) has been widely used as a non-invasive modality to evaluate neurological organ structures. However, brain MRI studies in cats with neurological signs are limited. This study evaluated the association between patient characteristics, neurological signs, and brain lesion locations identified by MRI. Blood profiles of cats with presumptive inflammatory and structural brain lesions were also determined. Materials and Methods: Medical records of 114 cats that underwent brain MRI were retrospectively reviewed. Cats were categorized into five groups based on the location of their lesion: Cerebrum, brainstem, cerebellum, multifocal, and non-structural. Patient characteristics, neurological signs, and hematological profiles were obtained from their medical records. Disease classification was categorized based on their etiologies. Associations were determined using Fisher's exact test. Blood parameters were compared using the Kruskal-Wallis test. Results: A total of 114 cats met the inclusion criteria. Lesions were identified in the cerebrum (21.1%), brainstem (8.8%), cerebellum (6.1%), multifocal (39.5%), and non-structural (24.6%) of the cats. Common neurological signs included seizure activity (56.1%), cerebellar signs (41.2%), and anisocoria (25.4%). The most common brain abnormality was inflammation (40.4%). There was no significant difference in hematological profiles between cats with presumptive inflammatory and non-inflammatory brain lesions. Neutrophils, platelets, total protein, and globulin concentrations were higher in cats with structural brain lesions. Conclusion: The most common neurological signs and brain disease category were seizure activity and inflammation, respectively. However, the hematological profile did not predict inflammatory and structural brain lesions. Further studies with a large number of birds are required to molecularly characterize the circulating strains of this virus in this area.

Background: Size of fourth ventricle varies in different pathologies, in the context of enlarged brain ventricles size observed in routine clinical practices, knowledge of the usual range of exact measurement is required. Aims and Objectives: This study is hospital-based observational study to derive normal measurement range of fourth ventricle and correlating it with measurements of cerebrum and age of patients. Materials and Methods: Hospital-based prospective study was conducted in the department of radiodiagnosis in a teaching medical college. Patients with virtually normal study on unenhanced head CT scan of both sex and age groups from 2 year to 60 years, were included in the study. Patients with CT scans showing gross pathological changes affecting the normal anatomy of ventricles were excluded from the study. Results: The mean age of the cases was 37.0±16.88 years. Mean fourth ventricle anterioposterior dimension is 7.5±2.5 mm and transverse dimension is 12±3.1 mm. Anteroposterior diameter of fourth ventricle showed non-significant correlation (r=0.06, P=0.56) with anteroposterior diameter of skull and no significant correlation with (r=0.07, P=0.45) transverse diameter (TD) of skull. AP diameter of fourth ventricle showed a positive correlation with age, which was statistically significant (r2=0.698, P=0.01). TD of fourth ventricle showed slight positive correlation (r=0.202 P=0.048) with anteroposterior diameter of skull and (r=0.142, P=0.168) TD of skull whereas nil with. TD of fourth ventricle showed a positive correlation with age, which was statistically non-significant (r2=0.659, P=0.01). It increases with age. Conclusion: Knowledge of normal measurements helps in assessing, dilated fourth ventricle in various pathologies.

Introduction: The measurement of brain volume is an important aspect of the assessment of brain structure and function. However, limited data is available on brain volumetry in the Nepalese population. The study aimed to find the mean intracranial volume of the brain among patients with normal magnetic resonance imaging referred to the Department of Radiology and Imaging of a tertiary care centre. Methods: A descriptive cross-sectional study was conducted among patients with normal magnetic resonance imaging referred to the Department of Radiology and Imaging in a tertiary care centre. All magnetic resonance imaging of the brain during the study period was reviewed by a radiologist. Magnetic resonance imaging with abnormal findings, clinical signs of neurological deficit, dementia and psychiatric symptoms were excluded from the study. A convenience sampling method was used. The point estimate was calculated at a 95% Confidence Interval. Results: Among 285 Magnetic Resonance Imaging datasets, the mean intracranial volume was 1286.30±129.88 cc (1271.22-1301.38, 95% of Confidence Interval). The mean cerebral volume was 985.06±106.4 cc, cerebellar volume was 126.99±13.05 cc and brain stem volume was 19.97±2.54 cc. Conclusions: The mean intracranial volume of the brain among patients with normal magnetic resonance imaging was found to be lower than other studies done in similar settings.

Este artigo apresenta um estudo envolvendo o protótipo de agente conversacional desenvolvido na plataforma Watson Assistant (IBM). O objetivo da investigação é analisar a usabilidade do agente conversacional como ferramenta de aprendizagem de matemática em equações algébricas. Para a avaliação, foi utilizado um sistema de avaliação de agentes conversacionais, denominado como ChatAval. A metodologia utilizada é qualitativa exploratória, pois consiste em analisar os dados obtidos pelos aplicativos tecnológicos Cerebrum e ChatAval. Os resultados da investigação de usabilidade do Cerebrum, com alunos da graduação de Licenciatura de Matemática, permitem concluir que a usabilidade do agente conversacional apresentou efetividade, eficiência e satisfação do usuário, acima do escore, na utilização do Cerebrum, sendo assim, é possível qualificar positivamente o seu desempenho e dar continuidade no seu desenvolvimento, implementado melhorias na ferramenta em estudo.

