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Article ; Online: Isolation of Human Microglia from Neuropathologically Diagnosed Cases in the Single-Cell Era.

Lue, Lih-Fen / Walker, Douglas G / Beh, Suet Theng / Beach, Thomas G

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2561, Page(s) 43–62

Abstract: This chapter describes the core procedures that we have developed over the last two decades to isolate routinely the microglia from postmortem human brains. The method is suitable for brain slices consisting of both gray and white matter.The ability to ... ...

Abstract	This chapter describes the core procedures that we have developed over the last two decades to isolate routinely the microglia from postmortem human brains. The method is suitable for brain slices consisting of both gray and white matter.The ability to concomitantly isolate vascular cells with glial cells provides the opportunity to investigate multiple cell types originating from the same donor. This represents a novel approach for -omics research, with the potential for discovering the shared or distinct molecular features among the glia and vascular cells from the same individual.
MeSH term(s)	Humans ; Microglia ; Neuroglia ; White Matter ; Brain
Language	English
Publishing date	2022-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2655-9_3
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Article: Advance in Plasma AD Core Biomarker Development: Current Findings from Immunomagnetic Reduction-Based SQUID Technology.

Lue, Lih-Fen / Kuo, Yu-Min / Sabbagh, Marwan

Neurology and therapy

2019 Volume 8, Issue Suppl 2, Page(s) 95–111

Abstract: New super-sensitive biomarker assay platforms for measuring Alzheimer's disease (AD) core pathological markers in plasma have recently been developed and tested. Research findings from these technologies offer promising evidence for identifying the ... ...

Abstract	New super-sensitive biomarker assay platforms for measuring Alzheimer's disease (AD) core pathological markers in plasma have recently been developed and tested. Research findings from these technologies offer promising evidence for identifying the earliest stages of AD and correlating them with brain pathological progression. Here, we review findings using immunomagnetic reduction, one of these ultrasensitive technologies. The principles, technology and assays developed, along with selected published findings will be discussed. The major findings from this technology were significant increases of amyloid beta (Aβ) 42 and total tau (t-tau) levels in subjects clinically diagnosed with early AD when compared with cognitively normal control (NC) subjects. The composite marker of the product of Aβ42 and t-tau discriminated subjects with early AD from NC subjects with high accuracy. The potential of this technology for the purpose of early or preclinical disease stage detection has yet to be explored in subjects who have also been assessed with brain imaging and cerebrospinal fluid AD core biomarker measurements.
Language	English
Publishing date	2019-12-12
Publishing country	New Zealand
Document type	Journal Article ; Review
ISSN	2193-8253
ISSN	2193-8253
DOI	10.1007/s40120-019-00167-2
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Article ; Online: Alzheimer's Disease Research Using Human Microglia.

Lue, Lih-Fen / Beach, Thomas G / Walker, Douglas G

Cells

2019 Volume 8, Issue 8

Abstract: Experimental studies of neuroinflammation in Alzheimer's disease (AD) have mostly investigated microglia, the brain-resident macrophages. This review focused on human microglia obtained at rapid autopsies. Studies employing methods to isolate and culture ...

Abstract	Experimental studies of neuroinflammation in Alzheimer's disease (AD) have mostly investigated microglia, the brain-resident macrophages. This review focused on human microglia obtained at rapid autopsies. Studies employing methods to isolate and culture human brain microglia in high purity for experimental studies were discussed. These methods were employed to isolate human microglia for investigation of a number of features of neuroinflammation, including activation phenotypes, neurotoxicity, responses to abnormal aggregated proteins such as amyloid beta, phagocytosis, and the effects of aging and disease on microglia cellular properties. In recent years, interest in human microglia and neuroinflammation has been renewed due to the identification of inflammation-related AD genetic risk factors, in particular the triggering receptor expressed on myeloid cells (TREM)-2. Because of the difficulties in developing effective treatments for AD, there has been a general need for greater understanding of the functions of microglia in normal and AD brains. While most experimental studies on neuroinflammation have employed rodent microglia, this review considered the role of human microglia in experimental studies. This review focused on the development of in vitro methodology for the culture of postmortem human microglia and the key findings obtained from experimental studies with these cells.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Microglia/cytology ; Microglia/metabolism ; Primary Cell Culture/methods
Language	English
Publishing date	2019-08-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8080838
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Article ; Online: Alzheimer’s Disease Research Using Human Microglia

Lih-Fen Lue / Thomas G. Beach / Douglas G. Walker

Cells, Vol 8, Iss 8, p

2019 Volume 838

Abstract: Experimental studies of neuroinflammation in Alzheimer’s disease (AD) have mostly investigated microglia, the brain-resident macrophages. This review focused on human microglia obtained at rapid autopsies. Studies employing methods to isolate and culture ...

