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American Journal of Human Genetics logoLink to American Journal of Human Genetics
. 2005 Nov 15;78(1):78–88. doi: 10.1086/498851

A Scan of Chromosome 10 Identifies a Novel Locus Showing Strong Association with Late-Onset Alzheimer Disease

Andrew Grupe 1, Yonghong Li 1, Charles Rowland 1, Petra Nowotny 2, Anthony L Hinrichs 2, Scott Smemo 2, John S K Kauwe 2, Taylor J Maxwell 2, Sara Cherny 2, Lisa Doil 1, Kristina Tacey 1, Ryan van Luchene 1, Amanda Myers 3, Fabienne Wavrant-De Vrièze 3, Mona Kaleem 3, Paul Hollingworth 4, Luke Jehu 4, Catherine Foy 5, Nicola Archer 5, Gillian Hamilton 5, Peter Holmans 4, Chris M Morris 6, Joseph Catanese 1, John Sninsky 1, Thomas J White 1, John Powell 5, John Hardy 3, Michael O’Donovan 4, Simon Lovestone 5, Lesley Jones 4, John C Morris 2, Leon Thal 7, Michael Owen 4, Julie Williams 4, Alison Goate 2
PMCID: PMC1380225  PMID: 16385451

Abstract

Strong evidence of linkage to late-onset Alzheimer disease (LOAD) has been observed on chromosome 10, which implicates a wide region and at least one disease-susceptibility locus. Although significant associations with several biological candidate genes on chromosome 10 have been reported, these findings have not been consistently replicated, and they remain controversial. We performed a chromosome 10–specific association study with 1,412 gene-based single-nucleotide polymorphisms (SNPs), to identify susceptibility genes for developing LOAD. The scan included SNPs in 677 of 1,270 known or predicted genes; each gene contained one or more markers, about half (48%) of which represented putative functional mutations. In general, the initial testing was performed in a white case-control sample from the St. Louis area, with 419 LOAD cases and 377 age-matched controls. Markers that showed significant association in the exploratory analysis were followed up in several other white case-control sample sets to confirm the initial association. Of the 1,397 markers tested in the exploratory sample, 69 reached significance (P<.05). Five of these markers replicated at P<.05 in the validation sample sets. One marker, rs498055, located in a gene homologous to RPS3A (LOC439999), was significantly associated with Alzheimer disease in four of six case-control series, with an allelic P value of .0001 for a meta-analysis of all six samples. One of the case-control samples with significant association to rs498055 was derived from the linkage sample (P=.0165). These results indicate that variants in the RPS3A homologue are associated with LOAD and implicate this gene, adjacent genes, or other functional variants (e.g., noncoding RNAs) in the pathogenesis of this disorder.


Alzheimer disease (AD [MIM 104300]) is the most significant cause of dementia in developed countries and is clinically characterized by memory loss of subtle onset followed by a slowly progressive dementia that has a course of several years. The risk of AD has a genetic component, as evidenced by an increased risk of AD among first-degree relatives of affected individuals. So far, three genes have been identified that lead to the rare autosomal dominant early-onset form of AD. Mutations in the three genes—β-amyloid precursor protein (APP [MIM 104760]) (Goate et al. 1991), presenilin 1 (PSEN1 [MIM 104311]) (Sherrington et al. 1995), and presenilin 2 (PSEN2 [MIM 600759]) (Levy-Lahad et al. 1995)—lead to an increase in the production of long amyloid β peptide (Aβ42), the main component in amyloid plaques. The great majority of AD cases are of late onset (age at onset >65 years) and show complex, non-Mendelian patterns of inheritance. Late-onset AD (LOAD [MIM 606626]) probably results from the combined effects of variation in a number of genes as well as from environmental factors. Early genetic studies of LOAD demonstrated that the ɛ4 variant of APOE (MIM 107741) is associated with increased risk of LOAD and with lower age at disease onset in a dose-dependent manner (Corder et al. 1993).

Genomewide linkage screens in patients with LOAD have identified several other chromosomal regions (reviewed by Pastor and Goate [2004]), implying that genetic risk factors other than APOE must exist. Putative LOAD-susceptibility loci on chromosomes 9, 10, and 12 have been reported in two or more sample sets by different groups (Pericak-Vance et al. 1997, 2000; Rogaeva et al. 1998; Kehoe et al. 1999; Myers et al. 2000, 2002; Blacker et al. 2003). Perhaps the most prominent among them is the linkage to chromosome 10, observed in a number of nonoverlapping samples from studies employing distinct approaches, including linkage analysis based on a genomewide screen, a candidate gene–based limited genome screen, and a genome screen that used plasma Aβ levels as a quantitative phenotype (Kehoe et al. 1999; Bertram et al. 2000; Ertekin-Taner et al. 2000; Myers et al. 2000; Blacker et al. 2003; Farrer et al. 2003). Several candidate genes that are under or near the chromosome 10 linkage peaks have been tested for association with LOAD, but none has been consistently replicated (Alzheimer Disease Forum).

To identify the genes and mutations for LOAD, we undertook a screen of putative functional SNPs in 677 genes under the linkage peak, using a powerful set of unrelated cases and controls. A similar approach was used to identify the glyceraldehyde-3-phosphate dehydrogenase gene (GAPD [MIM 138400]), located on the short arm of chromosome 12, as a putative LOAD risk gene (Li et al. 2004). Here, we report the findings from this scan of 1,412 SNPs on chromosome 10.

Material and Methods

Sample-Set Characteristics

Three white clinical case-control series were used in this study: (1) the WU series (422 cases; 382 controls), collected through the Washington University Alzheimer’s Disease Research Center (ADRC) patient registry; (2) the UK series (368 cases; 404 controls), collected as part of the Medical Research Council (MRC) Late-Onset AD Genetic Resource, including those from the Cardiff University Wales School of Medicine and from King’s College London; and (3) the UCSD series (217 cases; 409 controls), collected through the ADRC of the University of California–San Diego. In total, 1,007 AD cases and 1,195 controls were analyzed. Cases in these series had received a clinical diagnosis of dementia of the Alzheimer type (DAT), with use of criteria equivalent to NINCDS-ADRDA (National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association) (McKhann et al. 1984) but modified slightly to include AD as a diagnosis for individuals aged >90 years (Berg et al. 1998). The minimum age at onset of DAT was 60 years. Controls were nondemented individuals aged >60 years at assessment who were screened for dementia through use of neuropsychological tests and clinical interviews. Controls were matched with cases for age and sex. These samples all show an expected age and APOE ɛ4–genotype distribution and do not appear to have evidence of population stratification (Li et al. 2004). More-detailed information about these samples can be found elsewhere (Li et al. 2005).

A fourth case-control series was generated by selecting one case per family from our genetic linkage sample (Myers et al. 2002) and matching each of them to an equal number of white, nondemented controls collected in St. Louis (these controls are independent of the controls used in the exploratory sample above). There were 429 cases and 321 controls in this series (mean age at onset for the case series is 73.6 years; mean age at assessment for controls is 75.0 years). The linkage pedigrees from the National Institute of Mental Health (NIMH) series and the NIA series (292 pedigrees; 624 affected individuals) (Myers et al. 2002) were also genotyped for the single SNP significant in all case-control series.

Two small series that consisted of neuropathologically confirmed white cases and controls were derived from the U.S. ADRCs (contributing centers are listed in the Acknowledgments) and from Newcastle upon Tyne, United Kingdom. Of the samples in the U.S. series, 40% were assessed as being at either Braak and Braak stage 5 or 6 (cases) or Braak stage 2 or less (controls). The remaining samples (cases) met neuropathological criteria for AD. Both the controls and cases were selected to be largely free of such complicating pathologies as Lewy bodies and vascular events. The combined series included 360 cases (age range 65–97 years; 220 women) and 252 controls (age range 65–100 years; 123 women).

SNP Selection and Genotyping

Genotyping of all samples was performed with written informed consent/assent from the participating individuals and their caregivers and approval from the participating institutions. Polymorphisms used for genotyping were identified from either the Celera human genome database that includes publicly available SNP data or the Applera Genome Sequencing Initiative database. For this study, we chose gene-based SNPs, with a preference for putative functional mutations, as predicted in the Celera or public SNP databases, with the aim to screen as many predicted genes with at least one variant as possible (table A1 and fig. A1 [online only]). Thus, these SNPs consist of 367 missense/nonsense mutations, 1 donor splice-site variant, 172 putative transcription factor binding site mutations, 9 exon-skipping site variants, 109 variants in the UTR, and 739 variants of other types (intronic, silent, and unknown types [SNPs of unknown and silent types were annotated as functional variants in previous genome assemblies]). They cover a total of 677 of 1,270 annotated genes on chromosome 10. All genomic positions for all SNPs and genes are from the Celera Genome Assembly R27. All SNPs had a minor-allele frequency (MAF) of >2% in either cases or controls. The MAF was 2%–5% for 80 exploratory markers and 5%–10% for 165 markers. The remaining markers had MAFs of 10%–50%, with approximately equal numbers of SNPs in each 10% interval.

Genotyping of SNPs was undertaken by allele-specific real-time PCR for individual samples, by use of primers designed and validated in-house (Germer et al. 2000). Cases and controls were always run on the same plate in a blind fashion. Assay quality was scored by an individual who had no access to the sample phenotypes, before the genotyping results were subjected to statistical analysis. Overall, the accuracy of our genotyping was >99%, as determined by internal comparisons of differentially designed assays for the same marker and by comparisons of the same marker across different groups.

Genotyping was performed in stages—markers were first genotyped in one sample set, the exploratory set. Generally, the WU sample set was used as the exploratory sample set. However, when markers were tested for replication in another sample set, we also genotyped that sample set with novel assays that had passed our assay-validation step. Overall, we used the UK sample (105 assays) and the UCSD sample (1 assay) as exploratory sets for <8% of all tested assays. Significant exploratory markers (P<.05) were then genotyped in two additional clinical case-control series. After replication in at least one of these other sample sets, additional fine-mapping markers were genotyped near the replicated SNPs. When additional assays for markers near significant exploratory markers were immediately available, they were genotyped in the exploratory sample in parallel with attempting to replicate in the validation samples. Significant markers were followed up as described above. Five SNPs that showed some level of replication in one or both of the additional case-control series were genotyped in a case-control series derived from the families originally used for our genomewide linkage scan. One of these SNPs (rs498055) was also genotyped in the case-control series that was composed of neuropathologically confirmed AD cases and controls.

Statistical Analysis

To help exclude assays with possible genotyping errors from the analysis, Hardy-Weinberg equilibrium tests were first performed in both the case and the control samples. Assays with significant deviation from Hardy-Weinberg equilibrium in controls were then examined for genotyping quality (P<.05; 63 markers in the exploratory stage). As a result, two assays were dropped from our analysis. One remaining assay with an MAF <10% was significant in the exploratory set but did not validate in the other sample sets and was in Hardy-Weinberg equilibrium.