To study the effects of Cu overload on ER quality control in duck cerebrums, 144 ducks were treated with 8 mg/kg, 100 mg/kg, 200 mg/kg and 400 mg/kg Cu added in the feed for 45 days. From histopathological examination, we found that excessive Cu increased the amount of microglia and disintegrated neuron, decreased the number of Nissl bodies, perturbed nerve fibers in duck cerebrums. Cu poisoning also increased Cu, H2O2, T-SOD, and MDA levels, decreased Fe and CAT contents in duck cerebrums. Furthermore, Cu treatment upregulated the mRNA levels of the unfolded protein response genes (PERK, ATF6, and IRE1), ER-associated degradation genes (CNX, Derlin1, and Derlin2), autophagy genes (ATG5, ATG7, ATG10, Beclin1, LC3A, LC3B, and P62), and heat shock response genes (Hsp70 and Hsp90) in duck cerebrums; elevated the protein levels of p-PERK, CNX, SEL1L, Beclin1, P62, and LC3BII/LC3BI in duck cerebrums; increased the numbers of SEL1L and LC3B puncta in duck cerebrums. Thus, our data showed that excessive Cu could cause histopathological damage to duck cerebrums, disrupt the balance of the trace elements, induce oxidative stress and activation of ER quality control, thereby resulting in duck cerebrums damage. [ABSTRACT FROM AUTHOR]

Aim: The aim of the present study was to characterize age-associated changes in the spatial configuration of cerebral hemispheres (including changes in spatial complexity and space-filling capacity) using fractal analysis of silhouette magnetic resonance brain images. Material and Methods: Magnetic resonance brain images of 100 (44 male, 56 female) participants aged between 18-86 years were studied. Five magnetic resonance images were selected from the magnetic resonance imaging dataset of each brain, including four tomographic sections in the coronal plane and one in the axial plane. Fractal dimension values of the cerebral hemispheres silhouettes were measured using the two-dimensional box-counting algorithm. Morphometric parameters based on Euclidean geometry (perimeter, area, and their derivative values) were determined as well. Results: The average fractal dimension value of the five studied tomographic sections was 1.878±0.0009, the average value of four coronal sections was 1.868±0.0010. It was shown that fractal dimension values of cerebral silhouettes for all studied tomographic sections and four coronal sections significantly decrease with age (r=-0.512, p

Rabies, one of the earliest known diseases reported in the history of mankind, is a fatal acute viral disease of the central nervous system. Despite numerous studies on etiology of rabies, its exact mechanism of neuropathogenesis remains unidentified. Glutamate ammonia ligase (GLUL) is a protein present in brain which play an important role in the pathogenesis of many neurological conditions. GLUL was identified to be over expressed in brain of human rabies. Cerebral cortex is the part of brain primarily responsible for coordination of movements and behaviour in animals and humans. Hence the work was designed to study the immunohistochemical localisation of GLUL in cerebrum in rabid carcasses in order to elucidate its role in the pathology of this deadly viral infection. The carcasses of 219 rabies suspected dogs that were brought to the Department of Veterinary Pathology, CVAS, Mannuthy, for necropsy between January 2021 and August 2022 formed the materials for the study. One hundred and thirty-three cases were found positive for rabies using the gold standard test for rabies - Direct Fluorescent Antibody Test (dFAT) which was further confirmed by polymerase chain reaction targeting N gene with amplicon size 533 bp. Among these 133 confirmed cases, 30 selected samples (frontal, occipital, temporal, parietal lobes of cerebrum) were further processed for histopathological and immunohistochemical (IHC) studies. The IHC signals of GLUL obtained were compared with the clinical form of rabies. Immunohistochemical staining revealed localisation of GLUL in glial cells with different staining intensity in encephalitic and paralytic form of rabies. The study concluded that the IHC signals for GLUL were stronger for furious form of rabies and weak for dumb form of the disease. [ABSTRACT FROM AUTHOR]

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Background: Size of fourth ventricle varies in different pathologies, in the context of enlarged brain ventricles size observed in routine clinical practices, knowledge of the usual range of exact measurement is required. Aims and Objectives: This study is hospital-based observational study to derive normal measurement range of fourth ventricle and correlating it with measurements of cerebrum and age of patients. Materials and Methods: Hospitalbased prospective study was conducted in the department of radiodiagnosis in a teaching medical college. Patients with virtually normal study on unenhanced head CT scan of both sex and age groups from 2 year to 60 years, were included in the study. Patients with CT scans showing gross pathological changes affecting the normal anatomy of ventricles were excluded from the study. Results: The mean age of the cases was 37.0±16.88 years. Mean fourth ventricle anterioposterior dimension is 7.5±2.5 mm and transverse dimension is 12±3.1 mm. Anteroposterior diameter of fourth ventricle showed non-significant correlation (r=0.06, P=0.56) with anteroposterior diameter of skull and no significant correlation with (r=0.07, P=0.45) transverse diameter (TD) of skull. AP diameter of fourth ventricle showed a positive correlation with age, which was statistically significant (r2=0.698, P=0.01). TD of fourth ventricle showed slight positive correlation (r=0.202 P=0.048) with anteroposterior diameter of skull and (r=0.142, P=0.168) TD of skull whereas nil with. TD of fourth ventricle showed a positive correlation with age, which was statistically non-significant (r2=0.659, P=0.01). It increases with age. Conclusion: Knowledge of normal measurements helps in assessing, dilated fourth ventricle in various pathologies. [ABSTRACT FROM AUTHOR]

A comprehensive inference of the structural alterations that occur in the body after death plays a pivotal role in the accurate interpretation of the time since death in many human and animal death investigations. Particular estimation of post-mortem interval (PMI) is usually affected by many frequently changed environmental and other factors that influence the sequential changes that happen to a body after death. Histopathologic investigation in autopsy is a unique technique to investigate PMI. Moreover, it is a supplementary investigation in cases where macroscopic examinations fail to display a diagnostic pathology regarding death. Here, we investigated the post-mortem histopathological changes in rats' brains to pinpoint the time that elapsed since death. For this purpose, we used 72 male Sprague-Dawley rats divided into two main groups 36 young-aged rats and 36 adult-aged rats. The two main groups were subdivided into 6 subgroups (6 rats/subgroup). After accommodation, rats were cervically dislocated and intact brain was collected at 0-hour post-mortem and at the 2nd, 4th, 8th, 12th, and 24th h post-mortem at room temperature (RT) and 4°C. The histopathological changes of collected brain tissues revealed that the post-mortem changes begin to be emphasized after 8 h post-mortem in both young and adult rats at RT than at 4°C. Those changes included hemorrhage, mild neuronal degeneration, and apoptotic neurons that were prominent in the cerebral cortex. Moreover, cerebral cortex histopathologic changes continued till 24 h post-mortem. Also, the cerebellar changes followed the same path as the cerebral ones. However, the results deduced that the post-mortem changes were prominent at RT in young-aged rats. In conclusion, observation of the histopathological changes of brain tissue under certain individual and environmental circumstances can be an effective, inexpensive, and additional tool to accurately estimate the PMI. [ABSTRACT FROM AUTHOR]