Abstract	Experimental studies of neuroinflammation in Alzheimer’s disease (AD) have mostly investigated microglia, the brain-resident macrophages. This review focused on human microglia obtained at rapid autopsies. Studies employing methods to isolate and culture human brain microglia in high purity for experimental studies were discussed. These methods were employed to isolate human microglia for investigation of a number of features of neuroinflammation, including activation phenotypes, neurotoxicity, responses to abnormal aggregated proteins such as amyloid beta, phagocytosis, and the effects of aging and disease on microglia cellular properties. In recent years, interest in human microglia and neuroinflammation has been renewed due to the identification of inflammation-related AD genetic risk factors, in particular the triggering receptor expressed on myeloid cells (TREM)-2. Because of the difficulties in developing effective treatments for AD, there has been a general need for greater understanding of the functions of microglia in normal and AD brains. While most experimental studies on neuroinflammation have employed rodent microglia, this review considered the role of human microglia in experimental studies. This review focused on the development of in vitro methodology for the culture of postmortem human microglia and the key findings obtained from experimental studies with these cells.
Keywords	neuroinflammation ; microglia ; cell culture ; brain ; amyloid ; neurodegeneration ; autopsy ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2019-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Increased expression of toll-like receptor 3, an anti-viral signaling molecule, and related genes in Alzheimer's disease brains.

Walker, Douglas G / Tang, Tiffany M / Lue, Lih-Fen

Experimental neurology

2018 Volume 309, Page(s) 91–106

Abstract: The focus of this study is the expression of Toll-like receptor-3 (TLR-3), a receptor for double-stranded RNA, in human brains affected by Alzheimer's disease (AD) pathology. Toll-like receptors are a family of pattern recognition molecules primarily ... ...

Abstract	The focus of this study is the expression of Toll-like receptor-3 (TLR-3), a receptor for double-stranded RNA, in human brains affected by Alzheimer's disease (AD) pathology. Toll-like receptors are a family of pattern recognition molecules primarily involved in host defenses to microbial pathogens, but roles in neurodegenerative disease have also been shown, as amyloid beta (Aβ) can be a ligand for TLR-2 and -4 and α-synuclein for TLR-1 and TLR-2, while TLR-9 activation promotes Aβ removal. However, involvement of TLR-3 in AD has not been rigorously studied. Immunohistochemical analyses in human temporal cortical sections with a validated antibody for TLR-3 predominantly identified microglia, particularly strongly in cells associated with amyloid plaques, also brain vascular endothelial cells and subsets of astrocytes, but not neurons or p62-immunoreactive structures. Microglial TLR-3 colocalized with the endosomal/lysosomal marker CD68, which identifies phagocytic cells. Quantitative analyses of neuropathologically-staged human brain middle temporal gyrus samples using immunohistochemistry and mRNA expression methods demonstrated increased TLR-3 immunoreactivity and increased TLR-3 mRNA in AD compared to non-demented cases. There were significant positive correlations between TLR-3 mRNA levels and plaque or tangle loads in both series of samples. Increased expression of interferon beta (IFN-β) and interferon regulatory factor (IRF)-3 mRNA, two factors induced by TLR-3 signaling, were detected in the AD cases. Increased expression of TLR-4 and TLR-9 mRNA was also observed in these same samples, but not TLR-2. In vitro cultured human brain microglia responses to Aβ inflammatory activation were not altered by TLR-3 activation with activator polyinosinic;polycytidylic acid (poly I:C), while human brain endothelial cells showed reduction in responses when stimulated with both agents. Treatment of microglia with poly I:C did not increase their uptake and breakdown of Aβ.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Peptides/pharmacology ; Brain/metabolism ; Brain/pathology ; Calcium-Binding Proteins ; Case-Control Studies ; Cells, Cultured ; Cytokines/metabolism ; DNA-Binding Proteins/metabolism ; Endothelial Cells/drug effects ; Gene Expression/drug effects ; Gene Expression/physiology ; HEK293 Cells ; Humans ; Microfilament Proteins ; Microglia/metabolism ; Microglia/pathology ; Neuroglia/metabolism ; Neuroglia/pathology ; Peptide Fragments/pharmacology ; Phosphopyruvate Hydratase/metabolism ; Poly I-C/pharmacology ; RNA-Binding Proteins/metabolism ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism
Chemical Substances	AIF1 protein, human ; Amyloid beta-Peptides ; Calcium-Binding Proteins ; Cytokines ; DNA-Binding Proteins ; Microfilament Proteins ; P62 protein, human ; Peptide Fragments ; RNA-Binding Proteins ; TLR3 protein, human ; Toll-Like Receptor 3 ; Toll-Like Receptors ; amyloid beta-protein (1-42) ; Phosphopyruvate Hydratase (EC 4.2.1.11) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2018-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2018.07.016
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Article ; Online: Microglial Phenotyping in Neurodegenerative Disease Brains: Identification of Reactive Microglia with an Antibody to Variant of CD105/Endoglin.

