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  1. Book: Microglia in the regenerating and degenerating central nervous system

    Streit, Wolfgang J.

    2002  

    Author's details Wolfgang J. Streit, ed
    Keywords Zentralnervensystem ; Nervenregeneration ; Mikroglia ; Nervendegeneration
    Subject Neurodegenerative Krankheit ; Neurodegenerative Erkrankung ; Zentrales Nervensystem ; ZNS ; Systema nervosum centrale ; Central nervous system ; CNS ; Reinnervation
    Language English
    Size XI, 315 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place New York
    Publishing country United States
    Document type Book
    HBZ-ID HT013354659
    ISBN 0-387-95301-9 ; 978-0-387-95301-4
    Database Catalogue ZB MED Medicine, Health

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    2002 A 2623 order for loan Magazin

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  2. Article ; Online: Is microglial dystrophy a form of cellular senescence? An analysis of senescence markers in the aged human brain.

    Neumann, Pauline / Lenz, Dana E / Streit, Wolfgang J / Bechmann, Ingo

    Glia

    2022  Volume 71, Issue 2, Page(s) 377–390

    Abstract: Aging can cause morphological transformation in human microglia indicative of cell senescence, termed microglial dystrophy. However, cellular senescence is characterized by additional changes, such as an irregular cell cycle arrest, and a variety of ... ...

    Abstract Aging can cause morphological transformation in human microglia indicative of cell senescence, termed microglial dystrophy. However, cellular senescence is characterized by additional changes, such as an irregular cell cycle arrest, and a variety of metabolic and molecular changes including a senescence-associated secretory phenotype, dysfunction of degradation mechanisms, and altered DNA damage response. Here, we tested whether dystrophic microglia display customary markers of cell senescence by performing double and triple staining in sections of the temporal lobe and brain stem from 14 humans. We found that markers related to oxidative damage, such as upregulation of 8-hydroxy-2'-deoxyguanosine (8-OHdG), hemeoxygenase-1 (HO-1), and y-H2AX, as well as inclusion of lipofuscin, do not or only exceptionally colocalize with dystrophic microglia. Further, we did not observe a decline in lamin B1 around nuclear laminae in either dystrophic or ramified microglia within the same microscopic field. Only ferritin expression, which is known to increase with aging in CNS microglia, was frequently observed in dystrophic, but rarely in ramified microglial cells. We conclude that neither dystrophic nor ramified microglia in human brain exhibit significant expression of conventional senescence markers associated with oxidative stress, and that ferritin is the dominant immunophenotypic change related to microglial aging. We suggest that multiple pathogenic mechanisms other than those driving cellular senescence contribute to dystrophic transformation of microglia.
    MeSH term(s) Humans ; Aged ; Microglia/metabolism ; Cellular Senescence ; Brain/metabolism ; Aging/pathology ; Ferritins/metabolism
    Chemical Substances Ferritins (9007-73-2)
    Language English
    Publishing date 2022-10-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.24282
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  3. Article ; Online: Beyond Activation: Characterizing Microglial Functional Phenotypes.

    Lier, Julia / Streit, Wolfgang J / Bechmann, Ingo

    Cells

    2021  Volume 10, Issue 9

    Abstract: Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. While ramified cells were long regarded as "resting", amoeboid and phagocytic microglia were viewed as "activated". In aged human ... ...

    Abstract Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. While ramified cells were long regarded as "resting", amoeboid and phagocytic microglia were viewed as "activated". In aged human brains, a fourth, morphologically novel state has been described, i.e., dystrophic microglia, which are thought to be senescent cells. Since microglia are not replenished by blood-borne mononuclear cells under physiological circumstances, they seem to have an "expiration date" limiting their capacity to phagocytose and support neurons. Identifying factors that drive microglial aging may thus be helpful to delay the onset of neurodegenerative diseases, such as Alzheimer's disease (AD). Recent progress in single-cell deep sequencing methods allowed for more refined differentiation and revealed regional-, age- and sex-dependent differences of the microglial population, and a growing number of studies demonstrate various expression profiles defining microglial subpopulations. Given the heterogeneity of pathologic states in the central nervous system, the need for accurately describing microglial morphology and expression patterns becomes increasingly important. Here, we review commonly used microglial markers and their fluctuations in expression in health and disease, with a focus on IBA1 low/negative microglia, which can be found in individuals with liver disease.
    MeSH term(s) Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Brain/metabolism ; Brain/pathology ; Calcium-Binding Proteins/metabolism ; Histocompatibility Antigens Class II/metabolism ; Humans ; Membrane Proteins/metabolism ; Microfilament Proteins/metabolism ; Microglia/metabolism ; Microglia/pathology ; Nerve Tissue Proteins/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Phagocytes/metabolism ; Phagocytes/pathology ; Phenotype ; Receptors, Purinergic P2Y12/metabolism ; Signal Transduction
    Chemical Substances AIF1 protein, human ; Antigens, CD ; Antigens, Differentiation, B-Lymphocyte ; Antigens, Differentiation, Myelomonocytic ; CD68 antigen, human ; Calcium-Binding Proteins ; Histocompatibility Antigens Class II ; Membrane Proteins ; Microfilament Proteins ; Nerve Tissue Proteins ; P2RY12 protein, human ; Receptors, Purinergic P2Y12 ; Tmem119 protein, human ; invariant chain
    Language English
    Publishing date 2021-08-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10092236
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  4. Article ; Online: The PET-Degrading Potential of Global Metagenomes: From In Silico Mining to Active Enzymes.