Background: The therapeutic efficacy of stem cell therapy in many diseased organs based greatly on their paracrine effect. The neural stem cells are thought to have a role in improving the neurological functional, recovery, and reduction of cerebral infarction caused by cerebral ischemia/ reperfusion [I/R] injury in rats.Objective: This study was conducted to look at the histological alterations in the rat cerebral cortex after ischemia-reperfusion [I/R] injury and to assess any potential neuroprotective effects of neural stem cells conditioned media [NSC-CM] on on those changes.Material and Methods: Thirty adult male albino rats weighing about 150 - 250 gm each were used in the present work. The animals were equally divided into 3 groups [10 rats each]. Group A was subdivided into negative control group, A1, [5 rats], not subjected to any intervention, and the sham-control group, A2 [5 rats], the animal of which were subjected to a midline cervical incision with exposure of both common carotid arteries followed by closure of the incision. Group B included rats subjected to brain [I/R] to induce transient global brain ischemia. Group C included rats subjected to I/R injury [as group B] and received 1.5 ml NSC-CM injected slowly through the tail vein at 3 h, 24 h, and 48 h after ischemia onset. Animals were anaesthetized using ether inhalation, the cerebrum was dissected and fixed in 10% neutral buffered formalin and specimens from them were taken and processed for examination by light microscopes.Results: NSC-CM significantly ameliorated neurological defects by reducing cerebral infarct volume, significant inhibition of cell apoptosis in the ischemic cerebral hemisphereConclusion: NSC-CM might be an alternative and effective therapeutic intervention for ischemic stroke.

Objectives: Involvement of central nervous system (CNS) by Hydatid cyst is rare comprising 0.5-4% of all hydatid cysts and principally affecting those younger than 20 years, giving rise to cystic masses mostly in the cerebral hemispheres. To report the clinicopathological findings of CNS hydatid cysts, we diagnosed and review the findings of the previous studies. Materials and Methods: All cases reported in our Section between January 1, 2001, and June 30, 2022, were included in the study. By searching our files, cases were retrieved, and diagnosis was confirmed. Follow-up was received on telephone. Ethical exemption was obtained. Results: Thirty-three cases were diagnosed. Almost all were received from rural areas. There were 17 females and 16 males. Mean and median age were 20 and 19 years, respectively. Over 60% were younger than 20 years of age. All 33 involved the cerebral and cerebellar hemispheres. Seventy six percent were supratentorial while 24% were infratentorial. The most common signs and symptoms included weakness, headaches, and seizures. All appeared as solitary cystic masses on imaging. Almost 67% were clinically suspected to be hydatid cysts. Grossly, thin-walled transparent unilocular or multilocular cysts filled with viscous material were received intact in 52% and in multiple pieces in 48% cases. Intact cysts measured 7 cm on average. All demonstrated typical histology. Of the nine patients whose follow-up was available, one died from unspecified acute surgery related complications. Four patients were asymptomatic at the time of follow-up, whereas four developed recurrent cysts. All eight received albendazole therapy. Conclusion: Cerebellum/posterior fossa location was common. Several cases were received in multiple pieces with increased risk of recurrence. Clinicopathological features were similar to those reported in literature. This series will hopefully serve to increase awareness regarding CNS hydatid disease. [ABSTRACT FROM AUTHOR]

The major increase in cetacean brain size happened in the middle Miocene, about 15 million years ago, and involved the modern oceanic dolphin lineage Delphinoidea. In this paper, we describe a new specimen of an archaic dolphin, aff. Prosqualodon davidis, from the Gee Greensand, near Oamaru, New Zealand. The specimen is from the early Miocene, approximately 23–19–18 Ma, and includes an incomplete cranium, endocast, teeth, and some postcranial elements. Comparison of the median sulcus among previously reported endocasts and brains of the Cetacea suggests that the cerebrum was expanded incipiently in the Odontoceti from the early Miocene in the Eurhinodelphinidae + Delphinoidea lineage. Conversely, the olfactory fossa has been reduced in Odontoceti, and completely lost in at least two clades (Delphinoidea and Platanista gangetica), because olfaction was most likely no longer an essential sense for animals spending their life in water. Reduction and loss of the olfactory fossa saved energy, which may be related to the expansion of the cerebrum and cortex in an Odontoceti lineage that led to modern oceanic dolphins. The early Miocene appears to have been a transitional period for archaic and modern-type odontocetes, which were possibly and partly separated by these differences. [ABSTRACT FROM AUTHOR]

Copper (Cu) is an essential trace element for growth and development in most organisms. However, environmental exposure to high doses of Cu can damage multiple organs. To investigate the underlying mechanism of Cu toxicity on mitochondrial dynamics and mitophagy in the cerebrum of pigs, 60 30-day-old pigs were randomly divided into three groups and treated with different contents of anhydrous Cu sulfate in the diets (Cu 10 mg/kg, control group; Cu 125 mg/kg, group I; Cu 250 mg/kg, group II) for 80 days. The Cu levels and histological changes in the cerebrum were measured. Moreover, the protein and mRNA expression levels related to mitophagy and mitochondrial dynamics were determined. The results showed that the contents of Cu were increased in the cerebrum with increasing dietary Cu. Vacuolar degeneration was found in group I and group II compared to the control group. Additionally, the protein and mRNA expression levels of PINK1, Parkin, and Drp1 and the protein level of LC3-II were remarkably upregulated with increasing levels of dietary Cu. Nevertheless, the protein and mRNA expression levels of MFN1 and MFN2 and the mRNA expression of P62 were obviously downregulated in a Cu dose-dependent manner. Overall, these results suggested that excess Cu could trigger mitochondrial dynamics disorder and mitophagy in the pig cerebrum, which provided a novel insight into Cu-induced toxicology. [ABSTRACT FROM AUTHOR]

