Planta Med 2008; 74 - SL117
DOI: 10.1055/s-0028-1083997

Atypical parkinsonism induced by Annonaceae: Where are we yet?

P Champy 1, M Escobar-Khondiker 2, 3, IN Bajin 1, E Yamada 2, A Lannuzel 4, O Laprévote 5, M Ruberg 3, GU Höglinger 2
  • 1Laboratoire de Pharmacognosie, UMR CNRS 8076 BioCIS, Faculté de Pharmacie Paris-Sud 11, 92296, Châtenay-Malabry, France
  • 2Experimental Neurology, Univ. Friedrich, D-35033, Marburg, Germany
  • 3INSERM U679, Neurologie et Thérapeutique Expérimentale, Pitié-Salpêtrière, 75013, Paris, France
  • 4Service de Neurologie, CHU, 97159, Pointe-à-Pitre, Guadeloupe, France.
  • 5Spectrométrie de Masse ICSN, CNRS, 91198, Gif-sur-Yvette, France

Atypical parkinsonian syndromes are abnormally frequent in the French West Indies. They were linked epidemiologically to the consumption, for alimentary and medicinal means, of plants of the Annonaceae family, suggesting a possible toxic etiology [1,2]. We showed Annonaceous acetogenins, such as annonacin, to be neurotoxicants, in several in vitro [3,4] and in vivo [5,6] paradigms, with: a) degeneration in animals being reminiscent of post-mortem observations in patients at autopsy; b) influence on the distribution and expression of tau protein, e.g. in Tau transgenic mouse models. Nevertheless, we determined important concentrations of acetogenins in pulps and fruit juices of several edible Annona species [7,8] (A. muricata, A. squamosa), whereas leave tea only contained low amounts of these molecules. Alimentary consumption of several Annonaceae species would therefore be a major source of exposure to environmental neurotoxins. Our research efforts on these themes are ongoing.

High incidences of atypical parkinsonisms associated to Annonaceae were reported in several other countries. This public health issue could therefore constitute a worldwide problem, which urgently needs epidemiological reassesment [9,10].

References: 1. Caparros-Lefèbvre, D. et al. (1999) Lancet 354:281–286. 2. Lannuzel, A. et al. (2007) Brain, 130: 816–827. 3. Lannuzel, A. et al (2003) Neuroscience 121: 287–296. 4. Escobar-Khondiker, M. et al. (2007)J. Neurosciences 27:7827–7837. 5. Champy, P. et al. (2004)J Neurochem. 88: 63–69. 6. Yamada, E. et al. in preparation. 7. Champy, P. et al. (2005) Mov. Disord. 20:1629–1633. 8. Bajin, I. et al. in preparation. 9. Capparos-Lefèbvre, D. et al. (2005) Environ. Toxicol. Pharmacol. 19:407–413. 10. Höglinger, G.U, et al. (2006) Mov. Disord. 20:118–119.