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Association between the neuron-specific RNA-binding protein ELAVL4 and Parkinson disease

Content Provider	Springer Nature Link
Author	ureddine, Maher A. Qin, Xue Jun Oliveira, Sofia A. Skelly, Tara J. Walt, Joelle Hauser, Michael A. Pericak Vance, Margaret A. Vance, Jeffery M. Li, Yi Ju
Copyright Year	2005
Abstract	Inflammatory processes have been implicated in the cascade of events that lead to nerve cell death. In the nervous system, a number of genes involved in inflammation pathways are regulated post-transcriptionally via the interaction of their mRNAs with specific RNA-binding Hu proteins, the vertebrate homologues of the Drosophila ELAV (for embryonic lethal abnormal vision). The gene encoding ELAVL4, a member of the Hu family of proteins, is located 2 Mb from the chromosome 1p linkage region peak for age-at-onset (AAO) of Parkinson disease (PD) (LOD=3.41). Nine single-nucleotide polymorphisms (SNPs) in ELAVL4 were genotyped for 266 multiplex families (1,223 samples). Additional genotyping in 377 singleton families was performed for a subset of five SNPs (SNPs 1–5) that were not in linkage disequilibrium. SNP 2 (located in the first intron of ELAVL4) showed a strong significant association with AAO of PD (P=0.006), and SNP 5 (a coding SNP in ELAVL4) showed a moderately significant association (P=0.035). Haplotype analysis revealed that the A-C haplotype at SNPs 2 and 3 has the strongest significant association with AAO (P=0.0001) among all combinations of two or three loci. The A-C haplotype remained significant for AAO after the inclusion of the C allele at SNP 5 to this haplotype (A-C-C haplotype, P=0.00018). Although SNP 5 was found to associate with PD risk in the early-onset subset of PD families (at least one affected with AAO <40 years, 60 families), we believe that it is a by-product of its association with AAO. Taken together, these results suggest a potential role for ELAVL4 as a modifier gene for AAO of PD.
Starting Page	27
Ending Page	33
Page Count	7
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	117
Issue Number	1
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	2005-04-13
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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