Walker, Douglas G / Lue, Lih-Fen / Beach, Thomas G / Tooyama, Ikuo

Cells

2019 Volume 8, Issue 7

Abstract: Inflammation is considered a key pathological process in neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), but there are still mechanisms not understood. In the brain, most microglia are performing essential ... ...

Abstract	Inflammation is considered a key pathological process in neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), but there are still mechanisms not understood. In the brain, most microglia are performing essential homeostatic functions, but can also respond to pathogenic stimuli by producing harmful pro-inflammatory cytokines or free radicals. Distinguishing between damaging and homeostatic microglia in human diseased brain tissues is a challenge. This report describes findings using a monoclonal antibody to CD105/Endoglin (R&D Systems MAB1097) that identifies subtypes of activated microglia. CD105/Endoglin is a co-receptor for transforming growth factor beta (TGFβ) receptor that antagonizes TGFβ signaling. CD105/Endoglin is a marker for vascular endothelial cells, but was originally identified as a marker for activated macrophages. This antibody did not identify endothelial cells in brain sections, only microglia-like cells. In this study, we examined with this antibody tissue section from middle temporal gyrus derived from human brains from normal control subjects with low-plaque pathology, high-plaque pathology, and AD cases, and also substantia nigra samples from control and PD cases, in conjunction with antibodies to markers of pathology and microglia. In low-plaque pathology cases, CD105-positive microglia were mostly absent, but noticeably increased with increasing pathology. CD105-positive cells strongly colocalized with amyloid-beta plaques, but not phosphorylated tau positive tangles. In substantia nigra, strong microglial CD105 staining was observed in microglia associated with degenerating dopaminergic neurons and neuromelanin. In PD cases with few surviving dopaminergic neurons, this staining had decreased. By Western blot, this antibody identified polypeptide bands of 70 kDa in brain samples, and samples from microglia, macrophages, and brain endothelial cells. In comparison with other tested CD105 antibodies, this antibody did not recognize the glycosylated forms of CD105 on Western blots. Overall, the data indicate that this antibody and this marker could have utility for subtyping of microglia in pathologically-involved tissue.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/metabolism ; Biomarkers/metabolism ; Brain/metabolism ; Brain/pathology ; Cells, Cultured ; Endoglin/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Female ; Humans ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Microglia/metabolism ; Microglia/pathology ; Parkinson Disease/metabolism
Chemical Substances	Biomarkers ; ENG protein, human ; Endoglin
Language	English
Publishing date	2019-07-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8070766
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Article: Immune phenotypes of microglia in human neurodegenerative disease: challenges to detecting microglial polarization in human brains.

Walker, Douglas G / Lue, Lih-Fen

Alzheimer's research & therapy

2015 Volume 7, Issue 1, Page(s) 56

Abstract: Inflammatory responses in the brain, which can be demonstrated by changes in properties of microglia, the brain-resident macrophages, are a common feature of human neurodegenerative diseases. Different monocyte/macrophage phenotypes have been defined by ... ...

