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  1. Article ; Online: Astrocytic contributions to Huntington's disease pathophysiology.

    Khakh, Baljit S / Goldman, Steven A

    Annals of the New York Academy of Sciences

    2023  Volume 1522, Issue 1, Page(s) 42–59

    Abstract: Huntington's disease (HD) is a fatal, monogenic, autosomal dominant neurodegenerative disease caused by a polyglutamine-encoding CAG expansion in the huntingtin (HTT) gene that results in mutant huntingtin proteins (mHTT) in cells throughout the body. ... ...

    Abstract Huntington's disease (HD) is a fatal, monogenic, autosomal dominant neurodegenerative disease caused by a polyglutamine-encoding CAG expansion in the huntingtin (HTT) gene that results in mutant huntingtin proteins (mHTT) in cells throughout the body. Although large parts of the central nervous system (CNS) are affected, the striatum is especially vulnerable and undergoes marked atrophy. Astrocytes are abundant within the striatum and contain mHTT in HD, as well as in mouse models of the disease. We focus on striatal astrocytes and summarize how they participate in, and contribute to, molecular pathophysiology and disease-related phenotypes in HD model mice. Where possible, reference is made to pertinent astrocyte alterations in human HD. Astrocytic dysfunctions related to cellular morphology, extracellular ion and neurotransmitter homeostasis, and metabolic support all accompany the development and progression of HD, in both transgenic mouse and human cellular and chimeric models of HD. These findings reveal the potential for the therapeutic targeting of astrocytes so as to restore synaptic as well as tissue homeostasis in HD. Elucidation of the mechanisms by which astrocytes contribute to HD pathogenesis may inform a broader understanding of the role of glial pathology in neurodegenerative disorders and, by so doing, enable new strategies of glial-directed therapeutics.
    MeSH term(s) Animals ; Humans ; Mice ; Astrocytes/metabolism ; Disease Models, Animal ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Mice, Transgenic ; Neuroglia ; Neurons/metabolism
    Language English
    Publishing date 2023-03-02
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/nyas.14977
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Remyelination in the Central Nervous System.

    Franklin, Robin J M / Bodini, Benedetta / Goldman, Steven A

    Cold Spring Harbor perspectives in biology

    2024  Volume 16, Issue 3

    Abstract: The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, while this is largely true of the neuronal elements of the adult mammalian CNS, save for ... ...

    Abstract The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, while this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granule neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated and myelin sheaths are restored to denuded axons. Yet remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this work, we will (1) review the biology of remyelination, including the cells and signals involved; (2) describe when remyelination occurs and when and why it fails, including the consequences of its failure; and (3) discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.
    MeSH term(s) Animals ; Adult ; Child ; Humans ; Remyelination/physiology ; Demyelinating Diseases ; Nerve Regeneration/physiology ; Myelin Sheath/physiology ; Central Nervous System ; Mammals
    Language English
    Publishing date 2024-03-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1943-0264
    ISSN (online) 1943-0264
    DOI 10.1101/cshperspect.a041371
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  3. Article ; Online: Glial evolution as a determinant of human behavior and its disorders.

    Goldman, Steven A

    Annals of the New York Academy of Sciences

    2020  Volume 1471, Issue 1, Page(s) 72–85

    Abstract: Astroglial complexity and pleomorphism have increased significantly with hominid evolution. This suggests a potential association between glial evolution and the development of human cognition, as well as between glial evolution and the advent of human- ... ...

    Abstract Astroglial complexity and pleomorphism have increased significantly with hominid evolution. This suggests a potential association between glial evolution and the development of human cognition, as well as between glial evolution and the advent of human-selective neurodegenerative and neuropsychiatric disorders.
    MeSH term(s) Astrocytes/physiology ; Biological Evolution ; Brain/physiology ; Cognition/physiology ; Humans ; Neuroglia/physiology
    Language English
    Publishing date 2020-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/nyas.14372
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Astrocytes as master modulators of neural networks: Synaptic functions and disease-associated dysfunction of astrocytes.

    Stogsdill, Jeffrey A / Harwell, Corey C / Goldman, Steven A

    Annals of the New York Academy of Sciences

    2023  Volume 1525, Issue 1, Page(s) 41–60

    Abstract: Astrocytes are the most abundant glial cell type in the central nervous system and are essential to the development, plasticity, and maintenance of neural circuits. Astrocytes are heterogeneous, with their diversity rooted in developmental programs ... ...