    Chow, Jennifer / Pérez-García, Pablo / Dierkes, Robert F / Zhang, Hongli / Streit, Wolfgang R

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

    2022  Volume 2555, Page(s) 139–151

    Abstract: Against the background of the steadily increasing amount of plastic waste in the sea and on land, it is more important than ever to find ways out of this situation. In recent years, microorganisms have been discovered that are capable of degrading ... ...

    Abstract Against the background of the steadily increasing amount of plastic waste in the sea and on land, it is more important than ever to find ways out of this situation. In recent years, microorganisms have been discovered that are capable of degrading artificial polymers such as polyethylene terephthalate (PET). Even if the turnover rates of the enzymes responsible for this reaction may be too low to solve the global plastic pollution problem, it is still of great societal interest to find microorganisms that are able to degrade the polymer. The corresponding enzymes, PET esterases (PETases) can be used in biotechnological processes and could contribute to a resource-saving circular economy. In this chapter, we present a sequence-based in silico screening method to find new PETases in metagenomic datasets. This method can easily be adapted to find other enzyme classes. We also list a number of assays that can be used to test the enzymes for activity on PET as well as other substrates.
    MeSH term(s) Polyethylene Terephthalates/chemistry ; Polyethylene Terephthalates/metabolism ; Metagenome ; Esterases/genetics ; Esterases/chemistry ; Metagenomics ; Plastics ; Hydrolases/genetics ; Hydrolases/metabolism
    Chemical Substances Polyethylene Terephthalates ; Esterases (EC 3.1.-) ; Plastics ; Hydrolases (EC 3.-)
    Language English
    Publishing date 2022-10-28
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2795-2_10
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  5. Article ; Online: The Role of Microglia in Sporadic Alzheimer's Disease.

    Streit, Wolfgang J / Khoshbouei, Habibeh / Bechmann, Ingo

    Journal of Alzheimer's disease : JAD

    2020  Volume 79, Issue 3, Page(s) 961–968

    Abstract: Microglia constitute the brain's immune system and their involvement in Alzheimer's disease has been discussed. Commonly, and in line with the amyloid/neuroinflammation cascade hypothesis, microglia have been portrayed as potentially dangerous immune ... ...

    Abstract Microglia constitute the brain's immune system and their involvement in Alzheimer's disease has been discussed. Commonly, and in line with the amyloid/neuroinflammation cascade hypothesis, microglia have been portrayed as potentially dangerous immune effector cells thought to be overactivated by amyloid and producing neurotoxic inflammatory mediators that lead to neurofibrillary degeneration. We disagree with this theory and offer as an alternative the microglial dysfunction theory stating that microglia become impaired in their normally neuroprotective roles because of aging, i.e., they become senescent and aging neurons degenerate because they lack the needed microglial support for their survival. Thus, while the amyloid cascade theory relies primarily on genetic data, the dysfunction theory incorporates aging as a critical etiological factor. Aging is the greatest risk factor for the sporadic (late-onset) and most common form of Alzheimer's disease, where fully penetrant genetic mutations are absent. In this review, we lay out and discuss the human evidence that supports senescent microglial dysfunction and conflicts with the amyloid/neuroinflammation idea.
    MeSH term(s) Aging/pathology ; Alzheimer Disease/etiology ; Alzheimer Disease/immunology ; Alzheimer Disease/pathology ; Humans ; Microglia/immunology ; Microglia/pathology
    Language English
    Publishing date 2020-12-23
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-201248
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  6. Article ; Online: Beyond Activation

    Julia Lier / Wolfgang J. Streit / Ingo Bechmann

    Cells, Vol 10, Iss 2236, p

    Characterizing Microglial Functional Phenotypes

    2021  Volume 2236

    Abstract: Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. While ramified cells were long regarded as “resting”, amoeboid and phagocytic microglia were viewed as “activated”. In aged human ... ...