Abstract	Inflammatory responses in the brain, which can be demonstrated by changes in properties of microglia, the brain-resident macrophages, are a common feature of human neurodegenerative diseases. Different monocyte/macrophage phenotypes have been defined by changes in expression of cytokines, receptors and other markers as a response to different classes of stimuli. Monocytes, macrophages and microglia can have a range of phenotypes with associated properties depending on their microenvironment. Macrophage/microglia polarization states have been defined as classical activation (M1), alternative activation (M2a), type II alternative activation (M2b) or acquired deactivation (M2c). Available markers for identifying microglial phenotypes in human brains are still limited; those available provide incomplete information on the functions or polarization states of microglia observed in tissues from diseases such as Alzheimer's disease, Parkinson's disease and multiple sclerosis. The most widely used marker to describe activated microglia in human brains, particularly diseased brains, has been HLA-DR, the major histocompatibility complex II protein. HLA-DR-positive microglia can have a wide range of activation morphologies that are affected not only by disease pathology, but also by their differentiation states and brain regions. Two other widely used markers to identify microglia in human brains are ionized calcium binding adaptor molecule-1 and CD68. Although their expression changes in diseased brains, these markers do not show specificity for different phenotypes. Over the years there have been studies with additional markers that attempt to further define microglial properties, particularly in Alzheimer's disease brains. Most studies have employed immunohistochemical techniques to identify microglia in tissue sections, but recent advances in this field have allowed gene expression profiling of microglia upon immediate isolation from brains. We will review which markers might better define different activation phenotypes of microglia in human brains and whether they fit into current microglial polarization schemes.
MeSH term(s)	Biomarkers/metabolism ; Brain/immunology ; Brain/pathology ; Humans ; Macrophages/pathology ; Macrophages/physiology ; Microglia/pathology ; Microglia/physiology ; Neurodegenerative Diseases/immunology ; Neurodegenerative Diseases/pathology ; Phenotype
Chemical Substances	Biomarkers
Language	English
Publishing date	2015-08-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2506521-X
ISSN	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-015-0139-9
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Article: Amyloid Beta and Tau as Alzheimer's Disease Blood Biomarkers: Promise From New Technologies.

Lue, Lih-Fen / Guerra, Andre / Walker, Douglas G

Neurology and therapy

2017 Volume 6, Issue Suppl 1, Page(s) 25–36

Abstract: The utility of the levels of amyloid beta (Aβ) peptide and tau in blood for diagnosis, drug development, and assessment of clinical trials for Alzheimer's disease (AD) has not been established. The lack of availability of ultra-sensitive assays is one ... ...

Abstract	The utility of the levels of amyloid beta (Aβ) peptide and tau in blood for diagnosis, drug development, and assessment of clinical trials for Alzheimer's disease (AD) has not been established. The lack of availability of ultra-sensitive assays is one critical issue that has impeded progress. The levels of Aβ species and tau in plasma and serum are much lower than levels in cerebrospinal fluid. Furthermore, plasma or serum contain high levels of assay-interfering factors, resulting in difficulties in the commonly used singulex or multiplex ELISA platforms. In this review, we focus on two modern immune-complex-based technologies that show promise to advance this field. These innovative technologies are immunomagnetic reduction technology and single molecule array technology. We describe the technologies and discuss the published studies using these technologies. Currently, the potential of utilizing these technologies to advance Aβ and tau as blood-based biomarkers for AD requires further validation using already collected large sets of samples, as well as new cohorts and population-based longitudinal studies.
Language	English
Publishing date	2017-07-21
Publishing country	New Zealand
Document type	Journal Article ; Review
ISSN	2193-8253
ISSN	2193-8253
DOI	10.1007/s40120-017-0074-8
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Article: Studies on Colony Stimulating Factor Receptor-1 and Ligands Colony Stimulating Factor-1 and Interleukin-34 in Alzheimer's Disease Brains and Human Microglia.

Walker, Douglas G / Tang, Tiffany M / Lue, Lih-Fen

Frontiers in aging neuroscience

2017 Volume 9, Page(s) 244

Abstract: Microglia are dependent on signaling through the colony stimulating factor-1 receptor (CSF-1R/CD115) for growth and survival. Activation of CSF-1R can lead to cell division, while blocking CSF-1R can lead to rapid microglia cell death. CSF-1R has two ... ...