Pearson’s χ2 test was used to calculate P values for the association of an allele with disease status within a single study. This test of association was performed on the basis of the frequency counts of a 2×2 contingency table of allele and disease status. Two-sided P values are presented for the exploratory study. In the validation stage, one-sided P values were calculated if the odds ratios (ORs) were in the direction observed in the exploratory stage. P values were not adjusted for multiple comparisons unless otherwise stated. ORs and the 95% CIs for an allelic effect were also estimated. ORs and P values for meta-analyses that combine results of multiple sample sets were calculated using the Cochran-Mantel-Haenszel test, and were controlled for the sample set (Agresti 1990). Evidence of replication, rather than multiple testing corrections, was used to evaluate the significance of associated SNPs.

Linkage Analysis

To determine whether rs498055 contributed to our linkage signal on chromosome 10, we stratified families on the basis of the presence or absence of the risk allele of rs498055 in the proband of each family. The families used in this analysis were the NIMH and the National Cell Repository for Alzheimer's Disease families from our linkage screen (Myers et al. 2002). The analysis was performed in Mapmaker/SIBS (“All pairs, UNWEIGHTED”). For the “proband” analysis, the (numerically) first individual with the SNP genotype was identified as the proband.

Haplotype Analysis

Several studies have shown that placing individual SNPs into the context of a haplotype increases biological information (Balciuniene et al. 2002; Knoblauch et al. 2002; Van Eerdewegh et al. 2002). Similarly, placing haplotypes into their evolutionary context also increases biological information (Templeton et al. 2005). For the haplotype analysis, we used SNPs that were typed in all three series and were located within ∼40 kb of rs498055. These criteria resulted in a data set of 11 SNPs in 1,159 controls and 974 cases from the WU, UK, and UCSD case-control samples.

Haplotypes were estimated using the software PHASE (Stephens et al. 2001; Stephens and Donnelly 2003). A set of 95%-plausible haplotype trees was estimated using statistical parsimony in the program TCS (Clement et al. 2000; Templeton et al. 2000).

Association with LOAD was tested by tree scanning (Templeton et al. 2005), which was modified to manage case-control data (Nowotny et al. 2005). A tree scan uses the haplotype network to define tests that are based on each branch of the tree. Each branch represents an a priori defined pooling of haplotypes: haplotypes on one side of the branch are pooled together and define an allele, whereas the haplotypes on the other side are pooled to define a separate allele. This results in a biallelic locus that can be tested for association with the phenotype. A permutation-based analog of the sequential Bonferroni (Westfall and Young 1993) was used to obtain nominal and multiple-test–corrected significance values with the parametric P value used as the test statistic. This permutation method takes into account the correlation structure between tests while correcting for multiple tests.

Results

To identify genetic variation associated with LOAD on chromosome 10, we performed a SNP-based association study with three well-characterized LOAD case-control series. Our strategy was to test markers in one sample set (exploratory sample) and to follow up significant markers in the two remaining sample sets (validation samples). Using this paradigm, we first scanned a relatively large number of gene-based putative functional SNPs across chromosome 10, with the highest SNP density in regions directly under the linkage peak reported above. Significant markers were then genotyped in the other two sample sets to attempt replication of the initial association. Regions with markers showing strong association with the exploratory sample and replication in at least one other sample set were then tested with additional markers. Specifically, we genotyped a total of 1,397 SNPs by allele-specific PCR in the exploratory stage (fig. 1), targeting 674 genes. From these, we genotyped 408 genes with 1 marker, 141 with 2 markers, 57 with 3 markers, 47 with 4–7 markers, and the remainder with ⩾8 markers. The majority of exploratory markers (1,291) were tested in the WU sample set. In the UK sample set, 105 markers were genotyped, and 1 marker was genotyped in the UCSD sample set. Of the 1,397 tested SNPs, 69 were significantly associated with LOAD in the exploratory sample (P<.05). These markers were scattered across the chromosome, as would be expected because of the high probability of false-positive associations due to the large number of SNPs analyzed (fig. 1). We subsequently genotyped the 69 markers in the two validation sample sets and found 5 that replicated in a meta-analysis combining the two validation sample sets (one-sided P<.05) (table 1). One marker, rs498055, located in LOC439999, a gene with high homology to RPS3A (MIM 180478), was significant (P<.05) in each of the three sample sets and was the most significant (P=.00004) marker in the three-sample meta-analysis (table 1). One other marker, rs4417206, located in a neighboring gene ALDH18A1 (or PYCS [MIM 138250]), was also significant in the combined validation study (P=.013). Markers rs4417206 in ALDH18A1 and rs498055 in LOC439999 are ∼41 kb apart and are in strong linkage disequilibrium (LD) with one another (D=0.98; r2=0.43).

Figure 1.

Figure  1

Allelic P values of 1,397 exploratory markers from the exploratory sample (middle), with a bar graph showing the distribution of annotated genes across chromosome 10 (bottom). Marker rs498055 is noted with an arrow, and a P value of .05 is marked with a line. The previously identified linkage peak regions are noted with solid lines and references (top). Studies with multipoint LOD scores >2 in white samples were included. Results of single-marker studies were not included.

Table 1.

Allelic Tests of Replicated Markers and LOAD

Cases
Controls
No. with Genotype
No. with Genotype
Marker, Gene, Position (bp) and Sample 11 12 22 Total MAF(%) 11 12 22 Total MAF(%) P OR (CIa) Power to Replicate
rs1057971, PCGF5, 86733401:
 WUb 2 54 363 419 6.9 0 33 344 377 4.4 .029 1.62 (1.05–.52)
 UCSDc 2 33 213 248 7.5 2 37 360 399 5.1 .044 1.49 (1.01–.19) .61
 UKc 1 39 307 347 5.9 3 32 345 380 5.0 .22 1.19 (.82–.75) .66
 UCSD and UKc 3 72 520 595 6.6 5 69 705 779 5.1 .042 1.33 (1.01–.74) .88
  All 5 126 883 1,014 6.7 5 102 1,049 1,156 4.8 .0068 1.43 (1.10–.85)
rs498055, LOC439999, 91096111:
 UKb 80 175 92 347 48.3 67 194 124 385 42.6 .029 1.26 (1.02–.55)
 UCSDc 64 107 48 219 53.7 85 156 102 343 47.5 .022 1.28 (1.04–.56) .59
 WUc 125 175 89 389 54.6 65 200 86 351 47.0 .0017 1.36 (1.14–.61) .71
 UCSD and WUc 189 282 137 608 54.3 150 356 188 694 47.3 .00021 1.32 (1.16–.51) .89
  All 269 457 229 955 52.1 217 550 312 1,079 45.6 .00004 1.3 (1.15–.47)
rs4417206, ALDH18A1, 91137678:
 UKb 36 153 158 347 32.4 61 169 154 384 37.9 .029 .79 (.63–.98)
 UCSDc 17 102 101 220 30.9 50 157 142 349 36.8 .021 .77 (.62–.95) .59
 WUc 45 155 190 390 31.4 38 165 148 351 34.3 .12 .88 (.73–.05) .71
 UCSD and WUc 62 257 291 610 31.2 88 322 290 700 35.6 .013 .83 (.72–.95) .90
  All 98 410 449 957 31.7 149 491 444 1,084 36.4 .0019 .81 (.71–.93)
rs600879, SORCS1, 102662200:
 WUb 6 87 325 418 11.8 4 54 319 377 8.2 .017 1.5 (1.07–.09)
 UCSDc 3 42 196 241 10.0 6 53 335 394 8.2 .15 1.23 (.89–.71) .67
 UKc 6 66 277 349 11.2 3 63 319 385 9.0 .079 1.28 (.96–.70) .74
 UCSD and UKc 9 108 473 590 10.7 9 116 654 779 8.6 .040 1.26 (1.01–.56) .92
  All 15 195 798 1,008 11.2 13 170 973 1,156 8.5 .0043 1.34 (1.10–.65)
rs1903908, hCG2039140, 102940843:
 WUb 14 97 308 419 14.9 5 77 294 376 11.6 .050 1.34 (1.00–.80)
 UCSDc 6 54 188 248 13.3 2 81 314 397 10.7 .079 1.28 (.96–.71) .53
 UKc 11 78 247 336 14.9 10 76 296 382 12.6 .10 1.22 (.94–.57) .57
 UCSD and UKc 17 132 435 584 14.2 12 157 610 779 11.6 .029 1.24 (1.03–.50) .80
  All 31 229 743 1,003 14.5 17 234 904 1,155 11.6 .0070 1.28 (1.07–.53)
a

95% CI for exploratory and total samples; 90% CI for validation samples.

b

Exploratory sample set.

c

Validation sample set: one-sided P value.

To determine whether any of the five SNPs that replicated in the meta-analysis (rs1057971, rs498055, rs4417206, rs600879, and rs1903908) were also associated with risk for LOAD in our original linkage study sample (Myers et al. 2002), we genotyped the entire series and performed two analyses. First, we used a case-control approach by selecting one case (proband) per family, and we matched each of them to an equal number of unrelated controls. We chose to use a case-control analysis rather than a discordant–sib-pair analysis because of the greater power in the case-control design and because discordant siblings were available for only a proportion of the cases. A one-sided χ2 test demonstrated significant evidence of association in the case-control sample with the same allele as in the other case-control series for rs498055 (P=.0165); all other SNPs failed to show any evidence of association (table 2). The ORs observed in the linkage series for rs498055 were similar to those observed in the other case-control series (OR=1.26; 95% CI 1.02–1.54).

Table 2.

Allelic Association in Linkage Case-Control Series[Note]

No. of Cases with Genotype
No. ofControlswith Genotype
Marker Location(Mb) 11 12 22 11 12 22 Pa OR (95% CI)
rs1057971 86.7 1 35 304 0 41 302 .73 .91 (.57–1.43)
rs498055 91.09 110 207 112 58 162 96 .017 1.26 (1.02–1.54)
rs4417206 91.13 45 163 145 59 139 131 .24 .87 (.70–1.09)
rs600879 102.66 285 62 6 275 56 8 1 1.01 (.72–1.43)
rs1903908 102.94 13 87 265 6 84 252 .45 1.12 (.84–1.51)

Note.— For cases, one affected sibling was genotyped from each family in the linkage sample (Myers et al. 2002) and was compared with a set of independent controls.

a

Allelic tests are two sided except for rs498055.

