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December 01, 1996; 47 (6 Suppl 3) Articles

Modulation of gene expression rather than monoamine oxidase inhibition

(-)-Deprenyl-related compounds in controlling neurodegeneration

W. G. Tatton
First published December 1, 1996, DOI: https://doi.org/10.1212/WNL.47.6_Suppl_3.171S
W. G. Tatton
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Citation
Modulation of gene expression rather than monoamine oxidase inhibition
(-)-Deprenyl-related compounds in controlling neurodegeneration
W. G. Tatton
Neurology Dec 1996, 47 (6 Suppl 3) 171S-183S; DOI: 10.1212/WNL.47.6_Suppl_3.171S

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Article Information

vol. 47 no. 6 Suppl 3 171S-183S
DOI: 
https://doi.org/10.1212/WNL.47.6_Suppl_3.171S

Published By: 
Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology
Print ISSN: 
0028-3878
Online ISSN: 
1526-632X
History: 
  • First Published December 1, 1996.

Copyright & Usage: 
Copyright 1996 by Advanstar Communications Inc.

Author Disclosures

    1. W. G. Tatton, MD, PhD, FRCPC, Chalmers-Redman, R.M.E., PhD
  1. W. G. Tatton, MD, PhD, FRCPC, Chalmers-Redman, R.M.E., PhD
  1. From the Departments of Physiology/Biophysics (Drs. Tatton and Chalmers-Redman), Psychology (Dr. Tatton), and the Institute for Neuroscience (Drs. Tatton and Chalmers-Redman), Dalhousie University, Halifax, Nova Scotia, Canada.
  2. Address correspondence and reprint requests to Dr. William G. Tatton, Institute for Neuroscience, 12th Floor Tupper Medical Building, Dalhousie University, Halifax, Nova Scotia, Canada, B3H4H7.
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  • Article
    • Abstract
    • The hypothetical basis for the benefits of MAO-B inhibition in Parkinson's disease.
    • Clinical benefits of (-)-deprenyl.
    • (-)-Deprenyl can increase neuronal survival in vivo and in vitro without inhibiting MAO-B.
    • Apoptosis may be involved in neurodegeneration.
    • Genes and proteins that promote or retard apoptosis.
    • Evidence that mitochondria contribute to the initiation of apoptosis and that (-)-deprenyl alters apoptosis through a mitochondrial mechanism.
    • (-)-Deprenyl alters the expression of genes that influence mitochondrial viability.
    • Do the selective changes in gene expression explain the capacity of (-)-deprenyl to maintain mitochondrial membrane potential and reduce neuronal apoptosis?
    • Do the actions of (-)-deprenyl on gene expression contribute to the benefits reported for (-)-deprenyl treatment in human neurodegenerative diseases?
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