GDNF in a Bind with Known Orphan: Accessory Implicated in New Twist

complement of dopaminergic neurons, and only minor GDNF: A Treatment for Parkinson’s Disease? losses of spinal motor neurons. Thus, the postulated Not long after success with ciliary neurotrophic factor role of GDNF as a developmentally important target(CNTF; Lin et al., 1989), Leu-Fen Lin and Frank Collins derived neurotrophic factor for nigral dopaminergic neurepeated the arduous task of characterizing a novel neurons and/or spinal or facial motor neurons would now rotrophic factor through protein purification and seseem to be in question. Although substantial deficits quencing. In doing so, they thought they had discovered in cranial sensory neurons (z40% loss in the nodose/ a new transforming growth factor b (TGFb)-like growth petrosal complex), sympathetic neurons (z35% loss in factor that was an extraordinarily specific and remarkthe superior cervical ganglion), and enteric neurons are ably potent target-derived neurotrophic factor for dopaindeed evident in GDNF2/2 mice, the most prominent minergic neurons (Lin et al., 1993). Follow-up work on and surprising phenotype of such null mutants is the the distribution of this factor, glial-derived neurotrophic complete absence of kidney tissue. Although surprising factor (GDNF), provided supportive evidence that this to the neurotrophic factor fraternity, the marked similarmolecule was in the right place at the right time to play ity in phenotype between GDNF null mutant mice and a crucial role in the genesis of the nigrostriatal dopaminan earlier knockout of the orphan receptor tyrosine kiergic pathway (Poulsen et al., 1994). Additionally, animal nase c-Ret (Ret) was cause for simultaneous illumination efficacy studies demonstrated protective effects of exof more than a few light bulbs. ogenousGDNF invarious models of Parkinson’s disease On primary and secondary structural characteristics,