ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ

Ahmet Hüsamettin Baran

doi:10.33483/jfpau.994367

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THE ROLE OF PHARMACOGENETICS IN INDIVIDUAL RESPONSE TO ANTIPARKINSONIAN DRUGS

Year 2022, Volume: 46 Issue: 2, 523 - 536, 29.05.2022

Ahmet Hüsamettin Baran

https://doi.org/10.33483/jfpau.994367

Abstract

Objective: Parkinson’s disease, the second most common neurodegenerative disorder after Alzheimer’s, is a progressive neurodegenerative disease characterized by tremor, rigidity, bradikinesis and postural instability. Environmental and genetic factors contribute to the pathophysiology of this disease. The pioneer of dopamine, L-DOPA, remains the gold standard of pharmacotherapy. Although current therapeutic options are clinically beneficial, since parkinson’s disease is a progressive disorder, all drugs used in treatment decline over time and increase in side effects.

Result and Discussion: Recent studies have shown that responses to antiparkinsonian drugs and their side effects exhibit significant interpersonal variability. Pharmacogenetics is a rapidly evolving and very promising field of research aiming to identify genetic markers associated with drug response. Studies in pharmacogenetics have shown that interpersonal genetic differences largely determine the response to drugs used to treat parkinson’s disease. Data obtained in this area will not only have the potential to present valuable therapeutic strategies for antiparkinson treatment, but also increase the probability of successful drug discovery. In this article, compiled studies to identify the role of genetic polymorphisms in better describing the variability in response to antiparkinson therapy and optimizing the pharmacotherapy of parkinson’s disease.

