Acetyl-levo-carnitine protects against MPTP-induced parkinsonism in primates

J Neural Transm Park Dis Dement Sect. 1991;3(1):63-72. doi: 10.1007/BF02251137.


Acetyl-levo-carnitine (ALC) protects against 1-methyl, 4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity in the nonhuman primate. ALC pretreated monkeys do not show signs of parkinsonism or electroretinographic changes typical of dopaminergic deficiency when given MPTP. In addition, pilot neurochemical and morphological data confirm a partial protection effect. While MAO-B inhibitors, like L-Deprenyl, are thought to protect dopaminergic neurons from MPTP-induced cell death by preventing the conversion of MPTP to its toxic metabolite MPP+, ALC is not known to have MAO-B affinity. Converging evidence suggests that ALC may affect directly mitochondrial respiration, which is known to be the target of MPP+ and affected in human neurodegenerative diseases, including Parkinson's disease. The results of this study point to new therapeutic avenues for the treatment of these nosologic entities.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acetylcarnitine / therapeutic use*
  • Animals
  • Carbidopa / therapeutic use
  • Caudate Nucleus / chemistry
  • Electroretinography
  • Female
  • Homovanillic Acid / analysis
  • Immunohistochemistry
  • Levodopa / therapeutic use
  • MPTP Poisoning*
  • Macaca fascicularis
  • Male
  • Parkinson Disease, Secondary / chemically induced*
  • Parkinson Disease, Secondary / drug therapy
  • Parkinson Disease, Secondary / physiopathology
  • Substantia Nigra / chemistry


  • Levodopa
  • Acetylcarnitine
  • Carbidopa
  • Homovanillic Acid