Parkinsonism - A Methyl-Donor Action for Mpp+

Charlton, Clivel George

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute of Neurological Disorders and Stroke (NINDS)
• Type: Research Project (R01)
• Project #: 5R01NS031177-04
• Application #: 2269105
• Study Section: Neurology A Study Section (NEUA)
• Program Officer: Oliver, Eugene J
• Project Start: 1993-01-01
• Project End: 1997-12-31
• Budget Start: 1996-03-01
• Budget End: 1997-12-31
• Support Year: 4
• Fiscal Year: 1996

Institution

• Name: Florida Agricultural and Mechanical University
• Department: Other Basic Sciences
• Type: Schools of Pharmacy
• City: Tallahassee
• State: FL
• Country: United States
• Zip Code: 32307

Publications

Zhao, Wan-Qian; Williams, Zakia; Shepherd, Kennie R et al. (2002) S-adenosyl-methionine-induced apoptosis in PC12 cells. J Neurosci Res 69:519-29

Lamango, N S; Charlton, C G (2000) Farnesyl-L-cysteine analogs block SAM-induced Parkinson's disease-like symptoms in rats. Pharmacol Biochem Behav 66:841-9

Lamango, N S; Nesby, R A; Charlton, C G (2000) Quantification of S-adenosylmethionine-induced tremors: a possible tremor model for Parkinson's disease. Pharmacol Biochem Behav 65:523-9

Charlton, C G (1997) Depletion of nigrostriatal and forebrain tyrosine hydroxylase by S-adenosylmethionine: a model that may explain the occurrence of depression in Parkinson's disease. Life Sci 61:495-502

Charlton, C G; Crowell Jr, B (1995) Striatal dopamine depletion, tremors, and hypokinesia following the intracranial injection of S-adenosylmethionine: a possible role of hypermethylation in parkinsonism. Mol Chem Neuropathol 26:269-84

Charlton, C G; Mack, J (1994) Substantia nigra degeneration and tyrosine hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain. Support for an excess methylation hypothesis for parkinsonism. Mol Neurobiol 9:149-61