Keywords

Parkinson's disease, dopamine, pharmacogenetics, polymorphism

References

1. Parkinson, J.J.T.J.o.n. and c. neurosciences. (2002). An essay on the shaking palsy. 14(2), 223-236.
2. Poewe, W., et al. (2017). Parkinson disease. Nature reviews Disease primers, 3(1), 1-21.
3. Cacabelos, R. (2017). Parkinson's Disease: From Pathogenesis to Pharmacogenomics. Int J Mol Sci, 18(3). doi:10.3390/ijms18030551
4. Raza, C., R. Anjum, and N.U.A. Shakeel. (2019). Parkinson's disease: Mechanisms, translational models and management strategies. Life Sci, 226, 77-90. doi:10.1016/j.lfs.2019.03.057
5. Balestrino, R. and A. Schapira. (2020). Parkinson disease. European journal of neurology, 27(1), 27-42.
6. Zesiewicz, T.A. (2019). Parkinson disease. CONTINUUM: Lifelong Learning in Neurology, 25(4), 896-918.
7. Paul, A. and K.S. Yadav. (2020). Parkinson's disease: Current drug therapy and unraveling the prospects of nanoparticles. Journal of Drug Delivery Science and Technology, 58, 101790.
8. Kurzawski, M., M. Białecka, and M. Droździk. (2015). Pharmacogenetic considerations in the treatment of Parkinson's disease. Neurodegenerative disease management, 5(1), 27-35.
9. Damasceno dos Santos, E.U., et al. (2019). Pharmacogenetic profile and the occurrence of visual hallucinations in patients with sporadic Parkinson's disease. The Journal of Clinical Pharmacology, 59(7), 1006-1013.
10. Redenšek, S., et al. (2020). Clinical and clinical-pharmacogenetic models for prediction of the most common psychiatric complications due to dopaminergic treatment in Parkinson’s disease. International Journal of Neuropsychopharmacology, 23(8), 496-504.
11. Shah, R.R. and D.R. Shah. (2012). Personalized medicine: is it a pharmacogenetic mirage? British journal of clinical pharmacology, 74(4), 698-721.
12. Spear, B.B., M. Heath-Chiozzi, and J. Huff. (2001). Clinical application of pharmacogenetics. Trends in molecular medicine, 7(5), 201-204.
13. Redenšek, S., et al. (2019). Dopaminergic Pathway Genes Influence Adverse Events Related to Dopaminergic Treatment in Parkinson's Disease. Frontiers in Pharmacology, 10(8). doi:10.3389/fphar.2019.00008
14. Dauer, W. and S. Przedborski. (2003). Parkinson's disease: mechanisms and models. Neuron, 39(6), 889-909. doi:10.1016/s0896-6273(03)00568-3
15. Simon, D.K., C.M. Tanner, and P. Brundin. (2020). Parkinson Disease Epidemiology, Pathology, Genetics, and Pathophysiology. Clinics in geriatric medicine, 36(1), 1-12. doi:10.1016/j.cger.2019.08.002
16. Trist, B.G., D.J. Hare, and K.L. Double. (2019). Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease. Aging Cell, 18(6), e13031. doi:10.1111/acel.13031
17. Puspita, L., S.Y. Chung, and J.-W. Shim. (2017). Oxidative stress and cellular pathologies in Parkinson's disease. Molecular brain, 10(1), 53-53. doi:10.1186/s13041-017-0340-9
18. Huot, P., et al. (2017). Serotonergic approaches in Parkinson’s disease: translational perspectives, an update. 8(5), 973-986.
19. Dietrichs, E. and P. Odin. (2017). Algorithms for the treatment of motor problems in Parkinson's disease. Acta Neurol Scand, 136(5), 378-385. doi:10.1111/ane.12733
20. Kalinderi, K., et al. (2011). Pharmacological treatment and the prospect of pharmacogenetics in Parkinson’s disease. 65(12), 1289-1294.
21. Tirozzi, A., et al. (2021). Analysis of Genetic and Non-genetic Predictors of Levodopa Induced Dyskinesia in Parkinson’s Disease. Frontiers in pharmacology, 12, 987.
22. Tappakhov, A., et al. (2020). Pharmacogenetics of drug-induced dyskinesias in Parkinson's disease. Neurology, Neuropsychiatry, Psychosomatics, 12(1), 87-92.
23. Cerri, S., L. Mus, and F. Blandini. (2019). Parkinson's Disease in Women and Men: What's the Difference? J Parkinsons Dis, 9(3), 501-515. doi:10.3233/jpd-191683
24. Olanow, C.W., M.B. Stern, and K. Sethi. (2009). The scientific and clinical basis for the treatment of Parkinson disease (2009). Neurology, 72(21 Suppl 4), S1-136. doi:10.1212/WNL.0b013e3181a1d44c
25. Liu, Y.Z., et al. (2009). Association of the DRD2 and DRD3 polymorphisms with response to pramipexole in Parkinson's disease patients. Eur J Clin Pharmacol, 65(7), 679-83. doi:10.1007/s00228-009-0658-z
26. Rao, S.S., L.A. Hofmann, and A. Shakil. (2006). Parkinson's disease: diagnosis and treatment. Am Fam Physician, 74(12), 2046-54.
27. Rezak, M. (2007). Current Pharmacotherapeutic Treatment Options in Parkinson’s Disease. Disease-a-Month, 53(4), 214-222. doi:https://doi.org/10.1016/j.disamonth.2007.05.002
28. Oertel, W. and J.B. Schulz. (2016). Current and experimental treatments of Parkinson disease: A guide for neuroscientists. J Neurochem, 139 Suppl 1, 325-337. doi:10.1111/jnc.13750
29. Kuhn, W. and T.J.N. Müller. (2020). Amantadine for Treating Parkinson’s Disease. 1-6.
30. Conrad Musey, B. Medical therapies for motor symptoms in Parkinson’s Disease.
31. Korczyn, A.D. (2004). Drug treatment of Parkinson's disease. Dialogues in clinical neuroscience, 6(3), 315-322. doi:10.31887/DCNS.2004.6.3/akorczyn
32. County, M.J.T.J.o.f.p. (2018). Parkinson’s disease: A treatment guide. 67(5).
33. Borovac, J.A. (2016). Side effects of a dopamine agonist therapy for Parkinson's disease: a mini-review of clinical pharmacology. The Yale journal of biology and medicine, 89(1), 37-47.
34. Philip, A.E., G. DeMaagd, and M.F.J.M.C.o.D.A.t.N.S. Khan. (2020). Parkinson Disease and Antiparkinsonian Drugs. 2, 321-376.
35. Masellis, M., et al. (2016). Dopamine D2 receptor gene variants and response to rasagiline in early Parkinson’s disease: a pharmacogenetic study. 139(7), 2050-2062.
36. Shah, R.R. and D.R.J.B.j.o.c.p. Shah. (2012). Personalized medicine: is it a pharmacogenetic mirage? , 74(4), 698-721.
37. Le Couteur, D.G., et al. (1997). Association of a polymorphism in the dopamine-transporter gene with Parkinson's disease. Mov Disord, 12(5), 760-3. doi:10.1002/mds.870120523
38. Higuchi, S., et al. (1995). Polymorphisms of dopamine receptor and transporter genes and Parkinson's disease. J Neural Transm Park Dis Dement Sect, 10(2-3), 107-13. doi:10.1007/bf02251226
39. Ziegler, D.A., et al. (2014). Motor impulsivity in Parkinson disease: Associations with COMT and DRD 2 polymorphisms. 55(3), 278-286.
40. Rascol, O., et al. (2000). A five-year study of the incidence of dyskinesia in patients with early Parkinson's disease who were treated with ropinirole or levodopa. N Engl J Med, 342(20), 1484-91. doi:10.1056/nejm200005183422004
41. Comi, C., et al. (2017). Polymorphisms of dopamine receptor genes and risk of l-dopa–induced dyskinesia in parkinson’s disease. 18(2), 242.
42. Liu, Y.-Z., et al. (2009). Association of the DRD2 and DRD3 polymorphisms with response to pramipexole in Parkinson’s disease patients. European Journal of Clinical Pharmacology, 65(7), 679-683. doi:10.1007/s00228-009-0658-z
43. Becker, M.L., et al. (2011). OCT1 polymorphism is associated with response and survival time in anti-Parkinsonian drug users. Neurogenetics, 12(1), 79-82. doi:10.1007/s10048-010-0254-5
44. Altmann, V., et al. (2016). Influence of genetic, biological and pharmacological factors on levodopa dose in Parkinson's disease. Pharmacogenomics, 17(5), 481-488.
45. Ferrari, M., et al. (2016). Polymorphisms of dopamine receptor genes and risk of visual hallucinations in Parkinson’s patients. European journal of clinical pharmacology, 72(11), 1335-1341.
46. Schumacher-Schuh, A.F., et al. (2013). Polymorphisms in the dopamine transporter gene are associated with visual hallucinations and levodopa equivalent dose in Brazilians with Parkinson's disease. International Journal of Neuropsychopharmacology, 16(6), 1251-1258. doi:10.1017/s1461145712001666
47. Białecka, M., et al. (2004). The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease. 110(4), 260-266.
48. Sampaio, T.F., et al. (2018). MAO‐B and COMT genetic variations associated with levodopa treatment response in patients with Parkinson's disease. 58(7), 920-926.

ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ

Year 2022, Volume: 46 Issue: 2, 523 - 536, 29.05.2022

Ahmet Hüsamettin Baran

https://doi.org/10.33483/jfpau.994367

Abstract

Amaç: Alzheimer hastalığından sonra ikinci en yaygın nörodejeneratif bozukluk olan Parkinson hastalığı, tremor, rijidite, bradikinezi ve postural instabilite ile karakterize ilerleyici bir nörodejeneratif hastalıktır. Çevresel ve genetik faktörler bu hastalığın patofizyolojisine katkıda bulunur. Dopaminin öncüsü olan L-DOPA, farmakoterapinin altın standardı olmaya devam etmektedir. Mevcut terapötik seçenekler klinik olarak faydalı olsa da parkinson hastalığı ilerleyici bir bozukluk olduğu için tedavisinde kullanılan tüm ilaçlarda zamanla etkinlik azalması ve yan etkilerde artış söz konusu olmaktadır.

Sonuç ve Tartışma: Son zamanlarda yapılan çalışmalardan elde edilen bulgular antiparkinson ilaçlara yanıtın ve yan etkilerin bireyler arası önemli değişkenlikler gösterdiğini işaret etmektedir. Farmakogenetik, ilaç yanıtı ile ilişkili genetik belirteçleri tanımlamayı amaçlayan, hızla gelişen ve çok umut verici bir araştırma alanıdır. Farmakogenetik alanında gerçekleştirilen araştırmalar, bireylerarası genetik farklılıkların parkinson hastalığının tedavisinde kullanılan ilaçlara yanıtı önemli ölçüde belirlediğini göstermiştir. Bu alanda elde edilen / edilecek veriler antiparkinson tedavide değerli terapötik stratejiler sunma potansiyelinin yanında başarılı ilaç keşfi ihtimalini de artıracaktır. Bu derlemede antiparkinson tedaviye yanıttaki değişkenliği daha iyi açıklamak ve parkinson hastalığının farmakoterapisini optimize etmek için genetik polimorfizmlerin rolünü tanımlamaya yönelik çalışmalar derlenmiştir.