A large amount of copper (Cu) used in production activities can lead to the enrichment of Cu in the environment, which can cause toxicity to animals. However, the toxicity mechanism of Cu on the cerebrum is still uncertain. Hence, a total of 240 chickens were separated into four groups in this study to reveal the potential connection between mitophagy and endoplasmic reticulum (ER) stress‐mediated apoptosis in the chicken cerebrum in the case of excess Cu exposure. The cu exposure situation was simulated by diets containing various levels of copper (11 mg/kg, control group; 110 mg/kg, group I; 220 mg/kg, group II and 330 mg/kg, group III) for 49 days. The results of histology showed that vacuolar degeneration was observed in the treated groups, and the mitochondria swell and autophagosomes formation were found under excess Cu treatment. Additionally, the expression of mitophagy (PINK1, Parkin, LC3I, LC3II and p62) and ER stress (GRP78, PERK, ATF6, IRE1α, XBP1, CHOP, and JNK) indexes were significantly upregulated under excess Cu exposure. Furthermore, the mRNA and protein expression of Bcl‐2 were decreased, while Bak1, Bax, Caspase12, and Caspase3 were increased compared to the control group. In summary, this study demonstrated that an overdose of Cu could induce mitophagy and ER stress‐mediated apoptosis in the chicken cerebrum. These findings revealed an important potential connection between Cu toxicity and cerebrum damage, which provided a new insight into Cu neurotoxicity. [ABSTRACT FROM AUTHOR]

Patients with COVID-19 have been reported to experience neurological complications, although the main cause of death in these patients was determined to be lung damage. Notably, SARS-CoV-2-induced pathological injuries in brains with a viral presence were also found in all fatal animal cases. Thus, an appropriate animal model that mimics severe infections in the lungs and brain needs to be developed. In this paper, we compared SARS-CoV-2 infection dynamics and pathological injuries between C57BL/6Smoc-Ace2em3(hACE2-flag-Wpre-pA)Smoc transgenic hACE2-C57 mice and Syrian hamsters. Importantly, the greatest viral distribution in mice occurred in the cerebral cortex neuron area, where pathological injuries and cell death were observed. In contrast, in hamsters, viral replication and distribution occurred mainly in the lungs but not in the cerebrum, although obvious ACE2 expression was validated in the cerebrum. Consistent with the spread of the virus, significant increases in IL-1β and IFN-γ were observed in the lungs of both animals. However, in hACE2-C57 mice, the cerebrum showed noticeable increases in IL-1β but only mild increases in IFN-γ. Notably, our findings revealed that both the cerebrum and the lungs were prominent infection sites in hACE2 mice infected with SARS-CoV-2 with obvious pathological damage. Furthermore, hamsters exhibited severe interstitial pneumonia from 3 dpi to 5 dpi, followed by gradual recovery. Conversely, all the hACE2-C57 mice experienced severe pathological injuries in the cerebrum and lungs, leading to mortality before 5 dpi. According to these results, transgenic hACE2-C57 mice may be valuable for studying SARS-CoV-2 pathogenesis and clearance in the cerebrum. Additionally, a hamster model could serve as a crucial resource for exploring the mechanisms of recovery from infection at different dosage levels.

Abstract A neonatal Dutch Warmblood colt was evaluated for inability to stand, incoordination and intention tremor. Despite partial improvement in clinical signs during the first 4 days of hospitalization, neurological deficits remained. Magnetic resonance imaging identified a unilateral infratentorial arachnoid cyst‐like lesion with ipsilateral compression and displacement of the cerebellar hemisphere, absent corpus collosum, polymicrogyria, suspect leukoencephalopathy, and noncompressive occipitoatlantal malformation. Improvement in clinical signs during the first 6 months of life suggests that horses can survive with complex congenital neurological malformations, but prognosis for athletic performance is poor. The accessibility of magnetic resonance imaging should improve the diagnostic accuracy of central nervous system disorders in neonatal foals in which congenital malformations are suspected. Euthanasia often is elected in foals with suspected congenital central nervous system disorders because of poor prognosis for athletic performance, limiting understanding of clinical progression in these cases.

Aim: The aim of the present study was to characterize age-associated changes in the spatial configuration of cerebral hemispheres (including changes in spatial complexity and space-filling capacity) using fractal analysis of silhouette magnetic resonance brain images. Material and Methods: Magnetic resonance brain images of 100 (44 male, 56 female) participants aged between 18-86 years were studied. Five magnetic resonance images were selected from the magnetic resonance imaging dataset of each brain, including four tomographic sections in the coronal plane and one in the axial plane. Fractal dimension values of the cerebral hemispheres silhouettes were measured using the two-dimensional box-counting algorithm. Morphometric parameters based on Euclidean geometry (perimeter, area, and their derivative values) were determined as well. Results: The average fractal dimension value of the five studied tomographic sections was 1.878±0.0009, the average value of four coronal sections was 1.868±0.0010. It was shown that fractal dimension values of cerebral silhouettes for all studied tomographic sections and four coronal sections significantly decrease with age (r=-0.512, p<0.001 and r=-0.491, p<0.001, respectively). The difference in the character of age-related changes in males and females was not statistically significant. Based on the age and the fractal dimension values of the studied sample, the confidence intervals of the fractal dimension values of cerebral hemispheres silhouettes were determined, which can be used as norm criteria in clinical neuroimaging. Conclusion: The fractal analysis and obtained data can be used in neuroimaging for assessing the degree of age-related cerebral atrophy and for differentiating between normal aging and neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Introduction: People living in highland areas may have factors that allow themto adapt to chronic hypoxia, but these physiologicalmechanisms remain unclear. This study aimed to investigate the brain mechanism in a cohort of adult residents of Tibet, a well-known plateau section in China, by observing differences in brain structure and function in non-plateau populations. Methods: The study included 27 Tibetan and 27 non-plateau region residents who were matched in age, sex, and education. All participants underwent high-resolution three-dimensional T1 weighted imaging (3D-T1WI) and resting-state functional magnetic resonance imaging (rs-fMRI) scans on a 1.5 Tesla MR. Gray matter volumes and regional spontaneous neuronal activity (SNA) were calculated and compared between the two groups. Results: When comparing graymatter in people living in high altitudes to those living in the flatlands, the results showed positive activation of gray matter in local brain regions (p < 0.05, false discovery rate (FDR) corrected), in the right postcentral [automated atomic labeling (aal)], left postcentral (aal), and right lingual (aal) regions. Comparing the people of high altitude vs. flat land in the brain function study (p < 0.05, FDR corrected), positive activation was found in the right superior motor area (aal) and left superior frontal (aal), and negative activation was found in the right precuneus (aal). Conclusion: In high-altitude individuals, larger regional gray matter volumes and higher SNA may represent a compensatory mechanism to adapt to chronic hypoxia. [ABSTRACT FROM AUTHOR]

