Selegiline Induces “Trophic-Like” Rescue of Dying Neurons without MAO Inhibition

  • William G. Tatton
  • K. Ansari
  • W. Ju
  • P. T. Salo
  • Peter H. Yu
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 363)

Abstract

Selegiline has been claimed to slow the progression of motor deficits in Parkinson’s Disease (PD)1 and cognitive decline in Alzheimer’s Disease (AD).2 It is controversial whether the slowing represents a symptomatic action due to improved dopaminergic neurotransmission or neuroprotection due to a decrease in the production of toxic oxidative radicals consequent on the inhibition of monoamine oxidase B (MAO-B). We propose a third action for selegiline — a “trophic-like” rescue of dying neurons.

Keywords

Monoamine MPTP Selegiline Deprenyl Salol 

References

  1. 1.
    The Parkinson Study Group: (1989) Effect of deprenyl on the progression of disability in early Parkinson’s disease. New Engl. J. Med. 321: 1364–1371.CrossRefGoogle Scholar
  2. 2.
    Mangoni, A, Grassi, MP, Frattola, L, Piolti, R, Brassi, S, Motta, A., Marcone, A and Smirne, S: (1991) Effects of a MAO-B inhibitor in the treatment of Alzheimer’s disease. Eur. Neurol. 31: 100–107.PubMedCrossRefGoogle Scholar
  3. 3.
    Tatton, WG and Greenwood, CE: (1991) Rescue of dying neurons: a new action for deprenyl in MPTP Parkinsonism. J. Neurosci. Res. 30: 666–672.PubMedCrossRefGoogle Scholar
  4. 4.
    Dipasquale, B, Marini, AM and Youle, RJ: (1991) Apoptosis and DNA degradation induced by 1-methl-4-phenypyridinium in neurons. Biochem Biophys Res. Comm. 181: 1442–1448.PubMedCrossRefGoogle Scholar
  5. 5.
    Raff, MC: (1992) Social controls on cell survival and cell death. Nature 356: 397–400.PubMedCrossRefGoogle Scholar
  6. 6.
    Salo, PT and Tatton, WG: Deprenyl reduces the death of motoneurons caused by axtomy. J. Neurosci Res. 31: 394-400.Google Scholar
  7. 7.
    Graeber, MB and Kreutzberg, GW: (1986) Astrocytes increase in glial fibrillary acidic protein during retrograde changes of ficial motor neurons. J. Neurocytol 15: 363–374.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • William G. Tatton
    • 1
  • K. Ansari
    • 1
  • W. Ju
    • 1
  • P. T. Salo
    • 1
  • Peter H. Yu
    • 2
  1. 1.Center for Research in Neurodegenerative DiseasesUniversity of TorontoTorontoCanada
  2. 2.Neuropsychiatry Research Unit Department of PsychiatryUniversity of SaskatchewanSaskatoonCanada

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