Neuroprotective mechanisms of antiparkinsonian dopamine D2-receptor subfamily agonists.

Abstract

Numerous studies have shown that endogenous and/or environmental neurotoxins and oxidative stress may participate in the pathogenesis of Parkinson's disease (PD), but the detailed mechanisms are still unclear. While dopamine (DA) replacement therapy with L-DOPA (levodopa) improves PD symptoms, it does not inhibit the degeneration of DA neurons in the substantia nigra. Recently, bromocriptine, pramipexole and several other agonists of the dopamine D2-receptor subfamily (including D2, D3 and D4-subtypes) have been shown to have neuroprotective effects in parkinsonian models in vitro and in vivo. Their neuroprotective effects may be mediated directly and/or indirectly by antioxidant effects, mitochondrial stabilization or induction of the antiapoptotic Bcl-2 family.

• Authors: Yoshihisa Kitamura, Takashi Taniguchi, Shun Shimohama, Akinori Akaike, Yasuyuki Nomura
• Journal: Neurochemical research (Neurochem Res) Vol. 28 Issue 7 Pg. 1035-40 (Jul 2003) ISSN: 0364-3190 [Print] United States
• PMID: 12737528 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antiparkinson Agents
• Dopamine Agonists
• Neuroprotective Agents
• Receptors, Dopamine D2

Topics

• Animals
• Antiparkinson Agents (therapeutic use)
• Dopamine Agonists (therapeutic use)
• Humans
• Neuroprotective Agents (therapeutic use)
• Parkinson Disease (drug therapy)
• Receptors, Dopamine D2 (agonists)