    Abstract Astrocytes are the most abundant glial cell type in the central nervous system and are essential to the development, plasticity, and maintenance of neural circuits. Astrocytes are heterogeneous, with their diversity rooted in developmental programs modulated by the local brain environment. Astrocytes play integral roles in regulating and coordinating neural activity extending far beyond their metabolic support of neurons and other brain cell phenotypes. Both gray and white matter astrocytes occupy critical functional niches capable of modulating brain physiology on time scales slower than synaptic activity but faster than those adaptive responses requiring a structural change or adaptive myelination. Given their many associations and functional roles, it is not surprising that astrocytic dysfunction has been causally implicated in a broad set of neurodegenerative and neuropsychiatric disorders. In this review, we focus on recent discoveries concerning the contributions of astrocytes to the function of neural networks, with a dual focus on the contribution of astrocytes to synaptic development and maturation, and on their role in supporting myelin integrity, and hence conduction and its regulation. We then address the emerging roles of astrocytic dysfunction in disease pathogenesis and on potential strategies for targeting these cells for therapeutic purposes.
    MeSH term(s) Humans ; Astrocytes/physiology ; Neuroglia ; Neurons/metabolism ; Myelin Sheath ; Neural Networks, Computer
    Language English
    Publishing date 2023-05-23
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/nyas.15004
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  5. Article ; Online: Transplanted neural progenitors bridge gaps to benefit cord-injured monkeys.

    Goldman, Steven A

    Nature medicine

    2018  Volume 24, Issue 4, Page(s) 388–390

    MeSH term(s) Animals ; Haplorhini ; Humans ; Neural Stem Cells/transplantation ; Spinal Cord
    Language English
    Publishing date 2018-06-08
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.4531
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  6. Article: Secreted in xylem 6 (

    Dilla-Ermita, Christine Jade / Goldman, Polly / Anchieta, Amy / Feldmann, Mitchell J / Pincot, Dominique D A / Famula, Randi A / Vachev, Mishi / Cole, Glenn S / Knapp, Steven J / Klosterman, Steven J / Henry, Peter M

    Molecular plant-microbe interactions : MPMI

    2024  

    Abstract: ... Fusarium ... ...

    Abstract Fusarium oxysporum
    Language English
    Publishing date 2024-03-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 743331-1
    ISSN 1943-7706 ; 0894-0282
    ISSN (online) 1943-7706
    ISSN 0894-0282
    DOI 10.1094/MPMI-02-24-0012-R
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  7. Article ; Online: Patience pays in spinal repair.

    Goldman, Steven A

    The Journal of clinical investigation

    2017  Volume 127, Issue 9, Page(s) 3284–3286

    Abstract: Transplantation of human neural stem cells has long been proposed as a potential strategy for treating CNS injury and disease; however, application of this approach has had limited therapeutic benefit. Yet compared with rodents and other experimental ... ...

    Abstract Transplantation of human neural stem cells has long been proposed as a potential strategy for treating CNS injury and disease; however, application of this approach has had limited therapeutic benefit. Yet compared with rodents and other experimental mammals, humans have a relatively long time window for development of the brain and spinal cord. In this issue of the JCI, Lu and colleagues asked whether the results of neural stem cell transplantation might be improved by accommodating the protracted development of human neural cells. They used a rodent model of spinal cord injury, in which human neural progenitor cells were transplanted at the site of damage. While there was no observable benefit at early time points after transplantation, both anatomic and functional improvements in the injured animals emerged over the course of a year. In particular, the human progenitor cell population differentiated, matured, and integrated into the rodent spinal cords over a time frame that aligned with the normal development of these cells in humans. This study demonstrates that neural stem cells may offer significant therapeutic benefit after CNS injury; however, this process may take time and demands patience on the part of investigators, patients, and clinicians alike.
    MeSH term(s) Animals ; Cell Differentiation ; Humans ; Neural Stem Cells/transplantation ; Spinal Cord ; Spinal Cord Injuries ; Stem Cell Transplantation
    Language English
    Publishing date 2017-08-21
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI96650
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  8. Article ; Online: Progenitor cell-based treatment of glial disease.