    Abstract Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. While ramified cells were long regarded as “resting”, amoeboid and phagocytic microglia were viewed as “activated”. In aged human brains, a fourth, morphologically novel state has been described, i.e., dystrophic microglia, which are thought to be senescent cells. Since microglia are not replenished by blood-borne mononuclear cells under physiological circumstances, they seem to have an “expiration date” limiting their capacity to phagocytose and support neurons. Identifying factors that drive microglial aging may thus be helpful to delay the onset of neurodegenerative diseases, such as Alzheimer’s disease (AD). Recent progress in single-cell deep sequencing methods allowed for more refined differentiation and revealed regional-, age- and sex-dependent differences of the microglial population, and a growing number of studies demonstrate various expression profiles defining microglial subpopulations. Given the heterogeneity of pathologic states in the central nervous system, the need for accurately describing microglial morphology and expression patterns becomes increasingly important. Here, we review commonly used microglial markers and their fluctuations in expression in health and disease, with a focus on IBA1 low/negative microglia, which can be found in individuals with liver disease.
    Keywords microglia ; IBA1 ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2021-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Dystrophic microglia in late-onset Alzheimer's disease.

    Streit, Wolfgang J / Khoshbouei, Habibeh / Bechmann, Ingo

    Glia

    2020  Volume 68, Issue 4, Page(s) 845–854

    Abstract: Here, we summarize current understanding of functional involvement of microglial cells in the most common neurodegenerative disease to affect humans, which is sporadic or late-onset Alzheimer's disease (LOAD). Our review narrowly focuses on insights ... ...

    Abstract Here, we summarize current understanding of functional involvement of microglial cells in the most common neurodegenerative disease to affect humans, which is sporadic or late-onset Alzheimer's disease (LOAD). Our review narrowly focuses on insights obtained from post-mortem neuropathological examinations of human brains paying particular attention to microglia as these cells have long been implicated as pivotal players in the cellular processes that lead to AD-type neurodegeneration. Although complete understanding of the roles played by microglia in AD neurodegeneration remains elusive, our studies thus far have illuminated microglial involvement in LOAD, showing that microglial dystrophy, the morphological manifestation of senescence, can be integrated with other hallmark pathological features of AD, such as intraneuronal neurofibrillary degeneration (NFD) and extracellular deposits of amyloid-beta (Aβ) protein. We have demonstrated an in situ correlation between microglial dystrophy and presence of NFD suggesting that neurodegeneration is secondary to aging-related microglial deterioration, a concept founded on the notion that proper neuronal function is dependent on presence of healthy microglia. Diseased or weakened glia are detrimental for neuronal well-being because their ability to provide neuronal support may be impaired. Our most recent work also links microglial dystrophy with Aβ deposits by showing that there is a chronic, yet futile microglial reaction to insoluble amyloid deposits. This inability of microglia to remove aggregated amyloid (a foreign body) causes microglial exhaustion and thereby exacerbates already ongoing aging-dependent microglial deterioration. An eventual total loss of functional microglia in advanced LOAD promotes widespread NFD, dementia, and brain failure.
    MeSH term(s) Aging/pathology ; Alzheimer Disease/pathology ; Brain/pathology ; Humans ; Microglia/pathology ; Neurofibrillary Tangles/pathology
    Language English
    Publishing date 2020-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.23782
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  8. Book: Microglia

    Streit, Wolfgang J. / Gräber, Manuel B.

    a pictorial ; with 1 table

    (Progress in histochemistry and cytochemistry ; 31,1)

    1996  

    Author's details W. J. Streit ; M. B. Graeber
    Series title Progress in histochemistry and cytochemistry ; 31,1
    Collection
    Keywords Microglia ; Mikroglia ; Neurohistologie ; Neuropathologie
    Subject Nervensystem
    Language English
    Size X, 89 S. : überw. Ill.
    Publisher Fischer
    Publishing place Stuttgart u.a.
    Publishing country Germany
    Document type Book
    HBZ-ID HT007297559
    ISBN 3-437-21036-X ; 1-56081-450-0 ; 978-3-437-21036-5 ; 978-1-56081-450-4
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Se 23 -31,1- verfügbar in Königswinter Königswinter

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  9. Article ; Online: Microglia and Other Myeloid Cells in Central Nervous System Health and Disease.

