Journal ArticleDOI
Levodopa in the treatment of Parkinson's disease.
TLDR
Maintaining good motor function and quality of life remain the primary goals of therapy and the principle that treatment must be tailored to the individual patient’s needs is paramount.Abstract:
The predominant motor features of Parkinson's disease (PD) are caused by degeneration of dopaminergic neurones and can be reversed in part or whole by dopamine replacement or augmentation strategies. Physicians have most experience with the use of levodopa, which remains the most potent oral dopaminergic treatment for PD. There are reservations about the long-term use of levodopa, most particularly in the context of its propensity to induce motor fluctuations and dyskinesias. Strategies exist to delay or diminish these complications, but the physician must lay the basis for these in the selection of drugs for early treatment and the sequence of drugs introduced subsequently. Levodopa efficacy and duration of effect may be enhanced by combination with a catechol-O-methyl transferase inhibitor. Maintaining good motor function and quality of life remain the primary goals of therapy and the principle that treatment must be tailored to the individual patient's needs is paramount.read more
Citations
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Journal ArticleDOI
Non-motor features of Parkinson disease.
TL;DR: Recent advances that have helped to establish the presence, severity and effect on the quality of life of non-motor symptoms in PD are discussed, and the neuroanatomical and neuropharmacological mechanisms involved are discussed.
Journal ArticleDOI
Clinical Approach to Parkinson's Disease: Features, Diagnosis, and Principles of Management
João Massano,Kailash P. Bhatia +1 more
TL;DR: This text is a roadmap to accurate diagnosis in PD, as it approaches clinical features, diagnostic methodology, and leading differential diagnoses.
Journal ArticleDOI
Levodopa therapy for Parkinson's disease: Pharmacokinetics and pharmacodynamics.
TL;DR: Several new pharmaceutical approaches are targeted at the unique physiology of l‐dopa uptake and are likely to improve the consistency of its anti‐Parkinsonian effect.
Journal ArticleDOI
Drosophila melanogaster in the Study of Human Neurodegeneration
TL;DR: Several signalling pathways including phosphatidylinositol 3-kinase (PI3K)/Akt and target of rapamycin (TOR), c-Jun N-terminal kinase (JNK) and bone morphogenetic protein (BMP) signalling, have been shown to be deregulated in models of proteinopathies, suggesting that two or more initiating events may trigger disease formation in an age-related manner.
Journal ArticleDOI
Molecular and clinical prodrome of Parkinson disease: implications for treatment.
TL;DR: A clearer perception has developed of the clinical prodrome ofPD, offering an opportunity to identify individuals who are at risk of PD, as well as those in the earliest clinical phase of the disease that might even precede the onset of motor symptoms.
References
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Journal ArticleDOI
Parkinsonism: Onset, progression, and mortality
Margaret M. Hoehn,Melvin D. Yahr +1 more
TL;DR: Controversy over the effectiveness of therapeutic measures for parkinsonism is due partially to this wide variability and to the paucity of clinical information about the natural history of the syndrome.
Journal ArticleDOI
Mitochondrial complex I deficiency in Parkinson's disease.
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Journal ArticleDOI
[Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system].
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TL;DR: The distribution of noradrenaline and dopamine in human adult and newborn brains has been investigated in this paper, where the greatest amounts of dopamine were found in the hypothalamus, the central gray matter of the mesencephalon, the reticular formation and in the area postrema.
Journal ArticleDOI
Levodopa and the progression of Parkinson's disease.
Stanley Fahn,David Oakes,Ira Shoulson,Karl Kieburtz,Alice Rudolph,Anthony E. Lang,C. W. Olanow,Caroline M. Tanner,Marek K +8 more
TL;DR: The clinical data suggest that levodopa either slows the progression of Parkinson's disease or has a prolonged effect on the symptoms of the disease, and the neuroimaging data suggest either thatlevodopa accelerates the loss of nigrostriatal dopamine nerve terminals or that its pharmacologic effects modify the dopamine transporter.
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