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We began analyzing https://link.springer.com/article/10.1007/s00401-012-1039-8, but it redirected us to https://link.springer.com/article/10.1007/s00401-012-1039-8. The analysis below is for the second page.

Title[redir]:
Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis | Acta Neuropathologica
Description:
The blood–brain barrier and blood–spinal cord barrier (BSCB) limit the entry of plasma components and erythrocytes into the central nervous system (CNS). Pericytes play a key role in maintaining blood–CNS barriers. The BSCB is damaged in patients with amyotrophic lateral sclerosis (ALS). Moreover, transgenic ALS rodents and pericyte-deficient mice develop BSCB disruption with erythrocyte extravasation preceding motor neuron dysfunction. Here, we studied whether BSCB disruption with erythrocyte extravasation and pericyte loss are present in human ALS. We show that 11 of 11 cervical cords from ALS patients, but 0 of 5 non-neurodegenerative disorders controls, possess perivascular deposits of erythrocyte-derived hemoglobin and hemosiderin typically 10–50 Îźm in diameter suggestive of erythrocyte extravasation. Immunostaining for CD235a, a specific marker for erythrocytes, confirmed sporadic erythrocyte extravasation in ALS, but not controls. Quantitative analysis revealed a 3.1-fold increase in perivascular hemoglobin deposits in ALS compared to controls showing hemoglobin confined within the vascular lumen, which correlated with 2.5-fold increase in hemosiderin deposits (r = 0.82, p < 0.01). Spinal cord parenchymal accumulation of plasma-derived immunoglobulin G, fibrin and thrombin was demonstrated in ALS, but not controls. Immunostaining for platelet-derived growth factor receptor-β, a specific marker for CNS pericytes, indicated a 54 % (p < 0.01) reduction in pericyte number in ALS patients compared to controls. Pericyte reduction correlated negatively with the magnitude of BSCB damage as determined by hemoglobin abundance (r = âˆ’0.75, p < 0.01). Thus, the BSCB disruption with erythrocyte extravasation and pericyte reductions is present in ALS. Whether similar findings occur in motor cortex and affected brainstem motor nuclei remain to be seen.

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Keywords {🔍}

article, google, scholar, pubmed, cord, cas, spinal, motor, lateral, amyotrophic, sclerosis, pericyte, subjects, hemoglobin, analysis, bscb, deposits, human, barrier, patients, cervical, hemosiderin, nndc, sections, neuron, sporadic, anterior, horn, neurol, cases, disruption, extravasation, fig, erythrocytes, pericytes, tissue, perivascular, zlokovic, erythrocyte, usa, mice, vascular, proteins, disease, neurons, capillaries, bloodspinal, controls, injury, study,

Topics {✒️}

blood–spinal cord barrier blood–spinal cord barriers blood–brain barrier integrity chromosome 9p21-linked als-ftd blood–brain barrier multiple plasma-derived proteins blood-gsf barrier article download pdf chromosome 9p-linked ftd goat anti-human podocalyxin bovine anti-goat cy3 z-stack images utilizing pdgf-b-deficient mice utilizing post-image thresholding iron-dependent oxidative injury lectin-positive capillary profiles lenalidomide regulate erythropoiesis controls cerebrovascular integrity maintaining blood–cns barriers amyotrophic lateral sclerosis endothelial cell-specific lectin pdgfrβ-positive surface area detect erythrocyte-derived products spinal cord capillaries open access spinal cord isolation impaired blood–brain pdgfrβ-positive pericyte coverage extravascular erythrocyte-derived hemoglobin perivascular hemosiderin deposits mm2 spinal cord pdgf beta receptor spinal cord tissues immediately snap frozen optimize pulse sequences spinal cord neurons serum-csf protein gradients pdgfrβ-positive pericyte number lumbar spinal cords motor neuron injury full access visualize neun-positive cells protein-bound iron including prussian blue staining human sod1 develop possess perivascular deposits endothelial tight junctions sporadic cd235a-positive erythrocytes rabbit anti-fibrinogen perivascular hemoglobin deposits

Questions {❓}

  • Andersen PM, Al-Chalabi A (2011) Clinical genetics of amyotrophic lateral sclerosis: what do we really know?