Keywords

Parkinson hastalığı, dopamin, farmakogenetik, polimorfizm

References

1. Parkinson, J.J.T.J.o.n. and c. neurosciences. (2002). An essay on the shaking palsy. 14(2), 223-236.
2. Poewe, W., et al. (2017). Parkinson disease. Nature reviews Disease primers, 3(1), 1-21.
3. Cacabelos, R. (2017). Parkinson's Disease: From Pathogenesis to Pharmacogenomics. Int J Mol Sci, 18(3). doi:10.3390/ijms18030551
4. Raza, C., R. Anjum, and N.U.A. Shakeel. (2019). Parkinson's disease: Mechanisms, translational models and management strategies. Life Sci, 226, 77-90. doi:10.1016/j.lfs.2019.03.057
5. Balestrino, R. and A. Schapira. (2020). Parkinson disease. European journal of neurology, 27(1), 27-42.
6. Zesiewicz, T.A. (2019). Parkinson disease. CONTINUUM: Lifelong Learning in Neurology, 25(4), 896-918.
7. Paul, A. and K.S. Yadav. (2020). Parkinson's disease: Current drug therapy and unraveling the prospects of nanoparticles. Journal of Drug Delivery Science and Technology, 58, 101790.
8. Kurzawski, M., M. Białecka, and M. Droździk. (2015). Pharmacogenetic considerations in the treatment of Parkinson's disease. Neurodegenerative disease management, 5(1), 27-35.
9. Damasceno dos Santos, E.U., et al. (2019). Pharmacogenetic profile and the occurrence of visual hallucinations in patients with sporadic Parkinson's disease. The Journal of Clinical Pharmacology, 59(7), 1006-1013.
10. Redenšek, S., et al. (2020). Clinical and clinical-pharmacogenetic models for prediction of the most common psychiatric complications due to dopaminergic treatment in Parkinson’s disease. International Journal of Neuropsychopharmacology, 23(8), 496-504.
11. Shah, R.R. and D.R. Shah. (2012). Personalized medicine: is it a pharmacogenetic mirage? British journal of clinical pharmacology, 74(4), 698-721.
12. Spear, B.B., M. Heath-Chiozzi, and J. Huff. (2001). Clinical application of pharmacogenetics. Trends in molecular medicine, 7(5), 201-204.
13. Redenšek, S., et al. (2019). Dopaminergic Pathway Genes Influence Adverse Events Related to Dopaminergic Treatment in Parkinson's Disease. Frontiers in Pharmacology, 10(8). doi:10.3389/fphar.2019.00008
14. Dauer, W. and S. Przedborski. (2003). Parkinson's disease: mechanisms and models. Neuron, 39(6), 889-909. doi:10.1016/s0896-6273(03)00568-3
15. Simon, D.K., C.M. Tanner, and P. Brundin. (2020). Parkinson Disease Epidemiology, Pathology, Genetics, and Pathophysiology. Clinics in geriatric medicine, 36(1), 1-12. doi:10.1016/j.cger.2019.08.002
16. Trist, B.G., D.J. Hare, and K.L. Double. (2019). Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease. Aging Cell, 18(6), e13031. doi:10.1111/acel.13031
17. Puspita, L., S.Y. Chung, and J.-W. Shim. (2017). Oxidative stress and cellular pathologies in Parkinson's disease. Molecular brain, 10(1), 53-53. doi:10.1186/s13041-017-0340-9
18. Huot, P., et al. (2017). Serotonergic approaches in Parkinson’s disease: translational perspectives, an update. 8(5), 973-986.
19. Dietrichs, E. and P. Odin. (2017). Algorithms for the treatment of motor problems in Parkinson's disease. Acta Neurol Scand, 136(5), 378-385. doi:10.1111/ane.12733
20. Kalinderi, K., et al. (2011). Pharmacological treatment and the prospect of pharmacogenetics in Parkinson’s disease. 65(12), 1289-1294.
21. Tirozzi, A., et al. (2021). Analysis of Genetic and Non-genetic Predictors of Levodopa Induced Dyskinesia in Parkinson’s Disease. Frontiers in pharmacology, 12, 987.
22. Tappakhov, A., et al. (2020). Pharmacogenetics of drug-induced dyskinesias in Parkinson's disease. Neurology, Neuropsychiatry, Psychosomatics, 12(1), 87-92.
23. Cerri, S., L. Mus, and F. Blandini. (2019). Parkinson's Disease in Women and Men: What's the Difference? J Parkinsons Dis, 9(3), 501-515. doi:10.3233/jpd-191683
24. Olanow, C.W., M.B. Stern, and K. Sethi. (2009). The scientific and clinical basis for the treatment of Parkinson disease (2009). Neurology, 72(21 Suppl 4), S1-136. doi:10.1212/WNL.0b013e3181a1d44c
