Format

Send to

Choose Destination
See comment in PubMed Commons below
Expert Rev Neurother. 2013 Jun;13(6):671-84. doi: 10.1586/ern.13.60.

Revelation in the neuroprotective functions of rasagiline and selegiline: the induction of distinct genes by different mechanisms.

Author information

1
Department of Health and Nutrition, Faculty of Psychological and Physical Science, Aichi Gakuin University, Nisshin, Aichi, Japan. mnaoi@dpc.agu.ac.jp

Abstract

In Parkinson's disease, cell death of dopamine neurons in the substantia nigra progresses and neuroprotective therapy is required to halt neuronal loss. In cellular and animal models, selegiline [(-)deprenyl] and rasagiline, inhibitors of type B monoamine oxidase (MAO)-B, protect neuronal cells from programmed cell death. In this paper, the authors review their recent results on the molecular mechanisms by which MAO inhibitors prevent the cell death through the induction of antiapoptotic, prosurvival genes. MAO-A mediates the induction of antiapoptotic bcl-2 and mao-a itself by rasagiline, whereas a different mechanism is associated with selegiline. Rasagiline and selegiline preferentially increase GDNF and BDNF in nonhuman primates and Parkinsonian patients, respectively. Enhanced neurotrophic factors might be applicable to monitor the neurorescuing activity of neuroprotection.

PMID:
23739004
DOI:
10.1586/ern.13.60
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center