Schema {🗺️}

WebPage:
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         headline:Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis
         description:The blood–brain barrier and blood–spinal cord barrier (BSCB) limit the entry of plasma components and erythrocytes into the central nervous system (CNS). Pericytes play a key role in maintaining blood–CNS barriers. The BSCB is damaged in patients with amyotrophic lateral sclerosis (ALS). Moreover, transgenic ALS rodents and pericyte-deficient mice develop BSCB disruption with erythrocyte extravasation preceding motor neuron dysfunction. Here, we studied whether BSCB disruption with erythrocyte extravasation and pericyte loss are present in human ALS. We show that 11 of 11 cervical cords from ALS patients, but 0 of 5 non-neurodegenerative disorders controls, possess perivascular deposits of erythrocyte-derived hemoglobin and hemosiderin typically 10–50 Οm in diameter suggestive of erythrocyte extravasation. Immunostaining for CD235a, a specific marker for erythrocytes, confirmed sporadic erythrocyte extravasation in ALS, but not controls. Quantitative analysis revealed a 3.1-fold increase in perivascular hemoglobin deposits in ALS compared to controls showing hemoglobin confined within the vascular lumen, which correlated with 2.5-fold increase in hemosiderin deposits (r = 0.82, p < 0.01). Spinal cord parenchymal accumulation of plasma-derived immunoglobulin G, fibrin and thrombin was demonstrated in ALS, but not controls. Immunostaining for platelet-derived growth factor receptor-β, a specific marker for CNS pericytes, indicated a 54 % (p < 0.01) reduction in pericyte number in ALS patients compared to controls. Pericyte reduction correlated negatively with the magnitude of BSCB damage as determined by hemoglobin abundance (r = −0.75, p < 0.01). Thus, the BSCB disruption with erythrocyte extravasation and pericyte reductions is present in ALS. Whether similar findings occur in motor cortex and affected brainstem motor nuclei remain to be seen.
         datePublished:2012-09-01T00:00:00Z
         dateModified:2012-09-01T00:00:00Z
         pageStart:111
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            Amyotrophic lateral sclerosis
            Pericytes
            Vascular injury
            Blood–brain barrier
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            Pathology
            Neurosciences
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      headline:Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis
      description:The blood–brain barrier and blood–spinal cord barrier (BSCB) limit the entry of plasma components and erythrocytes into the central nervous system (CNS). Pericytes play a key role in maintaining blood–CNS barriers. The BSCB is damaged in patients with amyotrophic lateral sclerosis (ALS). Moreover, transgenic ALS rodents and pericyte-deficient mice develop BSCB disruption with erythrocyte extravasation preceding motor neuron dysfunction. Here, we studied whether BSCB disruption with erythrocyte extravasation and pericyte loss are present in human ALS. We show that 11 of 11 cervical cords from ALS patients, but 0 of 5 non-neurodegenerative disorders controls, possess perivascular deposits of erythrocyte-derived hemoglobin and hemosiderin typically 10–50 Οm in diameter suggestive of erythrocyte extravasation. Immunostaining for CD235a, a specific marker for erythrocytes, confirmed sporadic erythrocyte extravasation in ALS, but not controls. Quantitative analysis revealed a 3.1-fold increase in perivascular hemoglobin deposits in ALS compared to controls showing hemoglobin confined within the vascular lumen, which correlated with 2.5-fold increase in hemosiderin deposits (r = 0.82, p < 0.01). Spinal cord parenchymal accumulation of plasma-derived immunoglobulin G, fibrin and thrombin was demonstrated in ALS, but not controls. Immunostaining for platelet-derived growth factor receptor-β, a specific marker for CNS pericytes, indicated a 54 % (p < 0.01) reduction in pericyte number in ALS patients compared to controls. Pericyte reduction correlated negatively with the magnitude of BSCB damage as determined by hemoglobin abundance (r = −0.75, p < 0.01). Thus, the BSCB disruption with erythrocyte extravasation and pericyte reductions is present in ALS. Whether similar findings occur in motor cortex and affected brainstem motor nuclei remain to be seen.
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      dateModified:2012-09-01T00:00:00Z
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         Amyotrophic lateral sclerosis
         Pericytes
         Vascular injury
         Blood–brain barrier
         Blood–spinal cord barrier
         Pathology
         Neurosciences
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                  name:University of Southern California
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            type:Organization
      name:Jenny S. Henkel
      affiliation:
            name:The Methodist Hospital Research Institute, The Methodist Hospital
            address:
               name:Department of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, USA
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      name:Center for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, USA
      name:Center for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, USA
      name:Department of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, USA
      name:Department of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, USA
      name:Center for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, USA

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