Although formaldehyde is the most widely used and largely available fixative for preserving cadavers through decomposition prevention, it promotes darkening and weight gain, in addition to being considered carcinogenic. Ethyl alcohol has been proven a potential substitute to formaldehyde due to its effectiveness in tissue penetration, thus preventing proliferation of microorganisms; however, it can only be used alone for fixation of small parts. In view of such fixatives limitations, saturated salt solution has been widely employed based on its antimicrobial effect and ability to maintain tissue similar to the original one, in addition to exerting no hazardous effects as there is no evaporation of harmful substances. This research aimed to observe anatomical brain behaviour submitted to formaldehyde, alcohol, and saturated salt solution as fixatives. Fixatives were tested in 15 adult Wistar rats' brain, submerged in 10 ml of intended solution after removal for 4 weeks. Weight of the brains fixed in saturated salt did not change over the weeks. However, the weight of formaldehyde‐fixed brains increased and the weight in alcohol‐fixed brains decreased; in addition, modifications in all solutions measures were also observed. Alcohol provides a peculiar dehydrating effect as formaldehyde clearly increases the length of the pieces. Thus, since the saturated salt solution showed no important adjustment over the experimental time, it proved an efficient alternative for replacing formaldehyde and alcohol as fixative solutions of anatomical study of the brain. [ABSTRACT FROM AUTHOR]

In rodent models, leukemia inhibitory factor (LIF) is involved in cerebral development via the placenta, and maternal immune activation is linked to psychiatric disorders in the child. However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA microarray analysis and quantitative RT-PCR on the fetal cerebrum after maternal intraperitoneal or fetal intracerebral ventricular injection of LIF at day 14.5 (E14.5) and determined that the expression of insulin-like growth factors (IGF)-1 and -2 was induced by LIF. Physiological IGF-1 and IGF-2 levels in fetal cerebrospinal fluid (CSF) increased from E15.5 to E17.5, following the physiological surge of LIF levels in CSF at E15.5. Immunostaining showed that IGF-1 was expressed in the cerebrum at E15.5 to E19.5 and IGF-2 at E15.5 to E17.5 and that IGF-1 receptor and insulin receptor were co-expressed in NPCs. Further, LIF treatment enhanced cultured NPC proliferation, which was reduced by picropodophyllin, an IGF-1 receptor inhibitor, even under LIF supplementation. Our findings suggest that IGF expression and release from the NPCs of the fetal cerebrum in fetal CSF is induced by LIF, thus supporting the involvement of the LIF–IGF axis in cerebral cortical development in an autocrine/paracrine manner. [ABSTRACT FROM AUTHOR]

Metformin is one of the most commonly used oral hypoglycemic drugs in clinical practice, with unique roles in neurodegeneration and vascular lesions. Neurodegeneration and vasculopathy coexist in many diseases and typically affect the neurovascular unit (NVU), a minimal structural and functional unit in the central nervous system. Its components interact with one another and are indispensable for maintaining tissue homeostasis. This review focuses on retinal (diabetic retinopathy, retinitis pigmentosa) and cerebral (ischemic stroke, Alzheimer's disease) diseases to explore the effects of metformin on the NVU. Metformin has a preliminarily confirmed therapeutic effect on the retinal NUV, affecting many of its components, such as photoreceptors (cones and rods), microglia, ganglion, Müller, and vascular endothelial cells. Since it rapidly penetrates the blood–brain barrier (BBB) and accumulates in the brain, metformin also has an extensively studied neuronal protective effect in neuronal diseases. Its mechanism affects various NVU components, including pericytes, astrocytes, microglia, and vascular endothelial cells, mainly serving to protect the BBB. Regulating the inflammatory response in NVU (especially neurons and microglia) may be the main mechanism of metformin in improving central nervous system related diseases. Metformin may be a potential drug for treating diseases associated with NVU deterioration, however, more trials are needed to validate its timing, duration, dose, clinical effects, and side effects. [ABSTRACT FROM AUTHOR]

