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  1. Article ; Online: Ole Isacson: development of new therapies for Parkinson's disease (interview).

    Isacson, Ole

    Journal of visualized experiments : JoVE

    2007  , Issue 3, Page(s) 189

    MeSH term(s) Biomedical Research/trends ; Humans ; Neurology/trends ; Parkinson Disease/etiology ; Parkinson Disease/therapy
    Language English
    Publishing date 2007
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ISSN 1940-087X
    ISSN (online) 1940-087X
    DOI 10.3791/189
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The Consequences of Coronavirus-Induced Cytokine Storm Are Associated With Neurological Diseases, Which May Be Preventable.

    Isacson, Ole

    Frontiers in neurology

    2020  Volume 11, Page(s) 745

    Keywords covid19
    Language English
    Publishing date 2020-07-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2020.00745
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  3. Article ; Online: The Consequences of Coronavirus-Induced Cytokine Storm Are Associated With Neurological Diseases, Which May Be Preventable

    Ole Isacson

    Frontiers in Neurology, Vol

    2020  Volume 11

    Keywords pandemic ; viral infection ; toll-like receptors ; Parkinson's disease (PD) ; interleukin-1 receptor antagonist (IL-1 ra) ; COVID-19 ; Neurology. Diseases of the nervous system ; RC346-429 ; covid19
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Sorting the wheat from the chaff in dopamine neuron-based cell therapies.

    Isacson, Ole

    Proceedings of the National Academy of Sciences of the United States of America

    2015  Volume 112, Issue 15, Page(s) 4512–4513

    MeSH term(s) Animals ; Dopaminergic Neurons/metabolism ; Female ; Gene Expression Profiling ; Male ; Neural Stem Cells/metabolism ; Stem Cell Transplantation/methods
    Language English
    Publishing date 2015-04-14
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1503859112
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    Zs.A 1148: Show issues Location:
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  6. Article ; Online: Lysosomes to combat Parkinson's disease.

    Isacson, Ole

    Nature neuroscience

    2015  Volume 18, Issue 6, Page(s) 792–793

    MeSH term(s) Animals ; Autophagy/genetics ; Dopamine/metabolism ; Humans ; LIM-Homeodomain Proteins/metabolism ; Lysosomes/metabolism ; Parkinson Disease/physiopathology ; Transcription Factors/metabolism
    Chemical Substances LIM-Homeodomain Proteins ; Transcription Factors ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2015-06
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.4027
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  7. Article ; Online: Upstream lipid and metabolic systems are potential causes of Alzheimer's disease, Parkinson's disease and dementias.

    Cooper, Oliver / Hallett, Penny / Isacson, Ole

    The FEBS journal

    2022  Volume 291, Issue 4, Page(s) 632–645

    Abstract: Brain health requires circuits, cells and molecular pathways to adapt when challenged and to promptly reset once the challenge has resolved. Neurodegeneration occurs when adaptability becomes confined, causing challenges to overwhelm neural circuitry. ... ...

    Abstract Brain health requires circuits, cells and molecular pathways to adapt when challenged and to promptly reset once the challenge has resolved. Neurodegeneration occurs when adaptability becomes confined, causing challenges to overwhelm neural circuitry. Studies of rare and common neurodegenerative diseases suggest that the accumulation of lipids can compromise circuit adaptability. Using microglia as an example, we review data that suggest increased lipid concentrations cause dysfunctional inflammatory responses to immune challenges, leading to Alzheimer's disease, Parkinson's disease and dementia. We highlight current approaches to treat lipid metabolic and clearance pathways and identify knowledge gaps towards restoring adaptive homeostasis in individuals who are at-risk of losing cognition.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Brain/metabolism ; Lipids
    Chemical Substances Lipids
    Language English
    Publishing date 2022-10-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16638
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    Zs.A 260: Show issues Location:
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  8. Article ; Online: Loss of Lipid Carrier ApoE Exacerbates Brain Glial and Inflammatory Responses after Lysosomal GBA1 Inhibition.

    Connolly, Kyle J / Margaria, Juliette / Di Biase, Erika / Cooper, Oliver / Hallett, Penelope J / Isacson, Ole

    Cells

    2023  Volume 12, Issue 21

    Abstract: Tightly regulated and highly adaptive lipid metabolic and transport pathways are critical to maintaining brain cellular lipid homeostasis and responding to lipid and inflammatory stress to preserve brain function and health. Deficits in the lipid ... ...

