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By C. Thomas Caskey

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18:1723–29 5. Seifert R, Wenzel-Seifert K. 2002. Constitutive activity of G-protein coupled receptors: cause of disease and common property of wild-type receptors. Naunyn. Schmiedebergs. Arch. Pharmacol. 366:381–416 6. Hamm H. 2001. How activated receptors couple to G proteins. Proc. Natl. Acad. Sci. USA 98:4819–21 7. Dessauer CW, Posner BA, Gilman AG. 1996. Visualizing signal transduction: receptors, G proteins and adenylate cyclases. Clin. Sci. 91:527–37 8. Neer EJ. 1995. Heterotrimeric G proteins: organizers of transmembrane signals.

J. Clin. Endocrinol. 80:1702–5 Hayward BE, Barlier A, Korbonits M, et al. 2001. Imprinting of the Gsα gene GNAS1 in the pathogenesis of acromegaly. J. Clin. Invest. 107:R31–36 Shenker A, Weinstein LS, Sweet DE, et al. 1994. An activating Gsα mutation is present in fibrous dysplasia of bone in the McCuneAlbright syndrome. J. Clin. Endocrinol. Metab. 79:750–55 Weinstein LS, Shenker A, Gejman PV, et al. 1991. Activating mutations of the stimulatory G protein in the McCune-Albright syndrome. N. Engl.

3. Disease progression: Despite the symptomatic value of levodopa, patients continue to deteriorate, and most eventually experience unacceptable disability. Indeed, there has been a theoretical concern that levodopa might actually accelerate neuronal degeneration and disease progression as a result of cytotoxic metabolites generated by the drug’s oxidative metabolism, although there is no direct evidence that this actually occurs in PD (9). Collectively, these problems limit the long-term value of levodopa, despite the drug’s profound symptomatic benefits.

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Annual Review of Medicine Volume 55 2004 by C. Thomas Caskey


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