Background: The anatomy of the substantia nigra on conventional MRI is controversial. Even using histological techniques it is difficult to delineate with certainty from surrounding structures. We sought to define the anatomy of the SN using high field spin-echo MRI of pathological material in which we could study the anatomy in detail to corroborate our MRI findings in controls and Parkinson's disease and progressive supranuclear palsy.
Methods: 23 brains were selected from the Queen Square Brain Bank (10 controls, 8 progressive supranuclear palsy, 5 Parkinson's disease) and imaged using high field 9.4 Tesla spin-echo MRI. Subsequently brains were cut and stained with Luxol fast blue, Perls stain, and immunohistochemistry for substance P and calbindin. Once the anatomy was defined on histology the dimensions and volume of the substantia nigra were determined on high field magnetic resonance images.
Results: The anterior border of the substantia nigra was defined by the crus cerebri. In the medial half it was less distinct due to the deposition of iron and the interdigitation of white matter and the substantia nigra. The posterior border was flanked by white matter bridging the red nucleus and substantia nigra and seen as hypointense on spin-echo magnetic resonance images. Within the substantia nigra high signal structures corresponded to confirmed nigrosomes. These were still evident in Parkinson's disease but not in progressive supranuclear palsy. The volume and dimensions of the substantia nigra were similar in Parkinson's disease and controls, but reduced in progressive supranuclear palsy.
Conclusions: We present a histologically validated anatomical description of the substantia nigra on high field spin-echo high resolution magnetic resonance images and were able to delineate all five nigrosomes. In accordance with the pathological literature we did not observe changes in the nigrosome structure as manifest by volume or signal characteristics within the substantia nigra in Parkinson's disease whereas in progressive supranuclear palsy there was microarchitectural destruction.
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http://dx.doi.org/10.1016/j.nicl.2016.11.015 | DOI Listing |
BMC Med Imaging
January 2025
Department of Physiology, Faculty of Medicine, AJA University of Medical Science, Tehran, Iran.
Background: Cognitive networks impairments are common in neuropsychiatric disorders like Attention Deficit Hyperactivity Disorder (ADHD), bipolar disorder (BD), and schizophrenia (SZ). While previous research has focused on specific brain regions, the role of the procedural memory as a type of long-term memory to examine cognitive networks impairments in these disorders remains unclear. This study investigates alterations in resting-state functional connectivity (rs-FC) within the procedural memory network to explore brain function associated with cognitive networks in patients with these disorders.
View Article and Find Full Text PDFParkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, primarily due to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Factors contributing to this neuronal degeneration include mitochondrial dysfunction, oxidative stress, and neuronal excitotoxicity. Despite extensive research, the exact etiology of PD remains unclear, with both genetic and environmental factors playing significant roles.
View Article and Find Full Text PDFJ Neurochem
January 2025
Department of Pathology, School of Veterinary Medicine, University of São Paulo, Sao Paulo, Brazil.
Autism spectrum disorder (ASD) is a complex developmental disorder characterized by several behavioral impairments, especially in socialization, communication, and the occurrence of stereotyped behaviors. In rats, prenatal exposure to valproic acid (VPA) induces autistic-like behaviors. Previous studies by our group have suggested that the autistic-like phenotype is possibly related to dopaminergic system modulation because tyrosine hydroxylase (TH) expression was affected.
View Article and Find Full Text PDFNeurosciences (Riyadh)
January 2025
From the School of Clinical Medicine (Liang, Luo, Jia), Shandong Second Medical University, Weifang, from the Department of Neurology (Liang, Zhao, Lin, Li, Luo, Jia) , Beijing Shijingshan Hospital, Shijingshan Teaching Hospital of Capital Medical University, Beijing, and from the Department of Neurology (Li), Affiliated Hospital of Weifang Medical University, Weifang, China.
Objectives: To identify a key Long chain non-coding RNAs (lncRNAs) related to PD and provide a new perspective on the role of LncRNAs in Parkinson's disease (PD) pathophysiology.
Methods: Our study involved analyzing gene chips from the substantia nigra and white blood cells, both normal and PD-inclusive, in the Gene Expression Omnibus (GEO) database, utilizing a weighted gene co-expression network analysis (WGCNA). The technique of WGCNA facilitated the examination of differentially expressed genes (DEGs) in the substantia nigra and the white blood cells of individuals with PD.
Int J Mol Sci
December 2024
Department of Anatomy, Dokkyo Medical University School of Medicine, 880 Kita-Kobayashi, Mibu-machi, Shimotsuga-gun 321-0293, Tochigi, Japan.
Recent findings have revealed that melanocortin 1 receptor (MC1R) deficiency leads to Parkinson's disease-like dopaminergic neurodegeneration in the substantia nigra (SN). However, its precise distribution and expressing-cell type in the SN remain unclear. Therefore, in this study, we analyzed the localization and characteristics of MC1R in the SN using histological methods, including in situ hybridization and immunohistochemistry.
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