Loading…
Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis
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, t...
Saved in:
| Published in: | Acta neuropathologica 2013-01, Vol.125 (1), p.111-120 |
|---|---|
| Main Authors: | , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3 |
| container_end_page | 120 |
| container_issue | 1 |
| container_start_page | 111 |
| container_title | Acta neuropathologica |
| container_volume | 125 |
| creator | Winkler, Ethan A. Sengillo, Jesse D. Sullivan, John S. Henkel, Jenny S. Appel, Stanley H. Zlokovic, Berislav V. |
| 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 μm 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
|
| doi_str_mv | 10.1007/s00401-012-1039-8 |
| format | article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3535352</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A352308685</galeid><sourcerecordid>A352308685</sourcerecordid><originalsourceid>FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3</originalsourceid><addsrcrecordid>eNp1Ustu1TAQtRCIXi58ABsUiQ2blPEzyQapVLykSmxgi-U4k1uXxA52Aro7_qF_2C_B0S0tRaBZjMZz5thzfAh5SuGYAlQvE4AAWgJlJQXelPU9sqGCsxIk5_fJBiB3FWfsiDxK6SJXrBLyITlirBGUMbUhX14PIXRXPy_T5LwZChtiV7QmRoexaCOar1344Qvju2LC6Ox-xiJit9jZBZ8Kl1vjPswxTOfOFoOZMWaWZAeMIbn0mDzozZDwyXXeks9v33w6fV-efXz34fTkrLQK-Fw2koLthBWGttJyo1qba9WAEdjXoJhqRGdbw3tlBW-V4QrAVrYS2Kiat3xLXh14p6UdsbPo5_wOPUU3mrjXwTh9t-Pdud6F75rLNVgmeHFNEMO3BdOsR5csDoPxGJaks3KcSlnntCXP_4JehCVm8ZJmogYpVEXZLWpnBtTO91kkY1dSfbJeCLWqZUYd_wOVo8PR2eCxd_n8zgA9DNisb4rY3-xIQa-m0AdT6PzXejWFrvPMsz_FuZn47YIMYAdAyi2_w3i70f9ZfwH76cMy</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2480546712</pqid></control><display><type>article</type><title>Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis</title><source>Springer Link</source><creator>Winkler, Ethan A. ; Sengillo, Jesse D. ; Sullivan, John S. ; Henkel, Jenny S. ; Appel, Stanley H. ; Zlokovic, Berislav V.</creator><creatorcontrib>Winkler, Ethan A. ; Sengillo, Jesse D. ; Sullivan, John S. ; Henkel, Jenny S. ; Appel, Stanley H. ; Zlokovic, Berislav V.</creatorcontrib><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 μm 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.</description><identifier>ISSN: 0001-6322</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s00401-012-1039-8</identifier><identifier>PMID: 22941226</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Aged ; Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - blood ; Amyotrophic Lateral Sclerosis - cerebrospinal fluid ; Amyotrophic Lateral Sclerosis - physiopathology ; Blood proteins ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - physiopathology ; Brain stem ; Capillary Permeability ; Central nervous system ; Cortex (motor) ; Deposits ; Endothelial Cells - metabolism ; Erythrocytes ; Extravasation ; Female ; Fibrin ; Genetic engineering ; Hemoglobin ; Humans ; Immunoglobulin G ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Motor Neurons - cytology ; Motor Neurons - pathology ; Motor nuclei ; Nervous system diseases ; Neurodegenerative diseases ; Neurosciences ; Original Paper ; Pathology ; Pericytes ; Pericytes - cytology ; Pericytes - metabolism ; Platelet-derived growth factor ; Spinal cord ; Spinal Cord - blood supply ; Spinal Cord - physiopathology ; Thrombin ; Tight Junctions - metabolism ; Tight Junctions - pathology</subject><ispartof>Acta neuropathologica, 2013-01, Vol.125 (1), p.111-120</ispartof><rights>The Author(s) 2012</rights><rights>COPYRIGHT 2013 Springer</rights><rights>The Author(s) 2012. This work is published under https://creativecommons.org/licenses/by/2.0 (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3</citedby><cites>FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22941226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Winkler, Ethan A.