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- W2060023105 abstract "Bezard and colleagues [ 1 Bezard E et al. Presymptomatic compensation in Parkinson's disease is not dopamine-mediated. Trends Neurosci. 2003; 26: 215-221 Abstract Full Text Full Text PDF PubMed Scopus (271) Google Scholar ] have to be congratulated on their studies and discussions of the mechanisms involved in compensation of striatal dopamine loss in Parkinson's disease (PD). To understand how PD begins and progresses is a major requirement in developing more definitive therapies for PD (A.E. Lang and J.A. Obeso, unpublished). Bezard et al. have conclusively shown that classically accepted dopamine-mediated mechanisms are not primarily involved in the initial compensation of striatal dopamine depletion in PD [ 1 Bezard E et al. Presymptomatic compensation in Parkinson's disease is not dopamine-mediated. Trends Neurosci. 2003; 26: 215-221 Abstract Full Text Full Text PDF PubMed Scopus (271) Google Scholar ]. They proposed a series of functional compensatory changes within and outside the basal ganglia. We would like to discuss an alternative hypothesis for the onset of PD and the role of compensatory changes. Before that, some methodological comments are also pertinent. The Bordeaux group has established an N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkey model that provokes a full parkinsonian syndrome within three weeks, unlike PD, which develops over several years. Importantly, PD has a unilateral or asymmetrical onset whereas MPTP-intoxicated monkeys exhibited bilateral symptoms from the beginning. Both differential features of the model are relevant when analysing the onset of PD and initial compensatory mechanisms." @default.
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- W2060023105 title "How does Parkinson's disease begin? The role of compensatory mechanisms" @default.
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- W2060023105 doi "https://doi.org/10.1016/j.tins.2003.12.006" @default.
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