Cervantes-Arriaga A, Rodríguez-Violante M, González-Latapí P, Dávila-Ortiz MDJ, Yescas P, Alonso-Vilatela E

Language: Spanish
References: 25
Page: 14-18
PDF size: 226.08 Kb.

ABSTRACT

Background: the expression of apolipoprotein E (apoE) polymorphisms has been proposed as a risk factor for early development of psychotic symptoms in patients with Parkinson’s disease. The association between apoE polymorphisms and motor complications is controversial. The aim was to determine the association between apoE polymorphisms and its allele frequency with the development of complications secondary to dopaminergic replacement therapy.
Methods: we evaluated 231 patients with the diagnosis of Parkinson’s disease. The presence of motor complications secondary to treatment was determined by a neurologist, and the genotypifi cation of apoE polymorphisms was performed. Descriptive statistics and X² test were used.
Results: genotype ε3/ε3 was expressed in 80.5 % of the sample; there was no association between genotype or allele frequency of apoE polymorphisms and the development of psychosis or dyskinesia. Patients who expressed the ε2 allele showed a tendency to develop motor fl uctuations, but without reaching statistical signifi cance (p = 0.08).
Conclusions: apoE polymorphisms are not associated with the development of complications from dopaminergic replacement therapy.

REFERENCES

1. Hely MA, Morris JG, Reid WG, Traffi cante R. Sydney Multicenter Study of Parkinson’s disease: non- L-dopa-responsive problems dominate at 15 years. Mov Disord. 2005;20(2):190-9.

2. The French Parkinson’s Disease Genetics Study Group. Apolipoprotein E genotype in familial Parkinson’s disease. J Neurol Neurosurg Psychiatry. 1997; 63(3):394-5.

3. Chapman J, Korczyn AD, Karussis DM, Michaelson DM. The effects of APOE genotype on age at onset and progression of neurodegenerative diseases. Neurology. 2001;57(8):1482-5.

4. Gallegos-Arreola MP, Figuera LE, Ortiz GG, Jiménez- Gil FJ, Ramírez-Vega J, Ruiz-Sandoval JL, et al. Apolipoprotein E genotypes in Mexican patients with Parkinson’s disease. Dis Markers. 2009; 27(5):225-30.

5. Gibb WR, Lees AJ. The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson’s disease. J Neurol Neurosurg Psychiatry. 1988;51(6):745-52.

6. Hoehn MM, Yahr MD. Parkinsonism: onset, progression and mortality. Neurology. 1967;17(5):427-42.

7. Ravina B, Marder K, Fernández HH, Friedman JH, McDonald W, Murphy D, et al. Diagnostic criteria for psychosis in Parkinson’s disease: report of an NINDS, NIMH work group. Mov Disord. 2007;22(8):1061-8.

8. Fox SH, Lang AE. Levodopa-related motor complications. Phenomenology. Mov Disord. 2008;23(Suppl 3):S509-14.

9. Ahlskog JE, Muenter MD. Frequency of levodoparelated dyskinesias and motor fl uctuations as estimated from the cumulative literature. Mov Disord. 2001;16(3):448-58.

10. Mack J, Rabins P, Anderson K, Goldstein S, Grill S, Hirsch ES, et al. Prevalence of psychotic symptoms in a community-based Parkinson disease sample. Am J Geriatr Psychiatry. 2012;20(2):123-32.

11. Friedman JH. Parkinson disease psychosis: update. Behav Neurol. 2012 Dec 14. [Epub ahead of print].

12. De la Fuente-Fernández R, Núńez MA, López E. The apolipoprotein E epsilon 4 allele increases the risk of drug-induced hallucinations in Parkinson’s disease. Clin Neuropharmacol. 1999;22(4):226-30.

13. Camicioli R, Rajput A, Rajput M, Reece C, Payami H, Hao C, et al. Apolipoprotein E epsilon 4 and catechol- O-methyltransferase alleles in autopsy-proven Parkinson’s disease: relationship to dementia and hallucinations. Mov Disord. 2005;20(8):989-94.l

14. Goetz CG, Burke PF, Leurgans S, Berry-Kravis E, Blasucci LM, Raman R, et al. Genetic variation analysis in Parkinson disease patients with and without hallucinations: case-control study. Arch Neurol. 2001;58(2):209-13.

15. Feldman B, Chapman J, Korczyn AD. Apolipoprotein epsilon 4 advances appearance of psychosis in patients with Parkinson’s disease. Acta Neurol Scand. 2006;113(1):14-7.

16. Irwin DJ, White MT, Toledo JB, Xie SX, Robinson JL, Van Deerlin V, et al. Neuropathologic substrates of Parkinson disease dementia. Ann Neurol. 2012;72(4):587-98.

17. Inzelberg R, Chapman J, Treves TA, Asherov A, Kipervasser S, Hilkewicz O, et al. Apolipoprotein E4 in Parkinson disease and dementia: new data and meta-analysis of published studies. Alzheimer Dis Assoc Disord. 1998;12(1):45-8.

18. Kurz MW, Dekomien G, Nilsen OB, Larsen JP, Aarsland D, Alves G. APOE alleles in Parkinson disease and their relationship to cognitive decline: a population-based, longitudinal study. J Geriatr Psychiatry Neurol. 2009;22(3):166-70.

19. Factor SA, Steenland NK, Higgins DS, Molho ES, Kay DM, Montimurro J, et al. Disease-related and genetic correlates of psychotic symptoms in Parkinson’s disease. Mov Disord. 2011;26(12):2190-5.

20. Aarsland D, Larsen JP, Cummins JL, Laake K. Prevalence and clinical correlates of psychotic symptoms in Parkinson disease: a community-based study. Arch Neurol. 1999;56(5):595-601.

21. Giladi N, Treves TA, Paleacu D, Shabtai H, Orlov Y, Kandinov B, et al. Risk factors for dementia, depression and psychosis in long-standing Parkinson’s disease. J Neural Transm. 2000;107(1):59-71.

22. Molchadski I, Korczyn AD, Cohen OS, Katzav A, Nitzan Z, Chapman J, et al. The role of apolipoprotein E polymorphisms in levodopa-induced dyskinesia. Acta Neurol Scand. 2011;123(2):117-21.

23. Halford J, Mazeika G, Slifer S, Speer M, Saunders AM, Strittmatter WJ, et al. APOE2 allele increased in tardive dyskinesia. Mov Disord. 2006;21(4):540-2.

24. Kiyohara C, Miyake Y, Koyanagi M, Fujimoto T, Shirasawa S, Tanaka K, et al. APOE and CYP2E1 polymorphisms, alcohol consumption, and Parkinson’s disease in a Japanese population. J Neural Transm. 2011;118(9):1335-44.

25. Aceves D, Ruiz B, Nuńo P, Román S, Zepeda E, Panduro A. Heterogeneity of apolipoprotein E polymorphism in different Mexican populations. Hum Biol. 2006;78(1):65-75.