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  1. Article ; Online: Levodopa is the best symptomatic therapy for PD: Nothing more, nothing less.

    Olanow, C Warren

    Movement disorders : official journal of the Movement Disorder Society

    2019  Volume 34, Issue 6, Page(s) 812–815

    MeSH term(s) Antiparkinson Agents/therapeutic use ; Humans ; Levodopa/therapeutic use ; Parkinson Disease/drug therapy ; Treatment Outcome
    Chemical Substances Antiparkinson Agents ; Levodopa (46627O600J)
    Language English
    Publishing date 2019-04-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.27690
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  2. Article ; Online: Reply to: "A New Approach to the Development of Disease-Modifying Therapies for PD".

    Kieburtz, Karl / Olanow, C Warren

    Movement disorders : official journal of the Movement Disorder Society

    2021  Volume 36, Issue 5, Page(s) 1281–1282

    MeSH term(s) Humans ; Pandemics ; Parkinson Disease/epidemiology
    Language English
    Publishing date 2021-05-15
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.28588
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  3. Article ; Online: Parkinson's Disease Modification Through Abl Kinase Inhibition: An Opportunity.

    Werner, Milton H / Olanow, C Warren

    Movement disorders : official journal of the Movement Disorder Society

    2021  Volume 37, Issue 1, Page(s) 6–15

    Abstract: ... of the disease. Animal models of PD suggest that activation of the Abelson tyrosine kinase (c-Abl) plays ... These studies demonstrate that internalization of misfolded α-synuclein activates c-Abl, which phosphorylates α ... synuclein and promotes α-synuclein pathology within the affected neurons. Additionally, c-Abl inactivates ...

    Abstract Parkinson's disease (PD) is the second most prevalent neurodegenerative disease of the central nervous system, with an estimated 5 000 000 cases worldwide. Historically characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, PD pathology is now known to be widespread and to affect serotonin, cholinergic and norepinephrine neurons as well as nerve cells in the olfactory system, cerebral hemisphere, brain stem, spinal cord, and peripheral autonomic nervous system. PD pathology is characterized by the accumulation of misfolded α-synuclein, which is thought to play a critical role in the etiopathogenesis of the disease. Animal models of PD suggest that activation of the Abelson tyrosine kinase (c-Abl) plays an essential role in the initiation and progression of α-synuclein pathology and neurodegeneration. These studies demonstrate that internalization of misfolded α-synuclein activates c-Abl, which phosphorylates α-synuclein and promotes α-synuclein pathology within the affected neurons. Additionally, c-Abl inactivates parkin, disrupting mitochondrial quality control and biogenesis, promoting neurodegeneration. Post-mortem studies of PD patients demonstrate increased levels of tyrosine phosphorylated α-synuclein, consistent with the activation of c-Abl in human disease. Although the c-Abl inhibitor nilotinib failed to demonstrate clinical benefit in two double-blind trials, novel c-Abl inhibitors have been developed that accumulate in the brain and may inhibit c-Abl at saturating levels. These novel inhibitors have demonstrated benefits in animal models of PD and have now entered clinical development. Here, we review the role of c-Abl in the neurodegenerative disease process and consider the translational potential of c-Abl inhibitors from model studies to disease-modifying therapies for Parkinson's disease. © 2021 Inhibikase Therapeutics, Inc. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society.
    MeSH term(s) Animals ; Brain/pathology ; Dopaminergic Neurons/metabolism ; Humans ; Neurodegenerative Diseases/pathology ; Parkinson Disease/drug therapy ; Parkinson Disease/pathology ; Proto-Oncogene Proteins c-abl/metabolism ; Randomized Controlled Trials as Topic
    Chemical Substances Proto-Oncogene Proteins c-abl (EC 2.7.10.2)
    Language English
    Publishing date 2021-11-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.28858
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  4. Article ; Online: Levodopa: effect on cell death and the natural history of Parkinson's disease.

    Olanow, C Warren

    Movement disorders : official journal of the Movement Disorder Society

    2015  Volume 30, Issue 1, Page(s) 37–44

    Abstract: This review article considers the question of whether or not levodopa is toxic in Parkinson's disease (PD). l-dopa is the most effective symptomatic treatment for PD and has provided benefit for millions of patients. However, there has been a ... ...

