2004
DOI: 10.1001/archneur.61.5.657
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Levodopa-Associated Increase of Homocysteine Levels and Sural Axonal Neurodegeneration

Abstract: This electrophysiological sign of peripheral neuronal dysfunction may be circumstantial evidence suggesting that, to a certain extent, sensory nerve action potentials are a surrogate marker for the levodopa metabolism-induced elevation of homocysteine levels and the aggravation of the ongoing central neurodegenerative process.

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Cited by 101 publications

(52 citation statements)
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“…Interestingly, symmetric dimethylarginine (SDMA), a uremic toxin that inhibits NOS, was associated with a lower PD risk at 10 to 15 years before diagnosis. These findings may indicate the involvement of endothelial function 55,56 and urea metabolism 57 in PD progression, and/or the initiation of levodopa treatment, which often increases homoarginine levels 58,59 . Consistent with previous investigations, 35‐38,53 several lipids were associated with clinical PD, and these replicated in prodromal samples.…”
Section: Discussion
supporting
confidence: 88%
“…These findings may indicate the involvement of endothelial function 55,56 and urea metabolism 57 in PD progression, and/or the initiation of levodopa treatment, which often increases homoarginine levels. 58,59 Consistent with previous investigations, [35][36][37][38]53 several lipids were associated with clinical PD, and these replicated in prodromal samples. Overall, relative to controls, lipid metabolites tended to be reduced or even decreased over the course of PD, especially sphingomyelins and ceramides.…”
Section: Discussion
supporting
confidence: 87%
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