    Gopinath, Adithya / Collins, Anthony / Khoshbouei, Habibeh / Streit, Wolfgang J

    The Journal of pharmacology and experimental therapeutics

    2020  Volume 375, Issue 1, Page(s) 154–160

    Abstract: Mononuclear macrophages derived from the bone marrow (myeloid cells) are key cellular components of the innate immune system in different organs. In this minireview, we are focused on both brain and blood macrophages, known as microglia and monocytes, ... ...

    Abstract Mononuclear macrophages derived from the bone marrow (myeloid cells) are key cellular components of the innate immune system in different organs. In this minireview, we are focused on both brain and blood macrophages, known as microglia and monocytes, respectively. We provide a succinct summary of the cells' functions under both normal and pathologic conditions, with particular reference to common neurodegenerative disorders, such as Alzheimer and Parkinson disease. SIGNIFICANCE STATEMENT: In this minireview, we aim to summarize available literature on microglial and myeloid involvement in CNS disease, directing the reader toward relevant and translatable interpretations of myeloid cell function in CNS health and neurodegeneration.
    MeSH term(s) Alzheimer Disease/blood ; Alzheimer Disease/immunology ; Alzheimer Disease/pathology ; Animals ; Central Nervous System/immunology ; Central Nervous System/pathology ; Humans ; Macrophages/immunology ; Macrophages/pathology ; Microglia/immunology ; Microglia/pathology ; Monocytes/immunology ; Monocytes/pathology ; Myeloid Cells/immunology ; Myeloid Cells/pathology ; Neuroimmunomodulation ; Parkinson Disease/blood ; Parkinson Disease/immunology ; Parkinson Disease/pathology
    Language English
    Publishing date 2020-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.120.265058
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  10. Article ; Online: Droplet Degeneration of Hippocampal and Cortical Neurons Signifies the Beginning of Neuritic Plaque Formation.

    Streit, Wolfgang J / Rotter, Jonas / Winter, Karsten / Müller, Wolf / Khoshbouei, Habibeh / Bechmann, Ingo

    Journal of Alzheimer's disease : JAD

    2021  Volume 85, Issue 4, Page(s) 1701–1720

    Abstract: Background: Neuritic plaques contain neural and microglial elements, and amyloid-β protein (Aβ), but their pathogenesis remains unknown.: Objective: Elucidate neuritic plaque pathogenesis.: Methods: Histochemical visualization of ... ...

    Abstract Background: Neuritic plaques contain neural and microglial elements, and amyloid-β protein (Aβ), but their pathogenesis remains unknown.
    Objective: Elucidate neuritic plaque pathogenesis.
    Methods: Histochemical visualization of hyperphosphorylated-tau positive (p-tau+) structures, microglia, Aβ, and iron.
    Results: Disintegration of large projection neurons in human hippocampus and neocortex presents as droplet degeneration: pretangle neurons break up into spheres of numerous p-tau+ droplets of various sizes, which marks the beginning of neuritic plaques. These droplet spheres develop in the absence of colocalized Aβ deposits but once formed become encased in diffuse Aβ with great specificity. In contrast, neurofibrillary tangles often do not colocalize with Aβ. Double-labelling for p-tau and microglia showed a lack of microglial activation or phagocytosis of p-tau+ degeneration droplets but revealed massive upregulation of ferritin in microglia suggesting presence of high levels of free iron. Perl's Prussian blue produced positive staining of microglia, droplet spheres, and Aβ plaque cores supporting the suggestion that droplet degeneration of pretangle neurons in the hippocampus and cortex represents ferroptosis, which is accompanied by the release of neuronal iron extracellularly.
    Conclusion: Age-related iron accumulation and ferroptosis in the CNS likely trigger at least two endogenous mechanisms of neuroprotective iron sequestration and chelation, microglial ferritin expression and Aβ deposition, respectively, both contributing to the formation of neuritic plaques. Since neurofibrillary tangles and Aβ deposits colocalize infrequently, tangle formation likely does not involve release of neuronal iron extracellularly. In human brain, targeted deposition of Aβ occurs specifically in response to ongoing ferroptotic droplet degeneration thereby producing neuritic plaques.
    MeSH term(s) Aged ; Aged, 80 and over ; Alzheimer Disease/pathology ; Autopsy ; Brain/pathology ; Female ; Hippocampus/pathology ; Humans ; Immunohistochemistry ; Male ; Microglia/pathology ; Neocortex/pathology ; Neurons/pathology ; Plaque, Amyloid/pathology
    Language English
    Publishing date 2021-12-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-215334
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