Marker rs498055 was also examined in two small series (183 cases/127 controls; 160 cases/106 controls) of neuropathologically confirmed cases and controls. The SNP was not associated with AD risk in these samples (P=.63 and P=.21, respectively). However, power to replicate our finding in these samples was low (40% and 36%, respectively; 60% power in the combined sample sets).

To further estimate the effect of rs498055 in the linkage sample, we performed a stratified linkage analysis of the stage II linkage data, on the basis of the genotype of the proband of each pedigree. We performed stratified linkage analyses using the pedigrees in which the proband had a copy of allele A and pedigrees in which the proband had a copy of allele G (table 3). We also considered pedigrees in which the proband was a homozygote for the A allele and in which the proband was a homozygote for the G allele. The results did not show an increase in LOD score in probands with the risk allele. In fact, although the first two groups were roughly the same size, the LOD score was substantially smaller in pedigrees in which the proband had a copy of the risk allele. This suggests that the rs498055 polymorphism (at 91.1 Mb) may have little direct effect on the linkage findings, which have their peak near D10S1211 (at 59.9 Mb), and that other loci contributing to disease have yet to be found in this region.

Table 3.

Linkage Analysis of Pedigrees Stratified by rs498055

Sample No. of Pedigrees No. Affected Peak LOD Location(cM)
All 343 733 3.84 68
Pedigrees with SNPs 292 624 3.18 68
Probands with A 228 488 3.37 68
Probands with G 221 471 2.38 50
Probands without A 64 136 .73 90
Probands without G 71 153 1.18 67

These findings prompted us to focus further follow-up on the region flanking these two genes. A total of 53 markers, covering a 1.49-Mb region, were typed in the exploratory sample, and association of these SNPs was examined. Ten of the markers resulted in a P value <.1 in the exploratory sample, and five were significant at P<.05 (fig. 2). After genotyping these markers in the validation samples, rs498055 remained the only marker that was significantly associated with LOAD in each of the three sample sets.

Figure 2.

Figure  2

Allelic P values of markers around the RPS3A homologue region (LOC43999) in both exploratory and validation samples, along with a gene map of the region and Celera assembly coordinates (in Mbp). Blue diamonds indicate two-sided explatory sample P values; the other symbols indicate one-sided replication sample P values for WU (red squares), UCSD (gray triangles), and UK (green circle).

We examined LD structure in this region, using genotypes from the UK and the WU sample sets. We observed a block of high LD extending from rs500470 to rs1418709, covering at least 190 kb of the genomic region that includes the most-significant markers, rs498055 and rs4417206. Although the D′ values among neighboring SNPs were high, the r2 values were generally low (table 4). The LD structure was comparable between cases and controls. The five significant markers with a P value <.05 (rs500470, rs533343, rs495998, rs498055, and rs4417206) were all located within this block and exhibited higher r2 values with rs498055 than with other neighboring SNPs. (All had r2>0.43 with rs498055.) Comparison of these results with data in the HapMap project indicates that the block containing rs498055 extends 419 kb and contains seven genes, LOC439999, ALDH18A1 (MIM 138250), C10orf61, ENTPD1 (MIM 601752), hCG2023951, hCG1781136, and C10orf130.

Table 4.

Measures of Pairwise D′ and r2 in UK Controls[Note]

Marker Distance rs500470 rs533383 rs533343 rs11594687 rs7895441 rs495998 rs17110999 rs7906450 rs498055 rs2296690 rs1804934 rs749049 hDV68531050 rs2986401 rs2275272 rs4417206 rs11188410 rs10882645 hDV68531048 rs11553577 hCV25943811 rs1418709
rs500470 .00 1.00 1.00 1.00 1.00 .89 1.00 1.00 .88 .95 1.00 .12 .92 .20 1.00 .98 1.00 .18 .92 .96 .92 .02
rs533383 5.78 .99 .99 1.00 1.00 .89 1.00 1.00 .88 .95 1.00 .11 .92 .20 1.00 .98 .96 .19 .92 .93 .92 .03
rs533343 .01 .74 .73 1.00 .66 .99 1.00 .92 .98 1.00 1.00 .04 1.00 .19 1.00 .98 1.00 .16 1.00 .97 1.00 .20
rs11594687 4.03 .07 .07 .05 1.00 1.00 1.00 1.00 1.00 1.00 .68 1.00 .05 1.00 1.00 1.00 1.00 1.00 .05 1.00 .05 1.00
rs7895441 1.40 .37 .37 .22 .03 1.00 1.00 .94 .98 1.00 .76 .50 .95 .63 1.00 1.00 .62 .60 .95 .25 .95 .88
rs495998 5.76 .54 .54 .48 .11 .25 1.00 1.00 .99 .77 1.00 .37 .91 .09 .76 .99 1.00 .09 .91 .94 .91 .23
rs17110999 2.17 .26 .27 .36 .02 .72 .18 1.00 1.00 1.00 .16 1.00 1.00 .96 1.00 1.00 .26 .94 1.00 .04 1.00 .86
rs7906450 5.57 .28 .28 .32 .02 .68 .19 .94 1.00 .85 .27 1.00 1.00 .90 1.00 1.00 .39 .95 1.00 .17 1.00 .87
rs498055 1.49 .52 .51 .47 .11 .24 .98 .18 .19 .78 1.00 .37 .91 .08 .77 .98 .94 .08 .91 .89 .91 .23
rs2296690 16.03 .09 .09 .07 .69 .04 .10 .03 .02 .10 1.00 .87 .44 1.00 1.00 1.00 1.00 .86 .44 1.00 .44 1.00
rs1804934 .20 .04 .04 .05 .00 .00 .02 .00 .00 .02 .00 1.00 1.00 1.00 .99 .98 1.00 1.00 1.00 1.00 1.00 1.00
rs749049 4.96 .01 .01 .00 .10 .06 .11 .19 .20 .11 .11 .02 1.00 .04 1.00 1.00 1.00 .02 1.00 .83 1.00 .41
hDV68531050 .02 .06 .06 .02 .00 .18 .04 .01 .01 .04 .00 .00 .04 1.00 .32 1.00 .93 1.00 1.00 .63 1.00 1.00
rs2986401 6.55 .03 .03 .04 .05 .19 .00 .33 .30 .00 .07 .01 .00 .02 1.00 1.00 1.00 .99 1.00 1.00 1.00 .94
rs2275272 5.51 .09 .09 .07 .74 .03 .09 .02 .03 .09 .94 .00 .13 .00 .07 1.00 1.00 1.00 .32 1.00 .32 1.00
rs4417206 8.31 .30 .29 .21 .05 .11 .44 .08 .09 .43 .07 .01 .54 .02 .23 .07 1.00 1.00 1.00 .86 1.00 .91
rs11188410 .09 .14 .13 .19 .01 .01 .10 .00 .00 .09 .01 .00 .08 .00 .04 .01 .04 1.00 .93 1.00 .93 1.00
rs10882645 7.81 .03 .03 .03 .05 .17 .00 .31 .33 .00 .06 .01 .00 .02 .95 .07 .23 .04 1.00 1.00 1.00 .94
hDV68531048 12.0 .06 .06 .02 .00 .18 .04 .01 .01 .04 .00 .00 .04 1.00 .02 .00 .02 .00 .02 .63 1.00 1.00
rs11553577 37.1 .14 .13 .19 .01 .00 .09 .00 .00 .08 .02 .00 .06 .00 .05 .01 .03 .95 .05 .00 .63 .94
hCV25943811 .24 .06 .06 .02 .00 .18 .04 .01 .01 .04 .00 .00 .04 1.00 .02 .00 .02 .00 .02 1.00 .00 1.00
rs1418709 65.0 .00 .00 .02 .11 .18 .05 .12 .13 .05 .15 .02 .16 .05 .42 .14 .41 .09 .42 .05 0 .05

Note.— Measures of pairwise D′ are shown above the diagonal; r2 values are shown below the diagonal.

The tree-scan analysis of 11 SNPs in the region surrounding rs498055 identified significant results across many branches of the haplotype network. However, the results of the conditional tests suggest that the association observed at these branches is due to their location in the network relative to a single branch. This branch was significant in both the original (P=.0008) and the conditional (P=.03) analyses (fig. 3). It is marked by mutations creating the SNPs rs498055 and rs495998.

Figure 3.

Figure  3

Haplotype networks. Each oval contains the haplotype identification number, the state at each locus, and the number of times it was inferred to occur in this sample set. To simplify the presentation of the network, haplotypes that appear only once in the sample are not shown, and selected haplotypes have been collapsed. The branch that was significant in the tree scan is denoted by the dashed line. P values for the original and conditional analyses are also provided. Mutations at rs498055 are indicated by “T⟷C”; the mutation at rs495998 is indicated by “A⟷C.”

Discussion

Genetic variants in several biological candidate genes under or near the chromosome 10 linkage peaks—including mutations in CTNNA3 (MIM 607667), PLAU (MIM 191840), IDE (MIM 146680), and others—have been reported to be associated with LOAD. However, none of the associations in these candidate genes has been consistently replicated (Alzheimer Disease Forum). Indeed, our own studies in the case-control series used in the present study showed no evidence of association with any of these genes (Myers et al. 2004; Nowotny et al. 2005). These findings suggest that the reported association may be false, although it remains possible that the lack of consistent replication may be due to type 1 error, genetic heterogeneity, population stratification, and/or a small genetic effect confounded by sample sizes insufficient to replicate the initial reports. With the technology that was available to us, we performed a broadly scaled and nonbiased genotyping program. This approach would inevitably be burdened by a requirement of multiple-testing corrections to assess potential associations. To mitigate this, we designed a two-step process in which we genotyped ∼1,400 SNPs in the exploratory sample set but only 69 markers in the subsequent validation sample sets. This strategy led us to identify five SNPs, located in five genes on chromosome 10, that are associated with LOAD. Although our genotyping scan covers the entire chromosome 10, these significant SNPs are located relatively close to linkage peaks identified in other studies (Bertram et al. 2000). Our analysis included 12 SNPs in IDE, 2 SNPs in PLAU, and 32 SNPs in CTNNA3, but none was significantly associated with LOAD (Busby et al. 2004; Nowotny et al. 2005).

The most consistently associated marker among the five significant SNPs is rs498055, which is significant in each of the three initially tested clinical case-control series employed here, with an allelic P value of .00004 in the meta-analysis of the three sample sets. The replication P value of .00021 is significant even after Bonferroni correction for 69 markers (P=.014), and the meta-analysis of these three case-control series used in the screening paradigm is marginally significant even after adjustment for 1,397 SNPs (P=.051). The linkage sample–derived case-control series replicates these results, whereas the smaller combined neuropathologically confirmed case-control sample set is not significant. The meta-analysis of all six sample sets maintains that rs498055 is significantly associated with AD risk (P=.0001).