• Studies have focused on brain analysis with manual volumetry being the main technique. • Structural and functional analysis in frail older people may expand the knowledge on the implications of frailty on the Central Nervous System. • More research is also needed on the brain areas where changes may impact frailty in older adults, notably those that are not age-related. Little is known about changes in the brain associated with frailty, in particular, which brain areas could be related to frailty in older people without cognitive impairment. This scoping review mapped evidence on functional and/or structural brain changes in frail older adults without cognitive impairment. The methodology proposed by the JBI® was used in this study. The search in PubMed, PubMed PMC, BVS/BIREME, EBSCOHOST, Scopus, Web of Science, Embase, and PROQUEST was conducted up to January 2023. Studies included following the population, concepts, context and the screening and data extraction were performed by two independent reviewers. A total of 9,912 records were identified, 5,676 were duplicates and were excluded. The remaining articles were screened; 31 were read in full and 17 articles were included. The results showed that lesions in white matter hyperintensities, reduced volume of the hippocampus, cerebellum, middle frontal gyrus, low gray matter volume, cortical atrophy, decreased connectivity of the supplementary motor area, presence of amyloid-beta peptide (aβ) in the anterior and posterior putamen and precuneus regions were more frequently observed in frail older adults, compared with non-frail individuals. Studies have suggested that such findings may be of neurodegenerative or cerebrovascular origin. The identification of these brain alterations in frail older adults through neuroimaging studies contributes to our understanding of the underlying mechanisms of frailty. Such findings may have implications for the early detection of frailty and implementation of intervention strategies. [ABSTRACT FROM AUTHOR]

Spider brain and central nervous system (CNS) have remained unexplored, due in part to the difficulty of observing these organs, usually only possible through histological preparations. Recently, internal anatomy studies have been supplemented by the inclusion of X‐ ray micro‐CT. Unmineralized tissue such as the body of invertebrates requires a staining process to enhance tissue X‐ray absorption and improve contrast during observation. Many current protocols are based on iodine staining requiring critical point drying (CPD) of the sample for optimal contrast. This process induces shrinking of the soft tissue generating artifacts in the morphology, volume, and even position of internal structures. Phosphotungstic acid (PTA) is an alternative staining agent recently used in marine invertebrate and plant studies. Here, we used several specimens of the common spider Araneus diadematus to visualize the spider brain and compare both contrast‐enhancing ethanol‐based solutions. We assessed a gradient of staining times, observed and tested the repercussions of CPD, and examined the use of vacuum to accelerate PTA diffusion. We show that PTA provides the best contrast on micro‐CT scans in ethanol eliminating the need for CPD, and offering more realistic in situ visualizations of the internal organs. In combination with different scanning settings, PTA allowed observation of internal organs like the CNS, digestive system, muscles, and finer structures like the retina, visual nerves, and optic neuropiles. This fast and less invasive method could facilitate the proper documentation of the internal anatomy in the context of evolutionary, developmental and functional studies. [ABSTRACT FROM AUTHOR]

Imidazole dipeptides (ID) are abundant in skeletal muscle and the brain and have various functions, such as antioxidant, pH-buffering, metal-ion chelation. However, the physiological significance of ID has not been fully elucidated. In this study, we orally administered ID to conventional carnosine synthase gene-deficient mice (Carns -KO mice) to investigate the pharmacokinetics. Carnosine or anserine was administered at a dose of 500 mg (~2 mmol) per kilogram of mouse body weight, and ID contents in the tissues were measured. No ID were detected in untreated Carns -KO mice. In the ID treatment groups, the ID concentrations in the tissues increased in a time-dependent manner in the gastrocnemius muscle, soleus muscle, and cerebrum after ID administration. Our findings suggest that the Carns -KO mice are a valuable animal model for directly evaluating the effects of dietary ID and for elucidating the physiological functions of oral ID administration. [ABSTRACT FROM AUTHOR]

Hyperlipidemia is a chronic disease characterized by elevated blood cholesterol and triglycerides and there is accumulated evidence that the disease might affect brain functions. Here we report on a proteomic analysis of the brain proteins in hyperlipidemic mice. Hyperlipidemia was successfully induced in mice by a 20 week high-fat diet (HFD) feeding (model group). A control group with a normal diet and a treatment group with HFD-fed mice treated with a lipid-lowering drug simvastatin (SIM) were established accordingly. The proteins were extracted from the left and right cerebrum hemispheres of the mice in the three groups and subjected to shotgun proteomic analysis. A total of 4,422 proteins were detected in at least half of the samples, among which 324 proteins showed significant difference (fold change >1.5 or <0.67, p < 0.05) in at least one of the four types of comparisons (left cerebrum hemispheres of the model group versus the control group, right cerebrums of model versus control, left cerebrums of SIM versus model, right cerebrums of SIM versus model). Biological process analysis revealed many of these proteins were enriched in the processes correlated with lipid metabolism, neurological disorders, synaptic events and nervous system development. For the first time, it has been reported that some of the proteins have been altered in the brain under the conditions of HFD feeding, obesity or hyperlipidemia. Further, 22 brain processes-related proteins showed different expression in the two cerebrum hemispheres, suggesting changes of the brain proteins caused by hyperlipidemia might also be asymmetric. We hope this work will provide useful information to understand the effects of HFD and hyperlipidemia on brain proteins. [ABSTRACT FROM AUTHOR]

Brain asymmetry is associated with handedness and cognitive function, and is also reflected in the shape of endocasts. However, comprehensive quantification of the asymmetry in endocast shapes is limited. Here, we quantify and visualize the variation of endocast asymmetry in modern humans using diffeomorphic surface matching. Our results show that two types of lobar fluctuating asymmetry contribute most to global asymmetry variation. A dominant pattern of local directional asymmetry is shared in the majority of the population: (1) the left occipital pole protrudes more than the right frontal pole in the left-occipital and right-frontal petalial asymmetry; (2) the left Broca's cap appears to be more globular and bulges laterally, anteriorly, and ventrally compared to the right side; and (3) the asymmetrical pattern of the parietal is complex and the posterior part of the right temporal lobes are more bulbous than the contralateral sides. This study confirms the validity of endocasts for obtaining valuable information on encephalic asymmetries and reveals a more complicated pattern of asymmetry of the cerebral lobes than previously reported. The endocast asymmetry pattern revealed here provides more shape information to explore the relationships between brain structure and function, to re-define the uniqueness of human brains related to other primates, and to trace the timing of the human asymmetry pattern within hominin lineages. [ABSTRACT FROM AUTHOR]