    Abstract This review article considers the question of whether or not levodopa is toxic in Parkinson's disease (PD). l-dopa is the most effective symptomatic treatment for PD and has provided benefit for millions of patients. However, there has been a longstanding concern that l-dopa might be toxic and accelerate neuronal degeneration and clinical progression as a consequence of reactive oxygen species generated by the drug's oxidative metabolism. In vitro, l-dopa can induce degeneration of dopaminergic neurons, but it is not clear that the effects of the drug on cultured dopamine neurons reflect what happens in the PD brain. In vivo, l-dopa has not been demonstrated to have toxic effects on dopamine neurons in normal, dopamine-lesioned, or oxidatively stressed animal models, but none of these models precisely replicates the PD condition. Clinical trials have tested the effect of l-dopa on clinical progression and have not demonstrated any findings indicative of toxicity. However, the symptomatic and long-duration effects of the drug could mask ongoing neuronal degeneration. Furthermore, l-dopa induces a greater decline in imaging measures of dopaminergic function than placebo or dopamine agonists, consistent with toxicity. Pathological studies have not demonstrated evidence of accelerated loss of dopamine neurons, but prospective and properly controlled studies with stereological unbiased counting have not been performed. Thus, although there is no hard evidence to suggest that l-dopa is toxic in PD patients, the issue has not been fully resolved. It is generally recommended that physicians continue to use l-dopa, but in the lowest dose that provides satisfactory clinical control.
    MeSH term(s) Animals ; Antiparkinson Agents/adverse effects ; Cell Death/drug effects ; Clinical Trials as Topic ; Humans ; In Vitro Techniques ; Levodopa/adverse effects ; Oxidative Stress/drug effects ; Parkinson Disease/drug therapy ; Parkinson Disease/epidemiology ; Parkinson Disease/pathology
    Chemical Substances Antiparkinson Agents ; Levodopa (46627O600J)
    Language English
    Publishing date 2015-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.26119
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  5. Article ; Online: Do prions cause Parkinson disease?: the evidence accumulates.

    Olanow, C Warren

    Annals of neurology

    2014  Volume 75, Issue 3, Page(s) 331–333

    MeSH term(s) Animals ; Humans ; Parkinson Disease/etiology ; Prions/pathogenicity ; alpha-Synuclein/genetics
    Chemical Substances Prions ; alpha-Synuclein
    Language English
    Publishing date 2014-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80362-5
    ISSN 1531-8249 ; 0364-5134
    ISSN (online) 1531-8249
    ISSN 0364-5134
    DOI 10.1002/ana.24098
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    Zs.MO 478: Show issues

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  6. Article ; Online: Parkinson disease: Gene therapy for Parkinson disease--a hope, or a dream?

    Olanow, C Warren

    Nature reviews. Neurology

    2014  Volume 10, Issue 4, Page(s) 186–187

    MeSH term(s) Antiparkinson Agents/administration & dosage ; Genetic Therapy/methods ; Genetic Vectors/administration & dosage ; Humans ; Infectious Anemia Virus, Equine/genetics ; Male ; Parkinson Disease/therapy ; Transfection/methods
    Chemical Substances Antiparkinson Agents
    Language English
    Publishing date 2014-03-25
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/nrneurol.2014.45
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  7. Article ; Online: Translating scientific advances into disease-modifying therapies for Parkinson's Disease.

    Cenci, M Angela / Olanow, C Warren

    Experimental neurology

    2017  Volume 298, Issue Pt B, Page(s) 135–136

    Language English
    Publishing date 2017-12
    Publishing country United States
    Document type Editorial
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2017.10.011
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  8. Article ; Online: Continuous Dopaminergic Stimulation as a Treatment for Parkinson's Disease: Current Status and Future Opportunities.

    Olanow, C Warren / Calabresi, Paolo / Obeso, Jose A

    Movement disorders : official journal of the Movement Disorder Society

    2020  Volume 35, Issue 10, Page(s) 1731–1744

    Abstract: Levodopa-induced motor complications remain an important source of disability for many patients with Parkinson's disease. Substantial laboratory evidence indicates that motor complications relate to the nonphysiological restoration of brain dopamine with ...