The tree-scan analysis identified a single branch in the network that is significantly associated with LOAD. This branch is marked by mutations at rs498055 and rs495998. Marker rs498055 is the most significant SNP in the single-marker association tests (see table 1), and rs495998 is in high LD with rs498055 (r2=0.98) (table 4). This suggests that the observed effect is a mutation on the background shared and defined by these SNPs. It is also interesting to note that rs498055 is homoplasious, with mutations inferred on four different haplotypic backgrounds (one major and three minor haplotypes). In some cases, the haplotype structure of a population allows for tests to be conducted at each branch that is marked by a particular SNP, which provides some evidence as to the “causal” nature of the polymorphism. Although no association was detected at the other transitions marked by rs498055 (a result that suggests that the SNP is not causal), the sample sizes for these tests are too small to provide strong evidence regarding the causality of this SNP. Inclusion of all the associated SNPs in this region in a logistic regression analysis by use of sequential regression (type 1) indicates that the significance derives only from LD with rs498055; that is, no other significant association is observed after first including the effect of rs498055.

Marker rs498055 is located in a gene annotated as an RPS3A homologue in the Entrez Gene database. Although the function of the RPS3A homologue is unknown, it appears that RPS3A itself is a strong biological candidate gene for AD. It has been reported that RPS3A mediates the interaction between BCL2 (encoded by BCL2 [MIM 151430]) and PARP—poly(ADP-ribose) polymerase—(PARP1 [MIM 173870]) and that BCL2 and RPS3A together prevent apoptosis by inhibiting PARP activity (Hu et al. 2000; Song et al. 2002). Thus, RPS3A is an important player in the early phase of apoptosis, a feature observed in AD-affected brains. However, we have been unable to detect transcripts of the RPS3A gene by RT-PCR in RNA from multiple tissues, including brain (data not shown). This may be due to constraints in transcript-specific primer design if a gene has multiple paralogues, as is the case with RPS3A. Alternatively, the annotated gene may not be expressed, and this SNP or variants that are in LD are located in a noncoding expressed sequence, such as a microRNA. It is also possible that this SNP, or variants that are in LD, modulate the transcription of neighboring genes. The SORBS1 (MIM 605264) coding sequence is located 33.7 kb downstream from this SNP and can be considered a strong biological candidate gene. It is involved in insulin signaling and was recently reported to be up-regulated in the hippocampus of AD-affected brains compared with controls (Blalock et al. 2004). ALDH18A1 (at 91.1 Mb and in tight LD with SNPs in RPS3A) encodes a member of the aldehyde dehydrogenase family, which is involved in proline biosynthesis via catalyzing the conversion of l-glutamate to l-glutamate 5-phosphate.

On the basis of the results in the combined validation sample sets, three other markers of interest were also identified, but they are not significant in all three individual samples. The power to replicate the original observation in the exploratory sample for these markers is relatively low in each of the validation samples (table 1). These markers are located in four different genes. PCGF5 (at 86.7 Mb) encodes polycomb group (PcG) ring finger 5, a component of a multimeric, chromatin-associated PcG protein complex, which is involved in stable repression of gene activity. SORCS1 (MIM 606283) (at 102.7 Mb) encodes a type 1 receptor containing a Vps10p-domain and a leucine-rich domain that is involved in endocytosis and intracellular sorting. It is most abundantly expressed in the brain (Hermey et al. 1999), and its expression can be differentially affected by neuronal activity (Hermey et al. 2004). hCG2039140 (at 102.9 Mb) is a predicted gene in the Celera Genome Assembly, encoding a 41-aa polypeptide with no apparent homology to any other known proteins. The potential relevance of these genes with LOAD remains to be examined. Moreover, it is possible that neighboring genes might have a role in AD, since the significant SNPs we identified or variants that are in LD may affect their function.

Although the association with rs498055 was replicated in the case-control series from the linkage sample, the pedigree analyses suggest that this association did not significantly contribute to the original linkage signal on chromosome 10. Although the power of this analysis is low, it suggests that there may be more than one AD susceptibility gene on chromosome 10.

In our screen, we did not attempt to systematically genotype chromosome 10; rather, we used an opportunistic approach to identify functionally relevant gene-based variants that show significant association with AD in at least two independently collected case-control sample sets. Therefore, we cannot exclude the majority of nonsignificant chromosome 10 genes from those that might contribute to the genetic risk of AD. This would require high-density SNP genotyping incorporating an LD-based approach to SNP selection in the case of the common disease–common variant hypothesis and, ultimately, deep resequencing of all genes, to exclude rare pathogenic variants. However, the results outlined above highlight five SNPs—particularly rs498055, which was replicated in four independent case-control series—and corresponding genes as likely AD risk factors on chromosome 10. These findings require functional experiments to validate potential links of the genes and genetic variation to pathways related to disease mechanisms for AD.

Acknowledgments

Some of the authors are employed by Celera Diagnostics, have personal financial interests in the company, or receive research funding from Celera Diagnostics. Funding for this work was partly provided by National Institutes of Health (NIH) ADRC grants P50 AG05681 (to J.C.M.), P50 AG05131 (to L.T.), RO1 AG16208 (to A. Goate), and PO1 AG03991 (to J.C.M.); the MRC UK (to J.W., M. Owen, S.L. M. O'Donovan, and L. Jones); and the Alzheimer Research Trust (to J.W., M. Owen, and S.L.). J.H. and A.M. were supported by the NIH intramural program and by the VERUM Foundation (DIADEM project). J.S.K.K. is supported by NIH training grant T32 HG000045, and T.J.M. is supported by MICORTEX and NIH grant GM065509. We acknowledge Mary Coats and Elizabeth Grant for coordinating the Washington University material, Mary Sundsmo for coordinating the UCSD case material, and Pamela Moore and Dragana Turic for providing clinical/DNA samples from MRC UK Genetic Resource for LOAD. Many data and biomaterials were collected in three projects that participated in the NIMH Alzheimer’s Disease Genetics Initiative. From 1991 to 1998, the research centers, grant numbers, and principal investigators and coinvestigators were as follows: Massachusetts General Hospital, Boston, U01 MH46281, Marilyn S. Albert and Deborah Blacker; Johns Hopkins University, Baltimore, U01 MH46290, Susan Bassett, Gary A. Chase, and Marshal F. Folstein; University of Alabama, Birmingham, U01 MH46373, Rodney C. P. Go and Lindy E. Harrell. Samples for this study also came from the National Cell Repository for Alzheimer’s Disease, which is supported by cooperative agreement NIA grant U24 AG021886. The neuropathological series were collected largely from several NIA–National Alzheimer's Coordinating Center–funded sites. Marcelle Morrison-Bogorad, Tony Phelps, and Walter Kukull are thanked for helping to coordinate this collection. The research centers, directors, pathologist, and technicians involved include: NIA, Bethesda, Ruth Seemann; Johns Hopkins ADRC, Baltimore (NIA grant AG 05146), Juan C. Troncoso and Olga Pletnikova; University of California–Los Angeles (NIA grant P50 AG16570), Harry Vinters and Justine Pomakian; the Kathleen Price Bryan Brain Bank, Duke University Medical Center, Durham, NC (NIA grant AG05128, National Institute of Neurological Disorders and Stroke grant NS39764, NIMH grant MH60451, and support from GlaxoSmithKline), Christine Hulette; Stanford University, La Jolla, Dikran Horoupian and Ahmad Salehi; New York Brain Bank, Taub Institute, Columbia University, New York, Jean Paul Vonsattel; Massachusetts General Hospital, Boston, E. Tessa Hedley-Whyte and Karlotta Fitch; University of Michigan, Ann Arbor (NIH grant P50-AG08671), Roger Albin, Lisa Bain, and Eszter Gombosi; University of Kentucky, Lexington, William Markesbery and Sonya Anderson, Mayo Clinic Jacksonville, Jacksonville, FL, Dennis W. Dickson and Natalie Thomas; University of Southern California, Los Angeles, Carol A. Miller, Jenny Tang, and Dimitri Diaz; ADRC, Washington University, St. Louis, Dan McKeel, John C. Morris, Eugene Johnson Jr., Virginia Buckles, and Deborah Carter; University of Washington, Seattle, Thomas Montine and Aimee Schantz. A.J.M. is a resident research associate of the National Academy of Sciences (U.S.A.).

Appendix A

Figure A1.

Figure  A1

Count of markers used in the exploratory samples by SNP types. Note that the categorization of the unknown (intergenic) and silent mutation SNPs is based on the most current genome assembly (Celera Genome Assembly R27). In previous genome assemblies, these SNPs belonged to functional categories as well.

Table A1.

Markers Genotyped as Part of the LOAD Screen of Chromosome 10[Note]

