B12, Levodopa ja PD

https://www.ncbi.nlm.nih.gov/pubmed/20027219
 

PLoS One. 2009 Dec 21;4(12):e8268. doi: 10.1371/journal.pone.0008268.

Vitamin B12-impaired metabolism produces apoptosis and Parkinson phenotype in rats expressing the transcobalamin-oleosin chimera in substantia nigra.

Orozco-Barrios CE¹, Battaglia-Hsu SF, Arango-Rodriguez ML, Ayala-Davila J, Chery C, Alberto JM, Schroeder H, Daval JL, Martinez-Fong D, Gueant JL.AbstractBACKGROUND:

Vitamin B12 is indispensable for proper brain functioning and cytosolic synthesis of S-adenosylmethionine. Whether its deficiency produces effects on viability and apoptosis of neurons remains unknown. There is a particular interest in investigating these effects in Parkinson disease where Levodopa treatment is known to increase the consumption of S-adenosylmethionine. To cause deprivation of vitamin B12, we have recently developed a cell model that produces decreased synthesis of S-adenosylmethionine by anchoring transcobalamin (TCII) to the reticulum through its fusion with Oleosin (OLEO).
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 In conclusion, the TCII-OLEO transfection was responsible for apoptosis in N1E-115 cells and rat substantia nigra and for Parkinson-like phenotype. This suggests evaluating whether vitamin B12 deficit could aggravate the PD in patients under Levodopa therapy by impairing S-adenosylmethionine synthesis in substantia nigra.