Neuroprotective mechanisms of antiparkinsonian dopamine D2-receptor subfamily agonists.
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.
Kitamura
Yoshihisa
Y
Department of Neurobiology, Kyoto Pharmaceutical University, Kyoto 607-8412, Japan. yo-kita@mb.kyoto-phu.ac.jp
Taniguchi
Takashi
T
Shimohama
Shun
S
Akaike
Akinori
A
Nomura
Yasuyuki
Y
D000818:Animals; D000978:Antiparkinson Agents / Q000627:therapeutic use*; D018491:Dopamine Agonists / Q000627:therapeutic use*; D006801:Humans; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010300:Parkinson Disease / Q000188:drug therapy*; D017448:Receptors, Dopamine D2 / Q000819:agonists*
D000978:Antiparkinson Agents; D018491:Dopamine Agonists; D018696:Neuroprotective Agents; D017448:Receptors, Dopamine D2