Gene
Sample
Marker 1 2 3 WU UCSC UK SNP Sequence
hCV1007164 hCG1811021 X TGTGTGTACGGGTGTGGTTGTGAAAGAGARAAGGAAGTCATTTTGTAGAGCTGTTTATTT
hCV11194331 IDE X CCCGGCTCAAGCAATCCTCCCGCCTCAGCMTCTGGAATAGTTGAGATTACTGGCACGTGC
hCV11196784 LOC119587 X GGGCAACCTGGAAAGGACAATGCTTGTTAWAAACAACGACAGATGCTGAAAGGGATGAGT
hCV11205455 MAT1A X AAGTTGCTGCTTCTGCTCCAGGAAGCCCASATAGGACTGGACTGGACTTAGACCACTTAC
hCV11208397 DMBT1 X AAGGATTCTTGTGTTCCCCTGTAGGATCTRAATCCAGTTTGGCCCTGAGGCTGGTGAATG
hCV11276238 PTPRE X TACCAGTTCATAATACCCATTTGTTGATGWCCTCAGGGGCTGACGGTGGCCGTTATGGTT
hCV11304669 SAMD8 X GAGGGTGGGAGGATCATTTCAAAAATATGWGATGTATGGTCCCTGTCCTCAGGAATATTA
hCV11374977 NA X CTTATTAGGTCTTCCACGATAACTATTTTRTTGCCTCATACACCACCTCTTTATCCTGTT
hCV11476780 VCL X TACTGTGGGCTATCAGGCTGCCTATATTTRGTGGGTGCCTTCATTTCTTTGGGTAGGCTC
hCV11568071 MRC1 X TACGCTACTAGGCAATGCCAATGGAGCAAYCTGTGCATTCCCGTTCAAGTTTGAAAACAA
hCV11568148 hCG1660695 X TGGGACCCCAGGAGCCCTCCTGTGACTCCRGAATCCTGAGAATGATGTCCCGGCGAGATG
hCV11596131 JMJD1C X GGGAATTATAAACTGTTTTTTCTGTGCTGKTTTTTTTTTTTTTTTCTGAGACACAGTCTC
hCV11640694 RSU1 X GCAACCAAAAGGGAAACGCGGGTTCCCCCYGTCAGGCAGAAAACTTCCCAGACAGACTAC
hCV11640699 CUBN X TTAGAAAGGGTAGCAGCAAGACCTACCACSAAGTAATCCCCCTGGTTGCAAGAAGAATCT
hCV11647845 CALML3 X CCTCCACGGCATGGCATCAGCTACTCTGAYTCAGTTCACCCACGGCAGTGAGTGTGTCCT
hCV11652239 KIN X CATACATACTATCTGTCCTAGTAAGAAAAYAGATCAACGCTGAGTAGAAACTATGGATGA
hCV11756797 HTR7 X AATGGGAAGTTGGACACACTTCCTGATACYCCCACCTTCAGGGGAGCCATCAGGCTTTCC
hCV11779483 ASAH2 X ATATAAACCCCAAACCCCCAGCTCCACAARCAGACAAGGAGATGAACAGAAAAGCAGAAT
hCV11877867 NCOA4 X TTGAGCCAAGGAGTTTAACACCAGCCTGGSCAACATACAGAGACCCTGTCTGTACAAAAA
hCV11880347 GALNAC4S-6ST X TTTTGTTTTCTCCTTTGCACGTGGGGCACRCCTGGTGACCGTGATGGGGGCCCCCTTGGC
hCV12014288 NA X ACCCACTGACACCGGTGATAGGGGCCTCTYTTCCACTGGACTGACAGCTACAAGGATGTA
hCV1213173 hCG1781406 TACC2 X ACAAAGTGAGCATGGGGTGTAACATGTCCRTTTGCTTACTATGCATGCACGCCCCTCTTC
hCV1229739 ADAMTS14 X CTAGTGAGGTGTTTTGTATTCATAAACAARGTTATTTAAAACAAAAAAGCTGGAGTATCC
hCV1251183 hCG1820432 X GAGCAAGAATGTGATGCTTTAGAAGAAAGRAATGAATGAAAGGCCAGGCTGGTTAAGCTG
hCV1345812 PKD2L1 X X X GGGAAGCCATCAGCTCCTGTTCTATCACCYACTCTACTGGGATCTCAGGACCAAGGCTCA
hCV1407029 hCG2041916 X CAGAACACAAATTATTATTATGATTCCTAWTATGAGCAATAGCTTCTGCCACCAAGTTCC
hCV1531925 SUPV3L1 X GCCAGCGGAGACTCCTTTTAGGATTCTTTRTCATTGAGGAGGCGCCGACTCATACCACGC
hCV1548908 hCG1643384 X TGAAGATGCTTCAGATTCAATCCGAGAAAKGTATCACTGCAGAGTTTATAGAAAATGAAG
hCV15792242 C10orf30 X GTTCGCTGGGAGCATATAAGGGAAATTGGRGGTTGTTGTCTGTTTTGAGTTCCAACTGCG
hCV15825497 NA X CTGGTTAATCGCAGGAGGCACTTTCAGCCMCTTATAGAGGATGGCTCTCTGCCGCTGCAA
hCV15834772 MKI67 X GGTCTCCCCTGACGTCCGTGTGAACTTGCYGACTGCTAGGAGCTCTTCTTTCACACCTAC
hCV16167035 hCG1655317 X TGATCTCATCCATCTTACTAAAGTTTGTGSAGTCTTGATCATTCCCCATTCCCCCAACAT
hCV16192725 C10orf35 X ACAGGTAGGTACTCATTTCCTGTGGAGTGRGACAGATGGCCTCCTGTGTACTGGCTACTC
hCV16264597 NA X CTCAGACTCCAGTTATGGCTCAACCCAAARAAGATGAAGAGGAAGATGATGATGTAGTGG
hCV1709930 LHPP X GACTTGGCCCAGGGCAGCCTCATAAAGCARTTCCCACCCAGGACCGCCCCGATCGATCGG
hCV1720473 C10orf7 X GCAGGTACAACATTTTTAAGACAGATACARTGTAAACCTTTCCAGTCTACTGACTGACTG
hCV1893544 JMJD1C X CATCCTACAAGATGTGGTAAATTTGAAAAKAATAACCCTGATCTTTACTTAAAGGAGTTG
hCV1912681 hCG39169 X CAGCGTCTGGTACAGCCACCTGTTCTTCCRGTACAGATGGAAGTGGAATTGACTATCTGT
hCV1974596 LOXL4 X TGGGCTTGAGCCGCACCTCCTCCAGCCGCYGGCCCTGCGGGGTGCACAGTCACCTGTGGG
hCV2008818 SORBS1 X ACAGCAGCTGAGGCACAGGCATTGAAAACRAATTTTGCCTACCTGTAAAGACTCTAGACT
hCV2009356 hCG2041919 X TTTTGTAGAAAGTATTTGAGGTGACGCTCWCAATTCAAGGAGATATCTCAGGGTGTAAGA
hCV2041328 hCG2041421 X TTTCAACTGAGAGGATAACAAAGAACATGRTAGGAGTTGGACTACATAAAAGTTAGTTTC
hCV204710 hCG23640 X TCTTTGACAAGTTTGAGTGTTGCTGGAACRGTTCGGATAGGTAAGGCCTGCGTGGAGATG
hCV21898 RPP30 X GAAGTTTGAATTTGTCTGTCAAGCCTGTAYACACTAGCATTGTCAGTAAGCTTTGTTTTT
hCV2376176 hCG1811015 X GATTCCTAGAGGGAACCTCCCTCCCCCCCWCAAGGGTGACACGCATGCTCGTGGGGTGAT
hCV2432147 TXNL2 X AGCGACATGCATCTAGTGGCTCCTTCCTAYCCAGCGCTAATGAACATCTTAAAGAAGATC
hCV247567 LOC220929 X ACACATGCATGTTTTCACTGAGAGCTGTAYTTGAAGAACAGCCTATATTCTGCTAAATTT
hCV25592823 CWF19L1 X CATAGGGCTCAAAGTCTTTCCGGAAGCGGYGAGCCAGGGTCTCCTCGTCTTCCTTGCTGA
hCV25595249 SYNPO2L X CCTGCTTGGGTGTTGCCCGAGGCCCCTGGKATTGGGCCTTAGGGAGAGTTCGGGCCGCCT
hCV25595681 NA X AACCAGAACAATGTCTTTTGACTTGCAGARATCCAGCAGTTTGCTCTGGTTGAGGTAAGG
hCV25596066 RGR X TCTATACGCAGTCATCGCAGACGTGACTTYCATCTCCCCCAAACTGCAGATGGTACAGAT
hCV25599810 MMRN2 X ACCCTTCTGCAGCTCAGCCATGGCAAAGASCGTTGCTGTGCTTCCACTCCCCTGCCCAGT
hCV25600248 ADAMTS14 X CGGGCCCCAACCCTGGCCCAGACCCTGGCYCAACCTCACTGCCCCCCTTCTCCACTCCTG
hCV25602992 DNTT X GTTTCAGAACTCTGAGTAAAGTAAGGTCGSACAAAAGCCTGAAATTTACACGAATGCAGA
hCV25603384 INA X CCAATCCAAGTTACCTGCTCCCACCTAGAMTCCTCAGTGCTACAACCTCCAAAGTCTCAT
hCV25603850 hCG23635 X GTCTTAGGTTTTAGTCTCTATGGAAAGCAYTGTGAAGTTAAAGTGCTTAATATTCACATA
hCV25603990 hCG23635 X GAGGTATTTTCTTAACAGGCACTGTGGGCRGCAATCTGTCAACAGAGAAAATAAAACTAT
hCV25604328 PPRC1 X AAACACCCCTTGAGATTTGCCTTGTGCCTRTAGGTCCCAGCCCTGCTTCTCCTAGTCCTG
hCV25604457 ITIH2 X GGACTATGATTTTTTGAAGAGACTGTCCARTGAAAACCATGGAATTGCACAAAGGATTTA
hCV25604675 ARHGAP19 X CAGCTCTCTCAGTGCCTCTTCCGTATGGTRCTGGGTCTCCTCCTGGTGAGGGCAGGAATC
hCV25605409 C10orf28 X CGAAGAGTTCAAAACAGAAGAGCAAGATGMCTCAGGGAGTATAGAATTTGGTGTATCTTT
hCV25606322 C10orf64 X CCTGGAGAGAGGGAAGTGAAGATTGAAGASGTCACACCGCTCTGGGAGGAGACGATGCTC
hCV25614719 OGDHL X GAGCTGGCCACACTGCCGATGTGGGTGAGSATGTCCTCAGGGATCCCCGTGGCTGGGCAT
hCV25624518 PNLIPRP2 X CTGTAAAATTACTTCCCTGGTCCCCCGAGSACATTGACACCCGCTTTCTTCTGTACACAA
hCV25624843 MCM10 X GAACCAAGAGGGTGGCTCGAACACCAAAGSCTTCACCTCCAGGTGTAGTACTTGCGGTCT
hCV25625205 JMJD1C X TATACCTTTTGAAGAAATTCCCTTATCTTSTCAACATCTTTCCCAGCATAAATATGCCAC
hCV25626240 FER1L3 X TTTCCCTGCATAAGGGTCACAGCGAAAGCRGTCCAGGCGCTCGATGGTGCACTGGCCGAC
hCV25626404 C10orf3 X AGAAATGTTACAACGATCTCTTGGCAAGTSCAAAAAAAGATCTTGAGGTTGAACGACAAA
hCV25638641 hCG1641533 X TACTGTTCGGTTCTGGTTCTACATGATTGWTCCCAGGAGTATGGGAATATTAAAGGTACA
hCV25639102 hCG1643351 X TATCAAAAGTATGCACGTATTTTATGTATRAGGTTCGCTACCCTAACAGCTCCACCGAGG
hCV25644235 hCG1655308 X TTTGACATTGATAGACTAGGAGAGGAAATYATCTCCAGGAAAAATGCCATGCATGACCAG
hCV25650689 MGC16186 X GAAGGAGGCCTTGAAGCAGGAATTCCTGCSAGGTACTTCCAGTCTGATTCCAGGAATGCC
hCV25651247 AMSH-LP X TGCGAAGTCAGCAAACCTCAGGGCTGTCARAGCAGATTGATGGGAGCGCTTTGTCCTGCT