</creatorcontrib><creatorcontrib>Sengillo, Jesse D.</creatorcontrib><creatorcontrib>Sullivan, John S.</creatorcontrib><creatorcontrib>Henkel, Jenny S.</creatorcontrib><creatorcontrib>Appel, Stanley H.</creatorcontrib><creatorcontrib>Zlokovic, Berislav V.</creatorcontrib><title>Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><addtitle>Acta Neuropathol</addtitle><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 μm 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.</description><subject>Aged</subject><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - blood</subject><subject>Amyotrophic Lateral Sclerosis - cerebrospinal fluid</subject><subject>Amyotrophic Lateral Sclerosis - physiopathology</subject><subject>Blood proteins</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - physiopathology</subject><subject>Brain stem</subject><subject>Capillary Permeability</subject><subject>Central nervous system</subject><subject>Cortex (motor)</subject><subject>Deposits</subject><subject>Endothelial Cells - metabolism</subject><subject>Erythrocytes</subject><subject>Extravasation</subject><subject>Female</subject><subject>Fibrin</subject><subject>Genetic engineering</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Motor Neurons - cytology</subject><subject>Motor Neurons - pathology</subject><subject>Motor nuclei</subject><subject>Nervous system diseases</subject><subject>Neurodegenerative diseases</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Pericytes</subject><subject>Pericytes - cytology</subject><subject>Pericytes - metabolism</subject><subject>Platelet-derived growth factor</subject><subject>Spinal cord</subject><subject>Spinal Cord - blood supply</subject><subject>Spinal Cord - physiopathology</subject><subject>Thrombin</subject><subject>Tight Junctions - metabolism</subject><subject>Tight Junctions - pathology</subject><issn>0001-6322</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1Ustu1TAQtRCIXi58ABsUiQ2blPEzyQapVLykSmxgi-U4k1uXxA52Aro7_qF_2C_B0S0tRaBZjMZz5thzfAh5SuGYAlQvE4AAWgJlJQXelPU9sqGCsxIk5_fJBiB3FWfsiDxK6SJXrBLyITlirBGUMbUhX14PIXRXPy_T5LwZChtiV7QmRoexaCOar1344Qvju2LC6Ox-xiJit9jZBZ8Kl1vjPswxTOfOFoOZMWaWZAeMIbn0mDzozZDwyXXeks9v33w6fV-efXz34fTkrLQK-Fw2koLthBWGttJyo1qba9WAEdjXoJhqRGdbw3tlBW-V4QrAVrYS2Kiat3xLXh14p6UdsbPo5_wOPUU3mrjXwTh9t-Pdud6F75rLNVgmeHFNEMO3BdOsR5csDoPxGJaks3KcSlnntCXP_4JehCVm8ZJmogYpVEXZLWpnBtTO91kkY1dSfbJeCLWqZUYd_wOVo8PR2eCxd_n8zgA9DNisb4rY3-xIQa-m0AdT6PzXejWFrvPMsz_FuZn47YIMYAdAyi2_w3i70f9ZfwH76cMy</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Winkler, Ethan A.</creator><creator>Sengillo, Jesse D.</creator><creator>Sullivan, John S.</creator><creator>Henkel, Jenny S.</creator><creator>Appel, Stanley H.</creator><creator>Zlokovic, Berislav V.</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130101</creationdate><title>Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis</title><author>Winkler, Ethan A. ; Sengillo, Jesse D. ; Sullivan, John S. ; Henkel, Jenny S. ; Appel, Stanley H. ; Zlokovic, Berislav V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aged</topic><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - blood</topic><topic>Amyotrophic Lateral Sclerosis - cerebrospinal fluid</topic><topic>Amyotrophic Lateral Sclerosis - physiopathology</topic><topic>Blood proteins</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - physiopathology</topic><topic>Brain stem</topic><topic>Capillary Permeability</topic><topic>Central nervous system</topic><topic>Cortex (motor)</topic><topic>Deposits</topic><topic>Endothelial Cells - metabolism</topic><topic>Erythrocytes</topic><topic>Extravasation</topic><topic>Female</topic><topic>Fibrin</topic><topic>Genetic engineering</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Immunoglobulin G</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Motor