Background: Intracerebral hemorrhage (ICH) can cause brain damage through a number of pathways. The purpose of the study was to explore the effect of thrombin, protease nexin-1 (PN-1) and protease activated receptor-1 (PAR-1) in rat and human cerebellum after ICH.
Methods: A model of ICH was produced in adult Sprague-Dawley rats by direct injection of autologous blood (50 microl) into caudate nucleus. Patients with injured hemorrhage were also enrolled in this study. Different expressions of thrombin, PAR-1, PN-1 were detected in rat and human cerebellum by immunohistochemistry and in situ hybridization.
Results: In rat cerebellum, thrombin protein significantly increased at 6 hours and reached the maximum 2 days after ICH. The expression of PAR-1 protein reached the maximum at 24 - 48 hours, and then began to decrease. The expression of PN-1 protein reached the maximum at 3 hours, decreased somewhat after that and increased a little at 5 days after ICH. While in human cerebellum, the changing tendency of thrombin, PAR-1 and PN-1 was almost conform to the rat.
Conclusion: In cerebellum, thrombin can activate PAR-1 expression after ICH, and PN-1 appears quickly after ICH in order to control the deleterious effect of thrombin.
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Cerebellum
January 2025
Department of Human Genetics, McGill University, Montréal, Québec, Canada.
Essential Tremor (ET) is the most common movement disorder and has a worldwide prevalence of 1%, including 5% of the population over 65 years old. It is characterized by an active, postural or kinetic tremor, primarily affecting the upper limbs, and is diagnosed based on clinical characteristics. The pathological mechanisms of ET, however, are mostly unknown.
View Article and Find Full Text PDFCerebellum
January 2025
Molecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.
Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a rare inherited condition described worldwide and characterized by a wide spectrum of heterogeneity in terms of genotype and phenotype. How sacsin loss leads to neurodegeneration is still unclear, and current knowledge indicates that sacsin is involved in multiple functional mechanisms. We hence hypothesized the existence of epigenetic factors, in particular alterations in methylation patterns, that could contribute to ARSACS pathogenesis and explain the pleiotropic effects of SACS further than pathogenic mutations.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Introduction: While cerebral amyloid angiopathy is likely responsible for intracerebral hemorrhage (ICH) occurring in superficial (grey matter, vermis) cerebellar locations, it is unclear whether hypertensive arteriopathy (HA), the other major cerebral small vessel disease (cSVD), is associated with cerebellar ICH (cICH) in deep (white matter, deep nuclei, cerebellar peduncle) regions. We tested the hypothesis that HA-associated neuroimaging markers are significantly associated with deep cICH compared to superficial cICH.
Patients And Methods: Brain MRI scans from consecutive non-traumatic cICH patients admitted to a referral center were analyzed for cSVD markers.
Front Neural Circuits
January 2025
Department of Advanced Medical and Surgical Sciences, Advanced MRI Research Center, University of Campania "Luigi Vanvitelli", Naples, Italy.
The substantia nigra pars compacta (SNc), one of the main dopaminergic nuclei of the brain, exerts a regulatory function on the basal ganglia circuitry via the nigro-striatal pathway but its possible dopaminergic innervation of the thalamus has been only investigated in non-human primates. The impossibility of tract-tracing studies in humans has boosted advanced MRI techniques and multi-shell high-angular resolution diffusion MRI (MS-HARDI) has promised to shed more light on the structural connectivity of subcortical structures. Here, we estimated the possible dopaminergic innervation of the human thalamus via an MS-HARDI tractography of the SNc in healthy human young adults.
View Article and Find Full Text PDFOrphanet J Rare Dis
January 2025
Department of Neurology of First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Background: Spinocerebellar ataxia type 3 (SCA3) is a hereditary disease caused by abnormally expanded CAG repeats in the ATXN3 gene. The study aimed to identify potential biomarkers for assessing therapeutic efficacy by investigating the associations between expanded CAG repeat size, brain and spinal cord volume loss, and motor functions in patients with SCA3.
Methods: In this prospective, cross-observational study, we analyzed 3D T1-weighted MRIs from 92 patients with SCA3 and 42 healthy controls using voxel-based morphometry and region of interest approaches.
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