hCV25651790 THNSL1 X GCCTGAAGACTGTGAACAGAAGGTTTCAGMAAAATTCTTTAGTGAAGCTGTAATTGAGGG
hCV25651880 NEBL X TGACCTTCCTTTAATCTCCTTCTCAAAATSCTCTTTGTAAACTTTCTGTTAAATAAGACC
hCV25652036 hCG1792626 X GCCTGACGTTCGTTCATCAGCTCCTGGTAMTCACGCCGCTGCCGCGCCATGTCCTGCTTG
hCV25652141 TCF7L2 X GTTAAAGAACATTAAATAAATTATATAAGKATGCCTACCTGTAACACTTTTATAAGGCAA
hCV25652286 SORCS3 X AGCAGAGGCCGTAAAAAAAAGTTTAAAGCRTGAAGCGAAATTCCACACCCATCCAGCGCT
hCV25767316 HECTD2 X AATTACTATTTACAAGATCTATAAACTTCRGAAGCAAAAATATCTTGCCTTGGCAGGAAA
hCV25921991 hCG2018011 X CTTACTGGGAAGGTTACGTTATGTAATATXTGCCAGCCATTTTTGCAAAGTGCTGTATAC
hCV25923481 hCG2023484 X ATTGAAAGCCATGGGAGAGGCTAAAGGAASAAGAGCCTCCAGATAACTTTCCTGAAAACA
hCV25930703 hCG1648656 hCG2042804 X TCCTTCTGACACTGGGTCCCTGTCACTTCYGAGGGAACAGGACCGTAGGATGATGTTTCC
hCV25931135 hCG1803570 X AAGCTGTGGAGAGCCACGAAGGTGGCAGGRGGCATTAGAGGGGCTGTAAAGGGACCGATG
hCV25932561 MGC32871 X ATTCAAATTAGTTTATCATTTACCTGCAAWCTTTTTCTTTGGTTCTGCAAGTCCGTGACT
hCV25933604 KNDC1 X TGACCCAGCCTCCTCGGCCGTGCTGACGAYGAGAATGCAGGTCAGTCCCCACCTCCGCCC
hCV25936294 NA X CGCGCCGGCACGAGGGTGTTTTCGACGTTRGCTGTGGGGAAACAGCAAGCGGCGTGGACG
hCV25943811 C10orf61 X X CGGGTCCGACGTAGGCCTCCGCGGTCTCCMATCGCATTGCCAGAGCGTGGGTGGGAGGAG
hCV25953510 hCG2024410 X CTTTGGTCACCCTGTGGTAGAAAGCCTTCRAAAGCAGCTAGGCCAGGACCCTTTCTTTGA
hCV25953694 hCG2017698 X GTGTCAGCCTGGACAACATAGCAAGACTCYATCTCTGAAAAAAAAACAACAACAAACTTT
hCV25966142 GPR123 X GGCGGGGTCACTTCGGTACCCCCAGTGACYTCATGTGGCAGATGGGCCCCCCACTCTGCT
hCV25971922 NUDT13 X CTGTTTCTTAGAGTTGGAAAGGCTCCTGGRTAAATTTGGACAGGATGCACAAAGAATAGA
hCV25990430 NA X TTCTCCTCTTGTAGCACCCAGTGACTGTGSGGGCCACTACACAGATGAATATGGCAGGAT
hCV29522 RPP30 X TTAAGCACAGATCTTAATTTTGTCACGATKTGGGCCCTTTTCTTTGGTTGTGGTGAAAAG
hCV3010735 hCG1993574 X GGGGAAAATGTCTGGGAAGAAGCTTTTCGKGACCAATGGTGAGCGGATGCCTTTCTCCAA
hCV3033543 NA X GCCTGAAGGGGAAAGCCACCTCGGAGGACMCCCTCAATCTAAGGTAATGGCGGGTAGCCA
hCV3061051 NA X GCTGGCAAGGCTGCGGAGAAAAGGGAATGYTTACACACTGTTGGTGGGAATGTAAATTTG
hCV3261312 KIAA1754 X CCCCCTCTGTCGGCAGCCATCTCCGACACRGCTCCTCCGAGCTCGCGCTCTCCATCGCGC
hCV382705 BTRC X CCAGGCCTCAGCTGGTAGTGTAGTTATTTMAAATAATATTTAATACAATAAATTCTATGG
hCV385555 hCG1657676 X CCCGAACAGAGGTAGATACCATGTGTAGAKAGAAACAGGCAGAGAAATAGGAGAGTTGAA
hCV7432608 KCNMA1 X CTTACCACGACCCAAAGAGCCTCACAGAAYAGATTTCGGAAAGTACGTGTGCGTGTGTGT
hCV7534313 hCG2041498 X TTGGTACAGGTAAGACCATCAGAGTGATTRCTGACATCTGGAATGTTGTTGTTCTTTTCA
hCV7548937 hCG25651 X ACAGTACATAAGAGAACACACAGAGGGGAKAAATCTTATTACTGTAATAAATGTGGGAAA
hCV8040921 CTNNA3 X CTATTGCATGATTGCTCGTACACATGTCTMTTCCTGGGTAATGAGCTCCATTATAGGAGG
hCV8171810 ABLIM1 X AATATCCTTGGGATTTAGCTCCGTAGCTAYACTTATGTTACATTCTCCATCTCTCCCACC
hCV9580408 CACNB2 X TTTATTTTTTCCCAGAGATGTTTTTATCTRTCTTTTGTGCCTTGTGACTTTGATAAGGTT
hDV60100216 NA X CTTGTCACAGCCGACAGGCTGAGGCCAGAKGTGAGGTCAGTGGGAGGAGGCTCCCCTGCC
hDV60100219 NA X TAACTGAAACCACAGAACTTGTATATCCTYAGGATTGAGTTGATGAAGGTCATAAAAGGT
hDV68531048 NA X CGCCCCCTGGCACTACCGCGGGTCCGCACYCCACGCCGGGCTGATTCCGGCGCTCGCTCA
hDV68531050 PYCS X CCTAAAGTCTGAAGGCTCACAGGCCTGCTSGAGTGTCAAGTCTGCTTGTAGTAGTGTCTT
rs1004256 CBARA1 X
rs10082391 MKI67 X
rs10082466 MBL2 X
rs1017822 ATRNL1 hCG2042431 X
rs1021362 SORCS3 X
rs10242 RPP38 X
rs1027190 SORCS3 X
rs1029074 LIPA X
rs1029077 ARHGAP12 X
rs10409 HNRPF X
rs1042454 RGR X
rs1043009 hCG2041852 X
rs1043098 EIF4EBP2 X
rs1044258 C10orf76 X
rs1044261 IDI2 X
rs1044563 PPP1R3C X
rs1044612 CAMK2G X
rs1044795 ARHGAP12 X
rs10450321 hCG2017076 hCG25653 X
rs1045170 WDR11 X
rs1046399 LDB1 X
rs1046528 hCG1640346 X
rs10466026 CDH23 X
rs10466280 SEC61A2 X
rs1047100 FGFR2 X
rs1047991 PAPD1 X
rs1048828 NA X
rs1049125 PNLIPRP1 X
rs1049455 NOLC1 X
rs1049632 RSU1 X
rs1050767 MKI67 X X X
rs10508773 EPC1 X
rs10509343 CBARA1 X
rs10509571 IFIT4 LIPA X X X
rs10509612 RPP30 X
rs10509613 RPP30 X
rs1051338 LIPA X
rs1051509 ARHGAP22 X
rs1051723 TLX1 X
rs1052289 SEC23IP X
rs1052420 hCG24072 X
rs1052895 hCG1781727 X
rs1053266 CCDC6 X
rs1053905 PYCS X
rs1054053 hCG1993574 X
rs1057108 CREM X
rs1057234 hCG1803442 X
rs1057910 CYP2C9 X X X
rs1057971 RNF159 X X X
rs1061135 HPS1 X
rs1061159 hCG1781474 X
rs1062465 MPHOSPH1 X
rs1063535 MKI67 X
rs10727 PANK1 X
rs10736069 KIF11 X
rs10736889 LOC399818 X
rs10740118 JMJD1C X
rs10745302 GPR123 X
rs10751331 hCG2006747 ZNF32 X
rs10751904 hCG2039878 hCG2041856 X
rs10752157 hCG2041860 X X X
rs10761471 ANK3 X
rs10761733 JMJD1C X
rs10761739 JMJD1C X X X
rs10762179 NA X
rs10762231 CXXC6 X
rs10762360 LRRC20 X
rs10762430 hCG1818231 UNC5B X
rs10762732 hCG1793822 X
rs10762760 KCNMA1 X
rs10764048 C10orf9 X
rs10764734 PTPRE X
rs10764882 hCG1796762 X
rs10764899 MGMT X
rs10764921 hCG41189 X
rs10765037 TCERG1L X
rs10776682 hCG1803640 X
rs10786050 KIF11 X
rs10786122 C10orf4 X
rs10786211 SORBS1 X
rs10786740 hCG2040253 X
rs10786775 OBFC1 X
rs10786783 C10orf78 X
rs10787227 SMNDC1 X
rs10787428 GPAM X
rs10787728 hCG1792255 X
rs10787879 hCG39777 X
rs10795417 RSU1 X
rs10795446 CUBN X
rs1079610 OPN4 X
rs10821668 ANK3 X
rs10821675 ANK3 X
rs10821937 hCG41574 X
rs10822156 JMJD1C X
rs10822160 JMJD1C X
rs10822988 CTNNA3 X
rs10823333 HK1 X
rs10823345 HK1 X
rs10823365 TACR2 X
rs10823435 COL13A1 X
rs10823935 CBARA1 X
rs10824119 ADK X
rs10826793 hCG1789973 X
rs10827628 hCG1641533 X
rs10828317 PIP5K2A X
rs10828395 ARMC3 X
rs10828833 GPR158 X
rs10829163 hCG25239 X X X
rs10829529 hCG1654004 X
rs10829970 TCERG1L X
rs10857625 C10orf64 X
rs10882617 SORBS1 X
rs10882645 PYCS X
rs10882993 ZFYVE27 X
rs10883100 HPSE2 X
rs10883565 C10orf6 X
rs10883841 NT5C2 X
rs10883974 C10orf79 hCG23142 X
rs10883979 C10orf79 hCG23143 X
rs10885330 hCG1811160 X
rs10885789 ATRNL1 X
rs10887621 KIAA0261 X
rs10887666 BMPR1A X
rs10901542 hCG1793036 X
rs10901614 hCG1660574 X
rs10903752 ZMYND11 X
rs10906818 THEDC1 X
rs10994860 ACF X
rs10997762 CTNNA3 X X X
rs10997795 hCG1786927 X
rs10997818 DNAJC12 X
rs10997823 DNAJC12 X
rs10998112 RUFY2 X
rs10998268 hCG1787108 X
rs10999147 TYSND1 X
rs10999212 GPR147 X
rs10999426 PRF1 X
rs10999511 MYST4 X
rs11000566 TTC18 X
rs11000911 ADK X
rs11001296 SAMD8 X
rs11001359 hCG1643166 X
rs11001456 NA X X X
rs11002528 hCG2041497 X
rs11006122 UBE2D1 X
rs11006128 TFAM X
rs11007349 hCG1820823 X
rs11008020 hCG1643739 X