    Abstract Tightly regulated and highly adaptive lipid metabolic and transport pathways are critical to maintaining brain cellular lipid homeostasis and responding to lipid and inflammatory stress to preserve brain function and health. Deficits in the lipid handling genes
    MeSH term(s) Humans ; Mice ; Animals ; Glucosylceramidase/genetics ; Glucosylceramidase/metabolism ; Brain/metabolism ; Lysosomes/metabolism ; Apolipoproteins E ; Glycolipids/metabolism
    Chemical Substances Glucosylceramidase (EC 3.2.1.45) ; Apolipoproteins E ; Glycolipids
    Language English
    Publishing date 2023-11-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12212564
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  9. Article ; Online: Acid ceramidase involved in pathogenic cascade leading to accumulation of α-synuclein in iPSC model of GBA1-associated Parkinson's disease.

    Kumar, Manoj / Srikanth, Manasa P / Deleidi, Michela / Hallett, Penelope J / Isacson, Ole / Feldman, Ricardo A

    Human molecular genetics

    2023  Volume 32, Issue 11, Page(s) 1888–1900

    Abstract: Bi-allelic mutations in GBA1, the gene that encodes β-glucocerebrosidase (GCase), cause Gaucher disease (GD), whereas mono-allelic mutations do not cause overt pathology. Yet mono- or bi-allelic GBA1 mutations are the highest known risk factor for ... ...

    Abstract Bi-allelic mutations in GBA1, the gene that encodes β-glucocerebrosidase (GCase), cause Gaucher disease (GD), whereas mono-allelic mutations do not cause overt pathology. Yet mono- or bi-allelic GBA1 mutations are the highest known risk factor for Parkinson's disease (PD). GCase deficiency results in the accumulation of glucosylceramide (GluCer) and its deacylated metabolite glucosylsphingosine (GluSph). Brains from patients with neuronopathic GD have high levels of GluSph, and elevation of this lipid in GBA1-associated PD has been reported. To uncover the mechanisms involved in GBA1-associated PD, we used human induced pluripotent stem cell-derived dopaminergic (DA) neurons from patients harboring heterozygote mutations in GBA1 (GBA1/PD-DA neurons). We found that compared with gene-edited isogenic controls, GBA1/PD-DA neurons exhibit mammalian target of rapamycin complex 1 (mTORC1) hyperactivity, a block in autophagy, an increase in the levels of phosphorylated α-synuclein (129) and α-synuclein aggregation. These alterations were prevented by incubation with mTOR inhibitors. Inhibition of acid ceramidase, the lysosomal enzyme that deacylates GluCer to GluSph, prevented mTOR hyperactivity, restored autophagic flux and lowered α-synuclein levels, suggesting that GluSph was responsible for these alterations. Incubation of gene-edited wild type (WT) controls with exogenous GluSph recapitulated the mTOR/α-synuclein abnormalities of GBA1/PD neurons, and these phenotypic alterations were prevented when GluSph treatment was in the presence of mTOR inhibitors. We conclude that GluSph causes an aberrant activation of mTORC1, suppressing normal lysosomal functions, including the clearance of pathogenic α-synuclein species. Our results implicate acid ceramidase in the pathogenesis of GBA1-associated PD, suggesting that this enzyme is a potential therapeutic target for treating synucleinopathies caused by GCase deficiency.
    MeSH term(s) Humans ; Parkinson Disease/metabolism ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism ; Induced Pluripotent Stem Cells/metabolism ; MTOR Inhibitors ; Acid Ceramidase/genetics ; Acid Ceramidase/metabolism ; Glucosylceramidase/genetics ; Glucosylceramidase/metabolism ; Gaucher Disease/metabolism ; Dopaminergic Neurons/metabolism ; TOR Serine-Threonine Kinases/genetics ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mutation ; Lysosomes/metabolism
    Chemical Substances alpha-Synuclein ; MTOR Inhibitors ; Acid Ceramidase (EC 3.5.1.23) ; Glucosylceramidase (EC 3.2.1.45) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2023-01-31
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddad025
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    Zs.A 3469: Show issues Location:
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  10. Book ; Thesis: Neural grafting in an animal model of huntington's disease

    Isacson, Ole

    1987  

    Keywords Huntington's Disease ; Disease Models, Animal ; Corpus Striatum ; Nerve Tissue / transplantation
    Size getr. Zählung : Ill., graph. Darst.
    Publishing country Sweden
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Lund, Univ., Diss., 1987
    HBZ-ID HT003176977
    ISBN 91-7900-258-7 ; 978-91-7900-258-9
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    88 E 2365 order for loan Magazin

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