RT Book, Section A1 Lindvall, Olle A2 Watts, Ray L. A2 Standaert, David G. A2 Obeso, Jose A. SR Print(0) ID 55794857 T1 Chapter 16. Restorative Therapies for Parkinson's Disease T2 Movement Disorders, 3e YR 2012 FD 2012 PB The McGraw-Hill Companies PP New York, NY SN 978-0-07-161312-5 LK neurology.mhmedical.com/content.aspx?aid=55794857 RD 2024/03/28 AB The main pathology underlying the motor symptoms in Parkinson's disease (PD) is a rather selective degeneration of the nigrostriatal dopamine (DA) neuron system. The experimental strategies to restore brain function in PD patients have all been based on a very simple principle, namely, to replace the dead dopaminergic neurons by new, transplanted DA-producing cells. The interest in cell replacement dates back to the late 1970s when it was demonstrated that intrastriatal grafts of embryonic mesencephalic tissue, rich in DA neuroblasts, induced functional recovery in rats with neurotoxin-induced lesions of the nigrostriatal DA system. There is now a solid experimental basis showing functional efficacy of such transplantation to the striatum in animal models of PD, and a biological mechanism underlying the observed improvement, that is, restoration of striatal DA transmission.1,2 Extensive animal studies have shown that the grafted DA neurons display many of the morphological and functional characteristics of the intrinsic mesencephalic DA neurons: they reinnervate the denervated striatum and form synaptic contacts with host neurons, are spontaneously active and release DA, and receive afferent inputs from the host. Reinnervation by the grafts ameliorates several aspects of the DA deficiency syndrome in rodents and monkeys.