rs11008032 hCG1643738 X
rs11009218 NA X
rs11010082 CUL2 hCG2040100 X
rs11011216 hCG1817887 hCG1817888 X
rs11011224 hCG25652 X
rs11013233 ARMC3 X
rs11015624 hCG1648219 X
rs11015640 ARMC4 X X X
rs11016076 MKI67 X
rs11016944 hCG1796998 X
rs11068 NET-7 X
rs1108616 RAI17 X
rs11101202 CHAT X
rs11106 MKI67 X
rs1111350 TLX1 X
rs1113394 NRAP X X X
rs11146301 NA X
rs11186275 hCG1787893 X
rs11186361 NA X
rs11186426 hCG1641715 X
rs11187265 CYP26C1 X
rs11187825 PLCE1 X
rs11187952 hCG1811021 X
rs11188410 ALDH18A1 X
rs11189211 KIAA0690 X
rs11189705 HPSE2 X
rs11190190 SLC25A28 X
rs11190780 SEMA4G X
rs11190812 KAZALD1 X
rs11191283 PSD X
rs11191865 OBFC1 X
rs11193438 hCG2039140 X
rs11196200 hCG1776259 TCF7L2 X
rs11196400 NRAP X
rs11196686 NA X
rs11199005 RGS10 X
rs11199755 hCG2040383 X
rs11200999 KIAA1128 X
rs11204210 ZNF488 X
rs11239851 hCG2040417 X
rs1124013 hCG1641930 X
rs11245007 hCG2023484 X X X
rs11245366 LOC399818 X
rs11248366 ACADSB X
rs11253042 AKR1C4 X
rs11253185 NET1 X
rs11254232 CUBN X
rs11254238 CUBN X
rs11256802 RBM17 X
rs11257462 UPF2 X
rs1125798 hCG1781035 X
rs1129614 GDI2 X X X
rs1132816 PIP5K2A X
rs1139943 DNMBP X
rs1148274 hCG25654 X
rs1148275 hCG25654 X
rs11509438 GSTO1 X
rs1152659 CTBP2 X
rs11541237 NA X
rs11542131 PEO1 X
rs11553577 C10orf61 X
rs11572080 CYP2C8 X
rs11591349 SEMA4G X
rs11592052 CCDC7 hCG2017386 X
rs11592502 hCG1781166 X
rs11592567 hCG2040099 hCG2040100 X
rs11592612 ACADSB X
rs11593766 CASP7 X
rs11594687 NA X
rs11594962 C10orf79 X
rs11595081 hCG1818441 X
rs11595114 SORBS1 X
rs11595603 LRRC20 X
rs11595684 ZNF248 X
rs11596193 HK1 X
rs11596235 SUFU X
rs11596518 HTR7 X
rs11597349 PRKG1 X
rs11597471 HTR7 X
rs11597812 hCG2041859 X
rs11597888 hCG2041374 X
rs11598232 ADK X
rs11598673 hCG24137 X
rs11599164 ANK3 X
rs11599210 ADAMTS14 X
rs11599234 PTPLA X
rs11600 hCG1643971 X
rs11601 CSTF2T X
rs1162759 HNRPH3 X
rs1171614 SLC16A9 X
rs11812465 hCG2040270 X
rs11812708 HTR7 X
rs11816811 COL13A1 X
rs11816967 C10orf59 X
rs11872 PDLIM1 X
rs1200814 ANKRD30A hCG1789874 X
rs1208606 ZNF25 X
rs1211373 hCG1745367 X
rs12217414 C10orf68 X
rs12221 STAM X
rs12221039 hCG32858 X
rs12240276 AKR1CL2 X
rs12241995 NRAP X
rs12243497 ANXA7 X
rs12244832 C10orf68 X
rs12247541 RSU1 X X X
rs12248786 BMPR1A hCG1994049 X
rs12251014 ADAM12 X
rs12253226 hCG1643166 X
rs12253240 CTNNA3 X
rs12254856 AMSH-LP X
rs12255505 USP54 X
rs12256352 HTR7 X
rs12256617 hCG1787893 X
rs12256853 VPS26 X
rs12261515 hCG32744 X
rs12262099 LRRC21 X X X
rs12263503 hCG1649846 X
rs12263945 hCG2040383 X X X
rs12266925 CCDC7 X
rs12268745 CUL2 hCG2040100 X
rs12268910 ADD3 X
rs1227049 CDH23 X
rs1227065 CDH23 X
rs1227236 hCG1640361 X
rs1228187 LIPF X
rs1229406 LIPF X
rs12354886 ZNF485 X
rs12356978 C10orf92 X
rs12357316 VCL X
rs12359728 hCG2040358 X
rs12359843 KAZALD1 X
rs12359948 hCG25653 X
rs1240373 hCG1994053 X
rs12412095 hCG1642404 X
rs12412249 IDE X
rs12413153 NA X
rs12414281 HERC4 X
rs12414693 SORBS1 X
rs12415681 SORBS1 X
rs12415976 SARA1 X
rs12416239 hCG40968 X
rs1244229 hCG1774090 X X X
rs1244422 ATP5C1 X
rs1244471 hCG2017949 X
rs1245560 SPOCK2 X
rs1247441 SVIL X
rs1247755 KCNMA1 X
rs1247766 KCNMA1 X
rs1248623 DLG5 X
rs1248634 DLG5 X
rs1248636 DLG5 X
rs1248638 DLG5 X
rs1248653 DLG5 X
rs1248674 DLG5 X
rs1248678 DLG5 X
rs1248688 DLG5 X
rs1248689 DLG5 X
rs1248690 DLG5 X X X
rs1248696 DLG5 X
rs1250533 RAI17 X
rs1250541 RAI17 X
rs1250556 RAI17 X
rs1250565 RAI17 X
rs1250580 RAI17 X
rs1250600 RAI17 X
rs1251363 KIF5B X
rs12570211 hCG24887 X
rs12570967 PP X
rs12570974 P4HA1 X
rs12572012 MPHOSPH1 X
rs12572520 C10orf70 X
rs12573590 ADK X
rs12573841 hCG2024499 X
rs1258184 OGDHL X
rs1264781 ATRNL1 X
rs1268514 DLG5 X
rs1268956 DLG5 X
rs1270911 DLG5 X
rs12761105 HTR7 X
rs12761705 hCG24649 X
rs12765373 C10orf107 X
rs12765826 hCG1744837 X
rs12766523 RPP30 X X X
rs12766938 hCG1643166 X
rs12767046 ARL8 X
rs12767142 ANXA11 X
rs12769629 hCG2036818 X
rs12769766 PCBD X
rs12770335 SGPL1 X
rs12770830 hCG25567 HSPA14 X
rs12771333 hCG1646071 X
rs12771404 hCG1648653 hCG41189 X
rs12772251 DOCK1 X
rs12772980 hCG2041102 X
rs12773574 SORBS1 X
rs12773592 hCG1646071 X
rs12774010 C10orf64 hCG1642860 X X X
rs12774061 CTNNA3 X
rs12774070 ADAMTS14 X
rs12776792 NA X
rs12779919 ABI1 X
rs12780826 NA X
rs12781453 hCG2040330 X
rs12782946 hCG1781474 X
rs12782963 PKD2L1 X
rs12784524 hCG40467 X
rs12784975 PIK3AP1 X
rs12915 hCG2040497 X
rs12917 MGMT X
rs13088 C10orf72 X X X
rs13134 ALOX5 X
rs1316312 PPIF X
rs1316313 PPIF X
rs1317894 C10orf64 X
rs1320496 LIPA X
rs1321934 PAPSS2 X
rs1322319 ZNF248 X
rs1324693 NA X
rs1326331 SEC15L1 X
rs1328323 SVIL X
rs1331326 NRP1 X
rs1334891 FRAT1 X
rs1336459 C10orf130 X
rs1338565 ZNF239 X
rs1338864 NA X
rs1339746 hCG1644292 X
rs1339907 hCG2038611 X
rs1340380 LOC143241 MGC16186 X
rs1341667 NA X
rs1341676 NA X
rs1342273 MXI1 X X X
rs1344089 CTNNA3 X
rs1344967 NA X
rs13500 LIPA X
rs1356090 KCNMA1 X
rs1359281 PARD3 X
rs1359511 RAI17 X
rs1359849 SHOC2 X
rs1360456 NRP1 X
rs1367024 NA X
rs1370562 hCG1781753 X
rs1374471 C10orf76 X
rs1380555 FAM13C1 X
rs1397617 EIF3S10 X
rs1403629 VCL X
rs1407696 PDCD4 X
rs1409313 CUEDC2 PSD X
rs1409322 PRPF18 X
rs1409354 PANK1 X
rs1410304 ATRNL1 X
rs1413772 ARMC4 X
rs1413835 FAM13C1 X
rs1417000 hCG25163 X
rs14177 LZTS2 X
rs1418362 MXI1 X
rs1418709 ENTPD1 X
rs1436186 PIK3AP1 X
rs1436214 hCG1745369 X
rs1439031 hCG1815393 X
rs1441735 ACTA2 AMSH-LP X
rs1443502 MRC1 X
rs1457523 KCNMA1 X
rs1459990 FAM13C1 X
rs1459996 FAM13C1 X
rs1468063 TNFRSF6 X X X
rs1471384 CTNNA3 X
rs1474 hCG1655317 X
rs1475435 EPC1 X
rs1477069 ADAMTS14 X X X
rs1477070 ADAMTS14 X
rs1477071 ADAMTS14 X
rs1477536 hCG1644026 X
rs1484247 SORCS3 X
rs1516510 KCNMA1 X
rs1536444 SORBS1 X
rs1538204 CNNM2 X
rs1538311 ADK hCG1644605 X
rs1538599 LGI1 X
rs1539163 DDX21 X
rs1541009 FRMD4 X
rs1541046 GBF1 PITX3 X
rs1544210 NA X
rs1551067 MYST4 X
rs1551687 hCG1773755 X
rs1555319 NRP1 X
rs1556612 hCG23658 X
rs1556641 ARMC4 X
rs1556864 hCG1647210 X
rs1561087 KCNMA1 X
rs1563824 FAM13C1 X
rs156697 GSTO2 X
rs157076 GSTO2 X
rs1571013 TNFRSF6 X
rs1571781 NRP1 X
rs1572798 ADAMTS14 X
rs1572934 TNKS2 X
rs15772 RPP38 X
rs1609746 hCG2042429 X