25. Liu, Y.Z., et al. (2009). Association of the DRD2 and DRD3 polymorphisms with response to pramipexole in Parkinson's disease patients. Eur J Clin Pharmacol, 65(7), 679-83. doi:10.1007/s00228-009-0658-z
26. Rao, S.S., L.A. Hofmann, and A. Shakil. (2006). Parkinson's disease: diagnosis and treatment. Am Fam Physician, 74(12), 2046-54.
27. Rezak, M. (2007). Current Pharmacotherapeutic Treatment Options in Parkinson’s Disease. Disease-a-Month, 53(4), 214-222. doi:https://doi.org/10.1016/j.disamonth.2007.05.002
28. Oertel, W. and J.B. Schulz. (2016). Current and experimental treatments of Parkinson disease: A guide for neuroscientists. J Neurochem, 139 Suppl 1, 325-337. doi:10.1111/jnc.13750
29. Kuhn, W. and T.J.N. Müller. (2020). Amantadine for Treating Parkinson’s Disease. 1-6.
30. Conrad Musey, B. Medical therapies for motor symptoms in Parkinson’s Disease.
31. Korczyn, A.D. (2004). Drug treatment of Parkinson's disease. Dialogues in clinical neuroscience, 6(3), 315-322. doi:10.31887/DCNS.2004.6.3/akorczyn
32. County, M.J.T.J.o.f.p. (2018). Parkinson’s disease: A treatment guide. 67(5).
33. Borovac, J.A. (2016). Side effects of a dopamine agonist therapy for Parkinson's disease: a mini-review of clinical pharmacology. The Yale journal of biology and medicine, 89(1), 37-47.
34. Philip, A.E., G. DeMaagd, and M.F.J.M.C.o.D.A.t.N.S. Khan. (2020). Parkinson Disease and Antiparkinsonian Drugs. 2, 321-376.
35. Masellis, M., et al. (2016). Dopamine D2 receptor gene variants and response to rasagiline in early Parkinson’s disease: a pharmacogenetic study. 139(7), 2050-2062.
36. Shah, R.R. and D.R.J.B.j.o.c.p. Shah. (2012). Personalized medicine: is it a pharmacogenetic mirage? , 74(4), 698-721.
37. Le Couteur, D.G., et al. (1997). Association of a polymorphism in the dopamine-transporter gene with Parkinson's disease. Mov Disord, 12(5), 760-3. doi:10.1002/mds.870120523
38. Higuchi, S., et al. (1995). Polymorphisms of dopamine receptor and transporter genes and Parkinson's disease. J Neural Transm Park Dis Dement Sect, 10(2-3), 107-13. doi:10.1007/bf02251226
39. Ziegler, D.A., et al. (2014). Motor impulsivity in Parkinson disease: Associations with COMT and DRD 2 polymorphisms. 55(3), 278-286.
40. Rascol, O., et al. (2000). A five-year study of the incidence of dyskinesia in patients with early Parkinson's disease who were treated with ropinirole or levodopa. N Engl J Med, 342(20), 1484-91. doi:10.1056/nejm200005183422004
41. Comi, C., et al. (2017). Polymorphisms of dopamine receptor genes and risk of l-dopa–induced dyskinesia in parkinson’s disease. 18(2), 242.
42. Liu, Y.-Z., et al. (2009). Association of the DRD2 and DRD3 polymorphisms with response to pramipexole in Parkinson’s disease patients. European Journal of Clinical Pharmacology, 65(7), 679-683. doi:10.1007/s00228-009-0658-z
43. Becker, M.L., et al. (2011). OCT1 polymorphism is associated with response and survival time in anti-Parkinsonian drug users. Neurogenetics, 12(1), 79-82. doi:10.1007/s10048-010-0254-5
44. Altmann, V., et al. (2016). Influence of genetic, biological and pharmacological factors on levodopa dose in Parkinson's disease. Pharmacogenomics, 17(5), 481-488.
45. Ferrari, M., et al. (2016). Polymorphisms of dopamine receptor genes and risk of visual hallucinations in Parkinson’s patients. European journal of clinical pharmacology, 72(11), 1335-1341.
46. Schumacher-Schuh, A.F., et al. (2013). Polymorphisms in the dopamine transporter gene are associated with visual hallucinations and levodopa equivalent dose in Brazilians with Parkinson's disease. International Journal of Neuropsychopharmacology, 16(6), 1251-1258. doi:10.1017/s1461145712001666
47. Białecka, M., et al. (2004). The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease. 110(4), 260-266.
48. Sampaio, T.F., et al. (2018). MAO‐B and COMT genetic variations associated with levodopa treatment response in patients with Parkinson's disease. 58(7), 920-926.