    Abstract Levodopa-induced motor complications remain an important source of disability for many patients with Parkinson's disease. Substantial laboratory evidence indicates that motor complications relate to the nonphysiological restoration of brain dopamine with intermittent doses of standard oral levodopa. Dopamine levels are normally maintained at a relatively constant level, even following a dose of levodopa. However, in the Parkinsonian state, where dopamine terminals have degenerated with a loss of their buffering capacity, intermittent doses of levodopa lead to dramatic peak and trough fluctuations in striatal dopamine levels. This results in pulsatile stimulation of dopamine receptors, molecular changes in striatal neurons, physiological changes in pallidal neurons, and ultimately the development of motor complications. These observations led to the hypothesis that continuous delivery of levodopa might be associated with a reduced risk of motor complications. This concept is known as continuous dopamine stimulation (CDS). Preliminary studies in animal models and patients with Parkinson's disease supported this hypothesis, suggesting a reduced risk of both motor fluctuations and dyskinesias. The present review considers the scientific advances and the more definitive clinical trials testing this concept that have taken place during the past decade and considers ongoing experimental studies and future opportunities. © 2020 International Parkinson and Movement Disorder Society.
    MeSH term(s) Animals ; Antiparkinson Agents ; Dopamine ; Dopamine Agonists ; Humans ; Levodopa/adverse effects ; Parkinson Disease/drug therapy
    Chemical Substances Antiparkinson Agents ; Dopamine Agonists ; Levodopa (46627O600J) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2020-08-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.28215
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  9. Article ; Online: On-Demand Therapy for OFF Episodes in Parkinson's Disease.

    Olanow, C Warren / Poewe, Werner / Rascol, Olivier / Stocchi, Fabrizio

    Movement disorders : official journal of the Movement Disorder Society

    2021  Volume 36, Issue 10, Page(s) 2244–2253

    Abstract: Levodopa is the most effective therapy for Parkinson's disease; however, chronic treatment is associated with the development of OFF episodes, in which there is a return of parkinsonian features following a dose of levodopa and prior to the onset of ... ...

    Abstract Levodopa is the most effective therapy for Parkinson's disease; however, chronic treatment is associated with the development of OFF episodes, in which there is a return of parkinsonian features following a dose of levodopa and prior to the onset of benefit from the subsequent dose. OFF episodes can be a major source of disability for PD patients and frequently result in depression, apathy and an unwillingness to participate in social activities. Most currently available medical and surgical therapies are designed to reduce total daily OFF time but do not provide a rapid and reliable "on-demand" therapy for individual OFF episodes. Indeed, responses to individual doses of levodopa during an acute OFF episode are unreliable, frequently leading to partial-ON, delayed-ON, or no-ON responses even at different times in the same patient. There are now 3 therapies that are available for the on-demand treatment of OFF episodes; subcutaneous injection of apomorphine, sublingual apomorphine film, and inhaled levodopa. The first has not enjoyed widespread use in the PD community, whereas the latter 2 therapies have only recently been approved. This review will consider the currently available on-demand therapies and their potential advantages and disadvantages. © 2021 International Parkinson and Movement Disorder Society.
    MeSH term(s) Antiparkinson Agents ; Apathy ; Apomorphine ; Humans ; Levodopa ; Parkinson Disease/drug therapy
    Chemical Substances Antiparkinson Agents ; Levodopa (46627O600J) ; Apomorphine (N21FAR7B4S)
    Language English
    Publishing date 2021-08-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.28726
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  10. Article ; Online: Targeting α-Synuclein as a therapy for Parkinson's disease: The battle begins.

    Olanow, C Warren / Kordower, Jeffrey H

    Movement disorders : official journal of the Movement Disorder Society

    2017  Volume 32, Issue 2, Page(s) 203–207

    MeSH term(s) Humans ; Neurons ; Parkinson Disease ; Substantia Nigra ; alpha-Synuclein
    Chemical Substances alpha-Synuclein
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.26935
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