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  1. Article ; Online: Balancing Scientific Advice with Political Realities during the Campaign to Pass California's Ballot Proposition 14.

    Goldstein, Lawrence S B

    Cell stem cell

    2021  Volume 28, Issue 1, Page(s) 12–16

    MeSH term(s) California ; Politics ; Science
    Language English
    Publishing date 2021-07-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2020.12.010
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  2. Article ; Online: Human fetal tissue is critical for biomedical research.

    Brumbaugh, Justin / Aguado, Brian A / Lysaght, Tamra / Goldstein, Lawrence S B

    Stem cell reports

    2023  Volume 18, Issue 12, Page(s) 2300–2312

    Abstract: Human fetal tissue and cells derived from fetal tissue are crucial for biomedical research. Fetal tissues and cells are used to study both normal development and developmental disorders. They are broadly applied in vaccine development and production. ... ...

    Abstract Human fetal tissue and cells derived from fetal tissue are crucial for biomedical research. Fetal tissues and cells are used to study both normal development and developmental disorders. They are broadly applied in vaccine development and production. Further, research using cells from fetal tissue is instrumental for studying many infectious diseases, including a broad range of viruses. These widespread applications underscore the value of fetal tissue research and reflect an important point: cells derived from fetal tissues have capabilities that cells from other sources do not. In many cases, increased functionality of cells derived from fetal tissues arises from increased proliferative capacity, ability to survive in culture, and developmental potential that is attenuated in adult tissues. This review highlights important, representative applications of fetal tissue for science and medicine.
    MeSH term(s) Adult ; Humans ; Fetus ; Fetal Research
    Language English
    Publishing date 2023-11-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2720528-9
    ISSN 2213-6711 ; 2213-6711
    ISSN (online) 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2023.10.008
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  3. Article ; Online: Human-Induced Pluripotent Stem Cell (hiPSC)-Derived Neurons and Glia for the Elucidation of Pathogenic Mechanisms in Alzheimer's Disease.

    Young, Jessica E / Goldstein, Lawrence S B

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

    2022  Volume 2561, Page(s) 105–133

    Abstract: Alzheimer's disease (AD) is a common neurodegenerative disorder and a mechanistically complex disease. For the last decade, human models of AD using induced pluripotent stem cells (iPSCs) have emerged as a powerful way to understand disease pathogenesis ... ...

    Abstract Alzheimer's disease (AD) is a common neurodegenerative disorder and a mechanistically complex disease. For the last decade, human models of AD using induced pluripotent stem cells (iPSCs) have emerged as a powerful way to understand disease pathogenesis in relevant human cell types. In this review, we summarize the state of the field and how this technology can apply to studies of both familial and sporadic studies of AD. We discuss patient-derived iPSCs, genome editing, differentiation of neural cell types, and three-dimensional organoids, and speculate on the future of this type of work for increasing our understanding of, and improving therapeutic development for, this devastating disease.
    MeSH term(s) Humans ; Induced Pluripotent Stem Cells ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Neurons/pathology ; Neuroglia/pathology ; Organoids/pathology
    Language English
    Publishing date 2022-11-18
    Publishing country United States
    Document type Review ; Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2655-9_6
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  4. Article ; Online: The cellular machinery of post-endocytic APP trafficking in Alzheimer's disease: A future target for therapeutic intervention?

    Goldstein, Lawrence S B / Das, Utpal

    Progress in molecular biology and translational science

    2020  Volume 177, Page(s) 109–122

    Abstract: Recent data establish multiple defects in endocytic functions as early events initiating various neurodegenerative disorders, including Alzheimer's disease (AD). The genetic landscape resulting from genome-wide association studies (GWAS) reveals changes ... ...