    Goldman, Steven A

    Progress in brain research

    2017  Volume 231, Page(s) 165–189

    Abstract: Diseases of glia, including astrocytes and oligodendrocytes, are among the most prevalent and disabling, yet least appreciated, conditions in neurology. In recent years, it has become clear that besides the overtly glial disorders of oligodendrocyte loss ...

    Abstract Diseases of glia, including astrocytes and oligodendrocytes, are among the most prevalent and disabling, yet least appreciated, conditions in neurology. In recent years, it has become clear that besides the overtly glial disorders of oligodendrocyte loss and myelin failure, such as the leukodystrophies and inflammatory demyelinations, a number of neurodegenerative and psychiatric disorders may also be causally linked to glial dysfunction and derive from astrocytic as well as oligodendrocytic pathology. The relative contribution of glial dysfunction to many of these disorders may be so great as to allow their treatment by the delivery of allogeneic glial progenitor cells, the precursors to both astroglia and myelin-producing oligodendrocytes. Given the development of new methods for producing and isolating these cells from pluripotent stem cells, both the myelin disorders and appropriate glial-based neurodegenerative conditions may now be compelling targets for cell-based therapy. As such, glial cell-based therapies may offer potential benefit to a broader range of diseases than ever before contemplated, including disorders such as Huntington's disease and the motor neuron degeneration of amyotrophic lateral sclerosis, which have traditionally been considered neuronal in nature.
    MeSH term(s) Demyelinating Diseases/therapy ; Humans ; Myelin Sheath ; Neuroglia/cytology ; Oligodendroglia/cytology ; Pluripotent Stem Cells/cytology
    Language English
    Publishing date 2017
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1875-7855 ; 0079-6123
    ISSN (online) 1875-7855
    ISSN 0079-6123
    DOI 10.1016/bs.pbr.2017.02.010
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  9. Article ; Online: Glymphatic failure as a final common pathway to dementia.

    Nedergaard, Maiken / Goldman, Steven A

    Science (New York, N.Y.)

    2020  Volume 370, Issue 6512, Page(s) 50–56

    Abstract: Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. Sleep quality decreases as we age, and disruption of the regular sleep architecture is a frequent antecedent to the onset of dementia in ... ...

    Abstract Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. Sleep quality decreases as we age, and disruption of the regular sleep architecture is a frequent antecedent to the onset of dementia in neurodegenerative diseases. The glymphatic system, which clears the brain of protein waste products, is mostly active during sleep. Yet the glymphatic system degrades with age, suggesting a causal relationship between sleep disturbance and symptomatic progression in the neurodegenerative dementias. The ties that bind sleep, aging, glymphatic clearance, and protein aggregation have shed new light on the pathogenesis of a broad range of neurodegenerative diseases, for which glymphatic failure may constitute a therapeutically targetable final common pathway.
    MeSH term(s) Aging ; Alzheimer Disease/etiology ; Alzheimer Disease/physiopathology ; Animals ; Aquaporin 4/genetics ; Cardiovascular Diseases/etiology ; Glymphatic System/physiopathology ; Humans ; Lymphatic System/physiopathology ; Mice ; Polymorphism, Genetic ; Prion Proteins/metabolism ; Protein Aggregates ; Sleep ; Sleep Wake Disorders/complications ; Sleep Wake Disorders/physiopathology
    Chemical Substances Aquaporin 4 ; Prion Proteins ; Protein Aggregates
    Language English
    Publishing date 2020-10-01
    Publishing country United States
    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 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abb8739
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  10. Article ; Online: Corticobasal Syndrome with TAR Binding Protein 43-Positive Oligodendrocyte Inclusions.

    Goldman, James E / Rippon, Gregory A / Chin, Steven S / Marder, Karen

    Movement disorders : official journal of the Movement Disorder Society

    2022  Volume 37, Issue 7, Page(s) 1564–1565

    MeSH term(s) Brain/metabolism ; Carrier Proteins/metabolism ; Corticobasal Degeneration ; Humans ; Inclusion Bodies/metabolism ; Oligodendroglia/metabolism
    Chemical Substances Carrier Proteins
    Language English
    Publishing date 2022-05-26
    Publishing country United States
    Document type Letter
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.29070
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