Gluten ataxia is a rare immune-mediated neurological disorder caused by the ingestion of gluten. The diagnosis is not straightforward as antibodies are present in only up to 38% of patients, but often at lower titers. The symptoms of ataxia may be mild at the onset but lead to permanent damage if remain untreated. It is characterized by damage to the cerebellum however, the pathophysiology of the disease is not clearly understood. The present study investigated the neurochemical profile of vermis and right cerebellum and structural changes in various brain regions of patients with gluten ataxia (n = 6, age range 40–65 years) and compared it with healthy controls (n = 10, 40–55 years). Volumetric 3-D T1 and T1-weighted magnetic resonance imaging (MRI) in the three planes (axial, coronal, and sagittal) of the whole brain and single-voxel 1H- magnetic resonance spectroscopy (MRS) of the vermis and right cerebellum were acquired on 3 T human MR scanner. The metabolite concentrations were estimated using LC Model (6.1–4A) while brain volumes were estimated using the online tool volBrain pipeline and CERES and corrected for partial volumes. The levels of neuro-metabolites (N-acetyl aspartate + N-acetyl aspartate glutamate, glycerophosphocholine + phosphocholine, and total creatine) were found to be significantly lower in vermis, while N-acetyl aspartate + N-acetyl aspartate glutamate and glycerophosphocholine + phosphocholine was lower in cerebellum regions in the patients with gluten ataxia compared to healthy controls. A significant reduction in the white matter of (total brain, cerebellum, and cerebrum); reduction in the volumes of cerebellum lobe (X) and thalamus while lateral ventricles were increased in the patients with gluten ataxia compared to healthy controls. The reduced neuronal metabolites along with structural changes in the brain suggested neuronal degeneration in the patients with gluten ataxia. Our preliminary findings may be useful in understanding the gluten-induced cerebral damage and indicated that MRI and MRS may serve as a non-invasive useful tool in the early diagnosis, thereby enabling better management of these patients. [ABSTRACT FROM AUTHOR]

A neonatal Dutch Warmblood colt was evaluated for inability to stand, incoordination and intention tremor. Despite partial improvement in clinical signs during the first 4 days of hospitalization, neurological deficits remained. Magnetic resonance imaging identified a unilateral infratentorial arachnoid cyst‐like lesion with ipsilateral compression and displacement of the cerebellar hemisphere, absent corpus collosum, polymicrogyria, suspect leukoencephalopathy, and noncompressive occipitoatlantal malformation. Improvement in clinical signs during the first 6 months of life suggests that horses can survive with complex congenital neurological malformations, but prognosis for athletic performance is poor. The accessibility of magnetic resonance imaging should improve the diagnostic accuracy of central nervous system disorders in neonatal foals in which congenital malformations are suspected. Euthanasia often is elected in foals with suspected congenital central nervous system disorders because of poor prognosis for athletic performance, limiting understanding of clinical progression in these cases. [ABSTRACT FROM AUTHOR]

Formalin is used for different purposes due to its preservation capability. But continuous exposure to formalin may result various health related issues leading to cancer and death. A new alcohol-based fixative, EMA (ethanol, methanol and acetic acid = 3:1:1) could be a safer option in this regard. To compare the health hazards of formalin and EMA, a total 15 adult male mice were randomly distributed into three groups- exposure groups (formalin and EMA) and control group. The mice were subjected to natural inhalation exposure of the fixatives followed by behavioral depression test (forced swimming test), histopathology and serum biochemical tests. Our results showed that the hazardous effects of formalin were remarkably higher than that of EMA. Formalin exposed group showed severe depression (P < 0.001) in the forced swimming test compared to EMA and control groups. Histopathologically, diffuse lymphocytic infiltrations around the lung alveoli and bronchioles and severe inflammation with accumulation of reactive cells in the cerebral cortex were detected in the formalin exposed group, whereas little or no inflammation with fibrinous exudates in the bronchioles was reported in the EMA group and no inflammatory cells were detected in the cerebral tissues. The serum biochemical analysis of the inflammatory mediators (Interleukin-6 and C-reactive protein) revealed that both significantly (P < 0.001) increased in the formalin exposed group compared to EMA and control groups. These results confer that EMA could be a safer option to reduce health hazards of formalin in the workplace environment. [ABSTRACT FROM AUTHOR]

Mitochondria, as the powerhouse of the cell, play a vital role in maintaining cellular energy homeostasis and are known to be a primary target of cadmium (Cd) toxicity. The improper targeting of proteins to mitochondria can compromise the normal functions of the mitochondria. However, the precise mechanism by which protein localization contributes to the development of mitochondrial dysfunction induced by Cd is still not fully understood. For this research, Hy-Line white variety chicks (1-day-old) were used and equally distributed into 4 groups: the Control group (fed with a basic diet), the Cd35 group (basic diet with 35 mg/kg CdCl 2), the Cd70 group (basic diet with 70 mg/kg CdCl 2) and the Cd140 group (basic diet with 140 mg/kg CdCl 2), respectively for 90 days. It was found that Cd caused the accumulation of heat shock factor 1 (HSF1) in the mitochondria, and the overexpression of HSF1 in the mitochondria led to mitochondrial dysfunction and neuronal damage. This process is due to the mitochondrial HSF1 (mtHSF1), causing mitochondrial fission through the upregulation of dynamin-related protein 1 (Drp1) content, while inhibiting oligomer formation of single-stranded DNA-binding protein 1 (SSBP1), resulting in the mitochondrial DNA (mtDNA) deletion. The findings unveil an unforeseen role of HSF1 in triggering mitochondrial dysfunction. The objective of this study was to investigate the significance of HSF1 localization in the development of mitochondrial dysfunction caused by Cd exposure. It discovered that Cd caused the accumulation of HSF1 in the mitochondria, and the overexpression of HSF1 in the mitochondria led to mitochondrial dysfunction and neuronal damage. This process is due to mtHSF1-mediated mitochondrial fission by increasing Drp1 content, while inhibiting oligomer formation of SSBP1, resulting in the mtDNA deletion. The results reveal an undiscovered function of HSF1 in inducing impaired mitochondrial function by Cd exposure. [Display omitted] • Cd caused the accumulation of HSF1 in mitochondria. • The overexpression of HSF1 in mitochondria led to mitochondrial dysfunction and neuronal damage. • MtHSF1 caused mitochondrial fission by increasing Drp1. • MtHSF1 inhibited oligomer formation of SSBP1, resulting in mtDNA deletion. [ABSTRACT FROM AUTHOR]

