Extracellular matrix components are regarded as important substrates for invasive tumor cells. The present work focuses on the expression of laminin in the brain in response to invading brain tumors. Biopsies obtained from tissue macroscopically evaluated as the border zone between tumor and normal brain, in 5 patients undergoing surgery for glioblastoma multiforme, were examined by immunocytochemistry and scanning confocal microscopy for the expression of laminin and glial fibrillary acidic protein. Laminin was mainly found in all the specimens associated with the basal lamina of blood vessels, but a variable degree of punctate laminin deposits were also observed in the parenchyma not associated with blood vessels. In the specimens with substantial deposits, scanning confocal microscopy showed that some of the laminin co-localized with intracellular glial fibrillary acidic protein. Punctate deposits of laminin were also seen in an intracranial BT4C rat glioma model, where it was particularly abundant in the brain/tumor confrontation zone. Previous in vitro studies have shown that laminin, among several extracellular matrix components, represent a highly permissive substrate for glioma cell migration. The presented results indicate that laminin can be produced by glial fibrillary acidic protein positive cells during glioma cell invasion in humans. This glycoprotein may thus represent one important substrate among many, which contribute to the invasive phenotype of gliomas.
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http://dx.doi.org/10.1016/s0736-5748(99)00055-6 | DOI Listing |
Alzheimers Dement (Amst)
January 2025
Neurochemistry Laboratory Department of Laboratory Medicine Amsterdam UMC Amsterdam The Netherlands.
Introduction: Blood-based glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and phosphorylated tau (pTau) have shown promising prognostic potential in Alzheimer's disease (AD), but their applicability in clinical settings where comorbidities are prevalent remains uncertain.
Methods: Simoa assays quantified GFAP, NfL, and pTau181 in retrospectively retrieved prediagnostic serum samples from 102 AD patients and 21 non-AD controls.
Results: Higher serum GFAP levels predicted earlier clinical presentation and faster subsequent Mini-Mental State Examination decline in AD patients.
Alzheimers Dement (Amst)
January 2025
Introduction: Increasing evidence links amyloid beta (Aβ) aggregation with inflammation. This pilot study investigated the use of an immunoassay panel to map biomarker changes in patients with Alzheimer's disease (AD). Furthermore, we evaluated the stability of protein quantification after multiple freeze-thaw cycles (FTCs).
View Article and Find Full Text PDFMol Neurobiol
January 2025
Research and Innovation Center, Shanghai Pudong Hospital, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, 200433, China.
Investigating plasma proteomic signatures of dementia offers insights into its pathology, aids biomarker discovery, supports disease monitoring, and informs drug development. Here, we analyzed data from 48,367 UK Biobank participants with proteomic profiling. Using Cox and generalized linear models, we examined the longitudinal associations between proteomic signatures and dementia-related phenotypes.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Orthopaedics, Tianjin Hospital, Tianjin University, Tianjin, China.
Neuropathic pain (NP) imposes a significant burden on individuals, manifesting as nociceptive anaphylaxis, hypersensitivity, and spontaneous pain. Previous studies have shown that traumatic stress in the nervous system can lead to excessive production of hydrogen sulfide (HS) in the gut. As a toxic gas, it can damage the nervous system through the gut-brain axis.
View Article and Find Full Text PDFFront Neurol
January 2025
14th European Reference Network in Neuromuscular Disorders (EURO-NMD), Scientific Laboratory of Molecular Genetics, Riga Stradins University, Riga, Latvia.
Background: Charcot-Marie-Tooth disease (CMT), a slowly advancing hereditary nerve disorder, presents a significant challenge in the medical field. Effective drugs for treatment are lacking, and we struggle to find sensitive markers to track the disease's severity and progression. In this study, our objective was to investigate the levels of neurofilament light chain (NfL), glial fibrillary acid protein (GFAP), fibroblast growth factor 21 (FGF-21) and growth differentiation factor 15 (GDF-15) in individuals with CMT and to compare them to a control group.
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