Neurons - cytology</topic><topic>Motor Neurons - pathology</topic><topic>Motor nuclei</topic><topic>Nervous system diseases</topic><topic>Neurodegenerative diseases</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Pericytes</topic><topic>Pericytes - cytology</topic><topic>Pericytes - metabolism</topic><topic>Platelet-derived growth factor</topic><topic>Spinal cord</topic><topic>Spinal Cord - blood supply</topic><topic>Spinal Cord - physiopathology</topic><topic>Thrombin</topic><topic>Tight Junctions - metabolism</topic><topic>Tight Junctions - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Winkler, Ethan A.</creatorcontrib><creatorcontrib>Sengillo, Jesse D.</creatorcontrib><creatorcontrib>Sullivan, John S.</creatorcontrib><creatorcontrib>Henkel, Jenny S.</creatorcontrib><creatorcontrib>Appel, Stanley H.</creatorcontrib><creatorcontrib>Zlokovic, Berislav V.</creatorcontrib><collection>SpringerOpen</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta neuropathologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Winkler, Ethan A.</au><au>Sengillo, Jesse D.</au><au>Sullivan, John S.</au><au>Henkel, Jenny S.</au><au>Appel, Stanley H.</au><au>Zlokovic, Berislav V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis</atitle><jtitle>Acta neuropathologica</jtitle><stitle>Acta Neuropathol</stitle><addtitle>Acta Neuropathol</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>125</volume><issue>1</issue><spage>111</spage><epage>120</epage><pages>111-120</pages><issn>0001-6322</issn><eissn>1432-0533</eissn><abstract>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 μm 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.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22941226</pmid><doi>10.1007/s00401-012-1039-8</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0001-6322 |
| ispartof | Acta neuropathologica, 2013-01, Vol.125 (1), p.111-120 |
| issn | 0001-6322 1432-0533 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3535352 |
| source | Springer Link |
| subjects | Aged Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - blood Amyotrophic Lateral Sclerosis - cerebrospinal fluid Amyotrophic Lateral Sclerosis - physiopathology Blood proteins Blood-brain barrier Blood-Brain Barrier - metabolism Blood-Brain Barrier - physiopathology Brain stem Capillary Permeability Central nervous system Cortex (motor) Deposits Endothelial Cells - metabolism Erythrocytes Extravasation Female Fibrin Genetic engineering Hemoglobin Humans Immunoglobulin G Male Medicine Medicine & Public Health Middle Aged Motor Neurons - cytology Motor Neurons - pathology Motor nuclei Nervous system diseases Neurodegenerative diseases Neurosciences Original Paper Pathology Pericytes Pericytes - cytology Pericytes - metabolism Platelet-derived growth factor Spinal cord Spinal Cord - blood supply Spinal Cord - physiopathology Thrombin Tight Junctions - metabolism Tight Junctions - pathology |
| title | Blood–spinal cord barrier breakdown and pericyte reductions in amyotrophic lateral sclerosis |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T11%3A22%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Blood%E2%80%93spinal%20cord%20barrier%20breakdown%20and%20pericyte%20reductions%20in%20amyotrophic%20lateral%20sclerosis&rft.jtitle=Acta%20neuropathologica&rft.au=Winkler,%20Ethan%20A.&rft.date=2013-01-01&rft.volume=125&rft.issue=1&rft.spage=111&rft.epage=120&rft.pages=111-120&rft.issn=0001-6322&rft.eissn=1432-0533&rft_id=info:doi/10.1007/s00401-012-1039-8&rft_dat=%3Cgale_pubme%3EA352308685%3C/gale_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c603t-9510cd4c4a1b5c3a6bc0cd690a4ef8062694dcba3f6c43b6a3600c7c74e9683b3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2480546712&rft_id=info:pmid/22941226&rft_galeid=A352308685&rfr_iscdi=true |