    Abstract Recent data establish multiple defects in endocytic functions as early events initiating various neurodegenerative disorders, including Alzheimer's disease (AD). The genetic landscape resulting from genome-wide association studies (GWAS) reveals changes in post-endocytic trafficking of amyloid precursor protein (APP) in neurons leading to an increase in amyloidogenic processing, deficits in amyloid beta (Aβ) clearance, increases in intracellular Aβ, and other endosomal pathogenic phenotypes. Multiple genetic factors regulate each segment of endosomal and post-endosomal trafficking. Intriguingly, several studies indicate endosomal dysfunctions preceding Aβ pathology and tau phosphorylation. In this chapter we highlight the role of various GWAS-identified endosomal and post-endosomal gene products in initiating AD pathologies. We also summarize the functions of various genetic modifiers of post-endocytic trafficking of APP that may work as targets for therapeutic intervention in AD.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Endosomes/metabolism ; Genome-Wide Association Study ; Humans ; Protein Transport
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor
    Language English
    Publishing date 2020-08-28
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2471995-X
    ISSN 1878-0814 ; 0079-6603 ; 1877-1173
    ISSN (online) 1878-0814
    ISSN 0079-6603 ; 1877-1173
    DOI 10.1016/bs.pmbts.2020.08.001
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  5. Article ; Online: Stem cells on the ballot.

    Goldstein, Lawrence S B / Klein, Robert N

    Science (New York, N.Y.)

    2021  Volume 371, Issue 6526, Page(s) 215

    MeSH term(s) Animals ; California ; Capital Financing ; Embryonic Stem Cells ; Federal Government ; Humans ; Mice ; Politics ; Regenerative Medicine/economics ; Regenerative Medicine/ethics ; Stem Cell Research/economics ; Stem Cell Research/ethics
    Language English
    Publishing date 2021-01-11
    Publishing country United States
    Document type Editorial
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abf8704
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  6. Article ; Online: Why we need fetal tissue research.

    Temple, Sally / Goldstein, Lawrence S B

    Science (New York, N.Y.)

    2019  Volume 363, Issue 6424, Page(s) 207

    MeSH term(s) Ethics, Medical ; Fetal Research ; Humans ; Models, Biological ; Organoids
    Language English
    Publishing date 2019-01-14
    Publishing country United States
    Document type Editorial
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aaw6299
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  7. Article ; Online: New frontiers in human cell biology and medicine: can pluripotent stem cells deliver?

    Goldstein, Lawrence S B

    The Journal of cell biology

    2012  Volume 199, Issue 4, Page(s) 577–581

    Abstract: Human pluripotent stem cells provide enormous opportunities to treat disease using cell therapy. But human stem cells can also drive biomedical and cell biological discoveries in a human model system, which can be directly linked to understanding disease ...

    Abstract Human pluripotent stem cells provide enormous opportunities to treat disease using cell therapy. But human stem cells can also drive biomedical and cell biological discoveries in a human model system, which can be directly linked to understanding disease or developing new therapies. Finally, rigorous scientific studies of these cells can and should inform the many science and medical policy issues that confront the translation of these technologies to medicine. In this paper, I discuss these issues using amyotrophic lateral sclerosis as an example.
    MeSH term(s) Cell Biology ; Humans ; Medicine ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Stem Cell Transplantation/methods
    Language English
    Publishing date 2012-11-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201209118
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  8. Article ; Online: An October call to arms: we are research!

    Goldstein, Lawrence S B

    Molecular biology of the cell

    2012  Volume 23, Issue 17, Page(s) 3279–3280

    Abstract: The American Society for Cell Biology is targeting the first week of October 2012 (the week before Nobel Prize winners are announced) to launch the We Are Research initiative. The goal of this initiative is to mobilize practicing junior and senior ... ...

    Abstract The American Society for Cell Biology is targeting the first week of October 2012 (the week before Nobel Prize winners are announced) to launch the We Are Research initiative. The goal of this initiative is to mobilize practicing junior and senior scientists, including graduate students, postdocs, and other lab members, to make contact with their elected officials and neighbors and explain to them why Federal support and investment in biomedical research is vital to the health and economic welfare of the United States. This initiative is designed to illustrate how important people are to scientific research and to supply our representatives with reliable and accurate information in the form of letters, emails, telephone calls, and personal visits.
    MeSH term(s) Biomedical Research ; Financing, Government ; Lobbying ; Research Support as Topic ; Societies, Scientific ; United States
    Language English
    Publishing date 2012-08-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1098979-1
    ISSN 1939-4586 ; 1059-1524
    ISSN (online) 1939-4586
    ISSN 1059-1524
    DOI 10.1091/mbc.E12-01-0064
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  9. Article ; Online: Axonal transport and neurodegenerative disease: can we see the elephant?