Abstract	Microglia are dependent on signaling through the colony stimulating factor-1 receptor (CSF-1R/CD115) for growth and survival. Activation of CSF-1R can lead to cell division, while blocking CSF-1R can lead to rapid microglia cell death. CSF-1R has two ligands, the growth factors colony stimulating factor-1 (CSF-1) and the more recently identified interleukin-34 (IL-34). Studies of IL-34 activation of rodent microglia and human macrophages have suggested it has different properties to CSF-1, resulting in an anti-inflammatory reparative phenotype. The goal of this study was to identify if the responses of human postmortem brain microglia to IL-34 differed from their responses to CSF-1 with the aim of identifying different phenotypes of microglia as a result of their responses. To approach this question, we also sought to identify differences between IL-34, CSF-1, and CSF-1R expression in human brain samples to establish whether there was an imbalance in Alzheimer's disease (AD). Using human brain samples [inferior temporal gyrus (ITG) and middle temporal gyrus (MTG)] from distinct cohorts of AD, control and high pathology, or mild cognitive impairment cases, we showed that there was increased expression of CSF-1R and CSF-1 mRNAs in both series of AD cases, and reduced expression of IL-34 mRNA in AD ITG samples. There was no change in expression of these genes in RNA from cerebellum of AD, Parkinson's disease (PD), or control cases. The results suggested an imbalance in CSF-1R signaling in AD. Using RNA sequencing to compare gene expression responses of CSF-1 and IL-34 stimulated human microglia, a profile of responses to CSF-1 and IL-34 was identified. Contrary to earlier work with rodent microglia, IL-34 induced primarily a classical activation response similar to that of CSF-1. It was not possible to identify any genes expressed significantly different by IL-34-stimulated microglia compared to CSF-1-stimulated microglia, but both cytokines did induce certain alternative activation-associated genes. These profiles also showed that a number of genes associated with lysosomal function and Aβ removal were downregulated by IL-34 and CSF-1 stimulation. Compared to earlier results our data indicate that CSF-1R stimulation by IL-34 or CSF-1 produced similar types of responses by elderly postmortem brain-derived microglia.
Language	English
Publishing date	2017-08-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2017.00244
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Article ; Online: Microglial Phenotyping in Neurodegenerative Disease Brains

Douglas G. Walker / Lih-Fen Lue / Thomas G. Beach / Ikuo Tooyama

Cells, Vol 8, Iss 7, p

Identification of Reactive Microglia with an Antibody to Variant of CD105/Endoglin

2019 Volume 766

Abstract: Inflammation is considered a key pathological process in neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD), but there are still mechanisms not understood. In the brain, most microglia are performing essential ... ...

Abstract	Inflammation is considered a key pathological process in neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD), but there are still mechanisms not understood. In the brain, most microglia are performing essential homeostatic functions, but can also respond to pathogenic stimuli by producing harmful pro-inflammatory cytokines or free radicals. Distinguishing between damaging and homeostatic microglia in human diseased brain tissues is a challenge. This report describes findings using a monoclonal antibody to CD105/Endoglin (R&D Systems MAB1097) that identifies subtypes of activated microglia. CD105/Endoglin is a co-receptor for transforming growth factor beta (TGFβ) receptor that antagonizes TGFβ signaling. CD105/Endoglin is a marker for vascular endothelial cells, but was originally identified as a marker for activated macrophages. This antibody did not identify endothelial cells in brain sections, only microglia-like cells. In this study, we examined with this antibody tissue section from middle temporal gyrus derived from human brains from normal control subjects with low-plaque pathology, high-plaque pathology, and AD cases, and also substantia nigra samples from control and PD cases, in conjunction with antibodies to markers of pathology and microglia. In low-plaque pathology cases, CD105-positive microglia were mostly absent, but noticeably increased with increasing pathology. CD105-positive cells strongly colocalized with amyloid-beta plaques, but not phosphorylated tau positive tangles. In substantia nigra, strong microglial CD105 staining was observed in microglia associated with degenerating dopaminergic neurons and neuromelanin. In PD cases with few surviving dopaminergic neurons, this staining had decreased. By Western blot, this antibody identified polypeptide bands of 70 kDa in brain samples, and samples from microglia, macrophages, and brain endothelial cells. In comparison with other tested CD105 antibodies, this antibody did not recognize the glycosylated ...
Keywords	neuroinflammation ; neuropathology ; transforming growth factor ; activation ; microglia ; immunohistochemistry ; human ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2019-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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