In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease

By C. Lee, A. Samii, V. Sossi, T. Ruth, M. Schulzer, J. Holden, J. Wudel, P. Pal, R. de la Fuente-Fernández, D. Calne and 1 more. Annals of Neurology, 2000

595 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/055878ef9237e3af47a684b7c935f2eda85a27bc

How researchers see this paper

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In Cellular and Molecular Neuroscience

1. Mark Hallett
2. Tao Wu
3. P. Brundin

In Neurology

1. Mark Hallett
2. Tao Wu
3. J. Lotharius
4. P. Brundin
5. Alvaro Pascual-Leone

Citations in the corpus

• Pathogenesis of parkinson's disease: dopamine, vesicles and α-synuclein (2002, background): “A selective reduction in dopamine-storage sites might be a pathogenic feature of Parkinson's disease, as an in vivo PET (positron emission tomography) imaging study of patients with idiopathic Parkinson's disease has revealed greater reductions in a marker for VMAT2 than in the signal arising from”
• The cerebellum in Parkinson’s disease (2013, background): “The motor symptoms of Parkinson’s disease usually present after 70% of dopaminergic neurons have degenerated (Fearnley and Lees, 1991; Lee et al., 2000).”
• Clinical Progression in Parkinson's Disease and the Neurobiology of Axons (2010, unknown): “It has been suggested that compensatory upregulation of aromatic acid decarboxylase may result in an underestimate of terminal losses by use of [(18)F]dopa positron emission tomography.(31,32) If we therefore restrict our attention to losses assessed by the other ligands, the estimates of 50 to 70% ”