    Goldstein, Lawrence S B

    Progress in neurobiology

    2012  Volume 99, Issue 3, Page(s) 186–190

    Abstract: Although it is well established that axonal transport defects are part of the initiation or progression of some neurodegenerative diseases, the precise role of these defects in disease development is poorly understood. Thus, in this article, rather than ... ...

    Abstract Although it is well established that axonal transport defects are part of the initiation or progression of some neurodegenerative diseases, the precise role of these defects in disease development is poorly understood. Thus, in this article, rather than enumerate the already well-reviewed evidence that there are transport deficits in disease, I will focus on a discussion of two crucial and unanswered questions about the possible role of axonal transport defects in HD and AD. (1) Are alterations in axonal transport caused by changes in the normal function of proteins mutated or altered in HD and AD and/or do such alterations in transport occur as a result of the formation of toxic aggregates of peptides or proteins? (2) Do alterations in axonal transport contribute to the causes of HD and AD or are they early, or late, secondary consequences of other cellular defects caused by disease-induction?
    MeSH term(s) Animals ; Axonal Transport/physiology ; Disease Progression ; Dyneins/metabolism ; Humans ; Kinesin/metabolism ; Neurodegenerative Diseases/diagnosis ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/physiopathology
    Chemical Substances Dyneins (EC 3.6.4.2) ; Kinesin (EC 3.6.4.4)
    Language English
    Publishing date 2012-04-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 185535-9
    ISSN 1873-5118 ; 0301-0082
    ISSN (online) 1873-5118
    ISSN 0301-0082
    DOI 10.1016/j.pneurobio.2012.03.006
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  10. Article ; Online: Amyloid-β-independent regulators of tau pathology in Alzheimer disease.

    van der Kant, Rik / Goldstein, Lawrence S B / Ossenkoppele, Rik

    Nature reviews. Neuroscience

    2019  Volume 21, Issue 1, Page(s) 21–35

    Abstract: The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. AD pathology is characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the ... ...

    Abstract The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. AD pathology is characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain. Genetic data, as well as autopsy and neuroimaging studies in patients with AD, indicate that Aβ plaque deposition precedes cortical tau pathology. Because Aβ accumulation has been considered the initial insult that drives both the accumulation of tau pathology and tau-mediated neurodegeneration in AD, the development of AD therapeutics has focused mostly on removing Aβ from the brain. However, striking preclinical evidence from AD mouse models and patient-derived human induced pluripotent stem cell models indicates that tau pathology can progress independently of Aβ accumulation and arises downstream of genetic risk factors for AD and aberrant metabolic pathways. This Review outlines novel insights from preclinical research that implicate apolipoprotein E, the endocytic system, cholesterol metabolism and microglial activation as Aβ-independent regulators of tau pathology. These factors are discussed in the context of emerging findings from clinical pathology, functional neuroimaging and other approaches in humans. Finally, we discuss the implications of these new insights for current Aβ-targeted strategies and highlight the emergence of novel therapeutic strategies that target processes upstream of both Aβ and tau.
    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/therapy ; Amyloid beta-Peptides/metabolism ; Animals ; Apolipoproteins E/metabolism ; Cholesterol/metabolism ; Endocytosis ; Humans ; Microglia/metabolism ; Plaque, Amyloid/pathology ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Apolipoproteins E ; tau Proteins ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2019-11-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2034150-7
    ISSN 1471-0048 ; 1471-0048 ; 1471-003X
    ISSN (online) 1471-0048
    ISSN 1471-0048 ; 1471-003X
    DOI 10.1038/s41583-019-0240-3
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