
DOI . ORG {
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Title[redir]:
Evidence for angiogenesis in Parkinsonās disease, incidental Lewy body disease, and progressive supranuclear palsy | Journal of Neural Transmission
Description:
Angiogenesis has not been extensively studied in Parkinsonās disease (PD) despite being associated with other neurodegenerative disorders. Post-mortem human brain tissues were obtained from subjects with pathologically confirmed Parkinsonās disease (PD) and progressive supranuclear palsy (PSP), a rapidly progressing Parkinsonian-like disorder. Tissues were also obtained from subjects with incidental Lewy body disease (iLBD) who had Lewy bodies in the substantia nigra pars compacta (SNpc) but had not been diagnosed with PD, and age-matched controls without Lewy body pathology. The SNpc, putamen, locus ceruleus (LC) and midfrontal cortex were examined for integrin αvβ3, a marker for angiogenesis, along with vessel number and activated microglia. All parkinsonian syndromes had greater αvβ3 in the LC and the SNpc, while only PD and PSP subjects had elevated αvβ3 in the putamen compared to controls. PD and PSP subjects also had increases in microglia number and activation in the SNpc suggesting a link between inflammation and clinical disease. Microglia activation in iLBD subjects was limited to the LC, an area involved at an early stage of PD. Likewise, iLBD subjects did not differ from controls in αvβ3 staining in the putamen, a late area of involvement in PD. The presence of αvβ3 reactive vessels in PD and its syndromes is indicative of newly created vessels that have not likely developed the restrictive properties of the blood brain barrier. Such angiogenic vessels could contribute to neuroinflammation by failing to protect the parenchyma from peripheral immune cells and inflammatory or toxic factors in the peripheral circulation.
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Keywords {š}
google, scholar, pubmed, article, cas, disease, parkinsons, angiogenesis, sisters, chicago, palsy, schneider, progressive, supranuclear, alzheimers, brain, vessels, neurol, neural, lewy, subjects, integrin, activation, blood, angiogenic, vascular, body, pathology, microglia, barrier, model, cell, incidental, carvey, hendey, αvβ, access, transm, endothelial, bennett, expression, rush, privacy, cookies, content, journal, desai, mouse, mcgeer, study,
Topics {āļø}
4-dihydroxyphenyl-l-alanine-induced dyskinesia l-dopa-induced angiogenic activity month download article/chapter pigment epithelium-derived factor clinic-based cohort study steele-richardson-olszewski syndrome dual-targeted contrast agent blood-brain barrier permeability hypoxia-induced integrin activation age-related cognitive decline α-synuclein pathology community-dwelling older persons progressive supranuclear palsy full article pdf striatal l-dopa l-dopa-carbidopa lewy body pathology community-based studies privacy choices/manage cookies alpha-synuclein deposition nigral dopaminergic neurons cohn research building blood brain barrier blood-brain barrier endothelial cell activation vascular integrin alpha alpha-synuclein pathology kenneth douglas foundation brooks pc carvey pm extracellular dopamine levels 6-hydroxydopamine-induced alterations peptide induced eae heterogeneous degeneration involving religious orders study hypoxia-induced retinopathy levodopa-induced dyskinesias brain blood vessels disease-related pathology parkinsonian substantia nigra endothelial cell proliferation check access instant access decision rules guiding vulnerable neuronal types 6-hydroxydopamine lesioned rats targeted proapoptotic peptidomimetic oligodendrocyte precursor differentiation abdominal aortic aneurysm 6-hydroxydopamine-lesioned rats
Questions {ā}
- Horton M (1990) Vitronectin receptor: tissue specific expression or adaptation to culture?
- Kirk S, Frank JA, Karlik S (2004) Angiogenesis in multiple sclerosis: is it good, bad or an epiphenomenon?
- Streit WJ (2006) Microglial senescence: does the brainās immune system have an expiration date?
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headline:Evidence for angiogenesis in Parkinsonās disease, incidental Lewy body disease, and progressive supranuclear palsy
description:Angiogenesis has not been extensively studied in Parkinsonās disease (PD) despite being associated with other neurodegenerative disorders. Post-mortem human brain tissues were obtained from subjects with pathologically confirmed Parkinsonās disease (PD) and progressive supranuclear palsy (PSP), a rapidly progressing Parkinsonian-like disorder. Tissues were also obtained from subjects with incidental Lewy body disease (iLBD) who had Lewy bodies in the substantia nigra pars compacta (SNpc) but had not been diagnosed with PD, and age-matched controls without Lewy body pathology. The SNpc, putamen, locus ceruleus (LC) and midfrontal cortex were examined for integrin αvβ3, a marker for angiogenesis, along with vessel number and activated microglia. All parkinsonian syndromes had greater αvβ3 in the LC and the SNpc, while only PD and PSP subjects had elevated αvβ3 in the putamen compared to controls. PD and PSP subjects also had increases in microglia number and activation in the SNpc suggesting a link between inflammation and clinical disease. Microglia activation in iLBD subjects was limited to the LC, an area involved at an early stage of PD. Likewise, iLBD subjects did not differ from controls in αvβ3 staining in the putamen, a late area of involvement in PD. The presence of αvβ3 reactive vessels in PD and its syndromes is indicative of newly created vessels that have not likely developed the restrictive properties of the blood brain barrier. Such angiogenic vessels could contribute to neuroinflammation by failing to protect the parenchyma from peripheral immune cells and inflammatory or toxic factors in the peripheral circulation.
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description:Angiogenesis has not been extensively studied in Parkinsonās disease (PD) despite being associated with other neurodegenerative disorders. Post-mortem human brain tissues were obtained from subjects with pathologically confirmed Parkinsonās disease (PD) and progressive supranuclear palsy (PSP), a rapidly progressing Parkinsonian-like disorder. Tissues were also obtained from subjects with incidental Lewy body disease (iLBD) who had Lewy bodies in the substantia nigra pars compacta (SNpc) but had not been diagnosed with PD, and age-matched controls without Lewy body pathology. The SNpc, putamen, locus ceruleus (LC) and midfrontal cortex were examined for integrin αvβ3, a marker for angiogenesis, along with vessel number and activated microglia. All parkinsonian syndromes had greater αvβ3 in the LC and the SNpc, while only PD and PSP subjects had elevated αvβ3 in the putamen compared to controls. PD and PSP subjects also had increases in microglia number and activation in the SNpc suggesting a link between inflammation and clinical disease. Microglia activation in iLBD subjects was limited to the LC, an area involved at an early stage of PD. Likewise, iLBD subjects did not differ from controls in αvβ3 staining in the putamen, a late area of involvement in PD. The presence of αvβ3 reactive vessels in PD and its syndromes is indicative of newly created vessels that have not likely developed the restrictive properties of the blood brain barrier. Such angiogenic vessels could contribute to neuroinflammation by failing to protect the parenchyma from peripheral immune cells and inflammatory or toxic factors in the peripheral circulation.
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