There are 48 citations in total.

Details

Primary Language	Turkish
Subjects	Pharmacology and Pharmaceutical Sciences
Journal Section	Collection
Authors	Ahmet Hüsamettin Baran 0000-0003-0830-313X
Publication Date	May 29, 2022
Submission Date	September 12, 2021
Acceptance Date	March 3, 2022
Published in Issue	Year 2022 Volume: 46 Issue: 2

Cite

APA	Baran, A. H. (2022). ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ. Journal of Faculty of Pharmacy of Ankara University, 46(2), 523-536. https://doi.org/10.33483/jfpau.994367
AMA	Baran AH. ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ. J. Fac. Pharm. Ankara. May 2022;46(2):523-536. doi:10.33483/jfpau.994367
Chicago	Baran, Ahmet Hüsamettin. “ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University 46, no. 2 (May 2022): 523-36. https://doi.org/10.33483/jfpau.994367.
EndNote	Baran AH (May 1, 2022) ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ. Journal of Faculty of Pharmacy of Ankara University 46 2 523–536.
IEEE	A. H. Baran, “ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ”, J. Fac. Pharm. Ankara, vol. 46, no. 2, pp. 523–536, 2022, doi: 10.33483/jfpau.994367.
ISNAD	Baran, Ahmet Hüsamettin. “ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University 46/2 (May 2022), 523-536. https://doi.org/10.33483/jfpau.994367.
JAMA	Baran AH. ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ. J. Fac. Pharm. Ankara. 2022;46:523–536.
MLA	Baran, Ahmet Hüsamettin. “ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ”. Journal of Faculty of Pharmacy of Ankara University, vol. 46, no. 2, 2022, pp. 523-36, doi:10.33483/jfpau.994367.
Vancouver	Baran AH. ANTİPARKİNSON İLAÇLARINA VERİLEN BİREYSEL YANITTA FARMAKOGENETİĞİN ROLÜ. J. Fac. Pharm. Ankara. 2022;46(2):523-36.

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The Journal of Faculty of Pharmacy of Ankara University is an international medium, an open access, peer-reviewed journal for the publication of original research reports, reviews and short communications in English or Turkish on relevant developments in pharmaceutical sciences., Proceeding of scientific meetings may be published as special issues of supplements to the journal. Additionally, it contains previous and forthcoming national and international scientific meetings with social activities in pharmaceutical areas.