Phenytoin, a drug of choice for Epilepsy is also known for its adverse effects. The most common adverse effect due to phenytoin is cognition impairment. Cognition impairment is a serious problem in society as it debars the person's social life. Thus to overcome such a problem demand for a solution arises. Huperzine, sesquiterpene alkaloids having immense neuroprotective properties. Thus in this study, it was aimed to evaluate the effectiveness of huperzine on Phenytoin-induced Cognition Impairment. The protective effect of huperzine on phenytoin-induced cognition impairment was evaluated in rats. The effect of Huperzine on phenytoin-induced cognitive impairment was evaluated by behavioral, biochemical, and histopathological studies. The co-administration of huperzine with phenytoin showed significant results. The treatment of Huperzine with phenytoin resulted in significant improvement in learning and memory. The oxidative stress induced by Phenytoin was reversed by huperzine. A significant decrease in cholinesterase activity was also observed. The histopathology showed damaged neuronal cells in periventricular regions and cortex due to phenytoin which was altered by Huperzine. Thus, the present study demonstrates the protective effect of huperzine on phenytoin-induced cognition impairment. [ABSTRACT FROM AUTHOR]

Lead toxicity is a common health issue. Lead (Pb) is harmful to vital organs of body particularly the nervous system. This study aimed to estimate the effects of lead on the cerebellum, cerebrum and spinal cord in rat model, focusing on histopathological changes. 24 female mature albino rats of 200-300g randomly divided into 2 groups, the first is the control, and the second group were treated with lead acetate at dose 30mg/kg B.W. for 30 days. Microscopic examination revealed degeneration and necrosis of Purkinje cells and molecular cells and decrease in the number of granular cells and molecular cells also observed. Some Purkinje cells lost axons and shrunken and some areas showed depletion of Purkinje cells. Congestion of blood vessels with perivascular cuffing of mononuclear inflammatory cells, hemorrhage, neurophagia, glial nodules were observed in the brain parenchyma. Demyelination reported in white matter, with microglial proliferation around vertebral canal of spinal cord. This study referred to the increased risk of central nervous system damage due to the exposure to lead.

In order to meet the increasing protein and income demand in Africa due to the rapid population growth, wildlife, such as the African grasscutter, is currently bred and domesticated as microlivestock. This study is one of the series on the brain morphology of this very large rodent, aimed at providing information that is lacking in the literature. Here, the gross anatomy of the cerebrum and brainstem in nine adult African grasscutters is described. The cerebral cortex was smooth, devoid of gyri and sulci, thus, placing the rodent in the lissencephalic group of mammals. However, blood vessels on the cortex created arterial and venous impressions. The cortex was asymmetrically-tapered oval in shape. The rostral and caudal colliculi were exposed through the cerebral transverse fissure. The rostro-caudal extent of the corpus callosum was from the mid-point of the frontal and parietal lobes, to a point just rostral to the occipital lobe. The rostral colliculi were grossly smaller than the caudal colliculi. The occulomotor and trochlear nerves emerged from the ventral midbrain, rostral to the pons. The pons was exceptionally large; it was pre-trigeminal. On either side of the ventral median fissure of the medulla oblongata were conspicuous pyramids. The trapezoid bodies were also conspicuous. These, and other findings, will be useful in future phylogenetic comparison of rodent brain morphology.

Background and Objectives: Hypoxia during pregnancy impairs fetal brain development. Fish oil acts as a reducer of oxidative stress, inflammation, and apoptosis in improving memory. This study aimed to determine the effect of fish oil on the histomorphometric changes of the offsprings' cerebrum and cerebellum caused by the hypoxia model during pregnancy rats. Materials and Methods: In this experimental study, 36 pregnant female Wistar rats were divided into six groups (n=6), including control, hypoxia, fish oil (1 mg/kg/day; orally), fish oil (0.5 mg/kg/day; orally), hypoxia + fish oil (1 mg/kg/day; orally), and hypoxia + fish oil (0.5 mg/kg/day; orally). The treatment period ranged from the sixth to the 15th day of pregnancy. On day 30 after birth, the rats were euthanized, and after removing the brain and measuring its weight, it was fixed in 10% formalin buffer. Histomorphometric changes of cerebrum and cerebellum were evaluated using hematoxylin and eosin (H&E) staining. Data were analyzed using one-way analysis of variance and Tukey's post hoc tests. Results: Hypoxia decreased the weight, volume, length, width, and thickness of the brain, and also increased the number of damaged neurons, the body size of Purkinje cells, and the percentage of damaged Purkinje cells (p<0.05). And administration of fish oil to hypoxic rats improved the mentioned parameters (p<0.05). Conclusion: According to the present study results, hypoxia during pregnancy can have destructive effects on offsprings' brains, and administration of fish oil can to some extent prevent the detrimental effects of hypoxia on offsprings' brains. [ABSTRACT FROM AUTHOR]

In the COVID-19 pandemic, direct and indirect effects on mental health have been reported, including neurological, neuropsychiatric, and neuropsychological symptoms with possible long-term effects. Also, it is suspected that in the coming years there could be a worldwide increase in the incidence of neurodegenerative disorders. The objective of this article is to review the most up-to-date information on brain damage associated with COVID-19, as well as the neuropsychiatric symptoms of the disease. The exact mechanisms of brain damage have not yet been clarified, and further longitudinal and international research--including studies that incorporate epidemiological, clinical, and diagnostic variables--is required to define these mechanisms and establish their impact on mental health, as well as their long-term consequences. [ABSTRACT FROM AUTHOR]