rs161229 TCF8 X
rs161254 TCF8 X
rs161255 TCF8 X
rs1638421 hCG2023700 X
rs1639134 KIF5B X
rs1650146 hCG2040947 X
rs1668154 ASCC1 X
rs166924 FAM13C1 X
rs1671308 RSU1 X
rs16924989 HERC4 X
rs16925584 CXXC6 X
rs17010003 hCG32744 X
rs17091403 hCG1781474 hCG2040349 X
rs17091424 TDRD1 X
rs17098707 GRK5 X
rs17101193 hCG1641930 X
rs17108179 hCG2040337 X
rs17108991 RBP4 X X X
rs17109671 PLCE1 X
rs17110999 NA X X X
rs17113613 PEO1 X
rs17116350 COL17A1 X X X
rs17133693 AKR1CL2 X
rs17152897 MCM10 X
rs17173698 PAPSS2 X
rs1720293 hCG1815358 X
rs1721804 FER1L3 X
rs17229970 hCG1802476 X
rs1735641 hCG25651 X
rs17366712 hCG1774090 X
rs1739 HPS1 X
rs17391197 SMBP X
rs17445028 IDE X
rs17445328 IDE X
rs17468739 IFIT2 X
rs17473271 PRG1 X
rs1749849 RAI17 X
rs1749851 RAI17 X
rs17506606 hCG2042945 X
rs17508082 PLCE1 X
rs17511 CTNNA3 X
rs1751658 hCG23635 X
rs17516758 PLCE1 X
rs17517578 C10orf117 X
rs17526356 SIRT1 X
rs1753586 PARD3 X
rs1761987 hCG2041939 X
rs1767174 SGPL1 X
rs17673844 hCG1811160 X
rs1769692 LIPF X
rs17730369 CWF19L1 X X X
rs17731 COPEB X
rs1775230 APBB1IP X
rs17756919 SVIL X
rs1775715 KIF5B X
rs17768650 ANUBL1 X
rs1777329 SVIL X
rs1781935 hCG20065 X
rs1782644 RAI17 X
rs1782645 RAI17 X
rs178598 TCF8 X
rs1786909 CTNNA3 X
rs17879914 CYP2C19 hCG2044079 X
rs17881479 SFTPA1 SFTPA2 X
rs17883804 CHUK X
rs17884026 CHUK X
rs17885900 SFTPD X
rs1797077 RSU1 X
rs1799939 RET X
rs1800373 SNCG X
rs1800451 MBL2 X
rs1800898 PAX2 X
rs1801222 CUBN X
rs1801230 CUBN X
rs1803997 MXI1 X
rs1804689 HPS1 X
rs1804934 PYCS X
rs180643 NA X
rs1830951 NA X
rs1832196 IDE X
rs1833477 NA X
rs1837949 hCG1788856 X
rs1837950 hCG1788856 X
rs1856564 IMPK X
rs1856591 hCG37897 X
rs1856679 DKFZP566K0524 X
rs1858610 PLCE1 X
rs1864590 NET-7 X
rs1865638 hCG2040457 hCG2042457 X
rs1866435 DLG5 X
rs1867998 CDH23 X
rs1868627 MYST4 X
rs1868751 FAM13C1 X
rs1871063 KCNMA1 X
rs1871065 KCNMA1 X
rs1871084 ADK X
rs1871446 CDC2 X
rs1874147 AP3M1 X
rs1874150 VCL X
rs1874151 VCL X
rs1874664 ATE1 X
rs1877993 KCNMA1 X
rs1880055 C10orf27 X
rs1880057 SGPL1 X
rs1880389 hCG1818441 X
rs1880676 CHAT X
rs1885434 NRAP X
rs1885517 NA X
rs188571 LIPF X
rs1886996 MPHOSPH1 X
rs1886997 MPHOSPH1 X
rs1887027 hCG1642404 X X X
rs1887922 IDE X
rs1888685 NRP1 X
rs1888686 NRP1 X
rs1889568 DUSP5 X
rs1890739 hCG1647787 X
rs1891110 FAM24B X
rs1891269 hCG1641716 X
rs1891386 hCG1818441 X
rs1891565 FER1L3 X
rs1892110 hCG1787893 X
rs1897367 RHOBTB1 X
rs1897516 hCG1658018 X
rs1898082 C10orf11 X
rs1900005 hCG1817383 X
rs1903870 CTNNA3 X
rs1903894 hCG2040450 KCNMA1 X
rs1903908 hCG2039140 X X X
rs1904416 CDC2 X
rs1904589 NODAL X
rs1904634 CTNNA3 X
rs1905542 KIAA1598 X
rs1907724 KCNMA1 X
rs1907732 KCNMA1 X
rs1907733 KCNMA1 X
rs1907737 KCNMA1 X
rs1907740 KCNMA1 X
rs1912277 hCG1818441 X
rs1914345 BTAF1 X
rs1915440 TMEM26 X
rs1916389 CTNNA3 hCG2038400 LRRTM3 X
rs1917138 NA X
rs1917155 hCG1818441 X
rs1923260 ATAD1 X
rs1923694 TLL2 X
rs1923696 TLL2 X
rs1923934 GLUD1 X
rs1924504 hCG23635 X
rs1925576 CTNNA3 hCG2038400 LRRTM3 X
rs1925591 CTNNA3 hCG1810898 LRRTM3 X
rs1925604 CTNNA3 hCG1810898 X
rs1925607 CTNNA3 hCG2038400 LRRTM3 X
rs1925621 CTNNA3 hCG2038400 LRRTM3 X
rs1925627 CTNNA3 hCG1810898 LRRTM3 X
rs1926564 ACSL5 X
rs1926736 MRC1 X
rs1928494 hCG2040451 X
rs1931757 hCG1811021 X
rs1932574 C10orf57 X
rs1934952 CYP2C8 X
rs1934963 CYP2C9 X
rs1935 JMJD1C X
rs1935347 HTR7 X
rs1935349 HTR7 X X X
rs1935350 HTR7 X
rs1935351 HTR7 X
rs1937348 STAM X
rs1953758 ATRNL1 X
rs1962336 hCG1653562 X
rs1969724 C10orf6 X
rs1969815 hCG2038406 HELLS X
rs1970473 hCG2040007 X X X
rs1973972 XPNPEP1 X X X
rs1977584 hCG2006597 X
rs1979363 CTNNA3 X
rs1979487 hCG2040312 X
rs1983864 LOXL4 X
rs1983894 C10orf45 X
rs1986558 hCG1818441 X
rs1991808 KCNMA1 X
rs1993986 C10orf64 X
rs1998709 PLCE1 X
rs1998756 HPSE2 X
rs1998864 DOCK1 X
rs1999240 MYO3A X
rs1999764 IDE X
rs2001245 MYST4 X
rs2001740 hCG1980421 X
rs2001813 NA X
rs2002773 PARD3 X
rs2004558 FER1L3 X
rs200910 hCG25654 X
rs2018728 hCG2036689 X X X
rs2020172 hCG20065 X
rs2024179 ATRNL1 X
rs2025453 TLL2 X
rs2025459 PARD3 X
rs2026015 ACBD5 X
rs2027108 NA X
rs2030057 CXXC6 X
rs2031612 TNFRSF6 X
rs2040009 ITGB1 X
rs2043618 ASAH2 X
rs2057227 hCG1815019 X
rs2062258 PPIF X
rs2062988 DHTKD1 X
rs2065364 NRP1 X
rs2066271 DNAJC1 X
rs2066323 NT5C2 X
rs2070845 IFIT2 X
rs2071496 MKI67 X
rs2095890 hCG2023943 X
rs2096181 FER1L3 X
rs211070 hCG1643662 X
rs211291 KIF5B X
rs211299 KIF5B X
rs211424 hCG1807268 X
rs2120902 hCG32855 X
rs2126750 CTNNA3 X
rs2133696 CTNNA3 X
rs2147289 hCG23635 X
rs2148493 hCG1811160 X
rs2152143 MKI67 X
rs2153779 HTR7 X
rs2162540 FGFR2 X
rs2163188 C10orf74 X
rs2170132 C10orf64 X
rs2172659 LOC220929 X
rs2182162 CTNNA3 hCG1810898 LRRTM3 X
rs220049 TCF8 X
rs220059 TCF8 X
rs2210497 hCG2036689 X
rs2227310 CASP7 X
rs2227564 PLAU X
rs2228059 IL15RA X
rs2228149 IL2RA X
rs2228527 PGBD3 X
rs2228529 PGBD3 X
rs2228638 NRP1 X
rs2230660 ZNF239 X
rs2230661 ZNF239 X
rs2232659 FAM26B X
rs2234962 BAG3 X
rs2234965 ANXA7 X
rs2236319 SIRT1 X
rs2236379 PRKCQ X
rs2240 MKI67 X
rs2240711 hCG2023700 X
rs2241666 hCG2024246 ZWINT X
rs2243897 hCG1652542 X
rs2244380 OPTN X
rs2244647 SFXN2 X
rs2250266 NA X
rs2251101 IDE X
rs2253545 KCNMA1 X
rs2254067 hCG2042943 X
rs2254174 C10orf27 X
rs2254266 CAMK2G X
rs2254419 C10orf92 X
rs2255607 KIAA1279 X
rs2262274 C10orf35 X
rs2270962 CWF19L1 X X X
rs2271362 PRDX3 X X X
rs2271690 hCG2041592 SARA1 X
rs2271904 HSGT1 X
rs2271908 MRPS16 X
rs2273697 ABCC2 X
rs2273740 XPNPEP1 X
rs2273747 C10orf119 INPP5F X
rs2273749 INPP5F X
rs2274109 MCM10 X
rs2274223 PLCE1 X X X
rs2274224 PLCE1 X X X
rs2274741 hCG25239 X
rs2275047 AVPI1 X
rs2275060 hCG23658 X
rs2275069 ITIH5 X
rs2275111 SFXN4 X
rs2275272 PYCS X
rs2275382 BA108L7.2 X
rs2275383 BA108L7.2 X
rs2275580 KIAA0690 X
rs2275586 MMS19L X
rs2275716 SLC25A16 X
rs2275720 ADAM8 X
rs2275799 NRAP X
rs2277212 CUGBP2 X
rs2277257 SLC29A3 X
rs2281699 hCG32858 X
rs2281797 C10orf49 X
rs2281854 hCG1817644 X
rs2281878 C10orf95 X
rs2281891 CYP2C18 X
rs2284665 PRSS11 X
rs2286735 NRAP X
rs2286748 TRIM8 X
rs2290167 hCG1655308 X
rs2292307 KIAA0913 X
rs2292584 C10orf64 X
rs2292948 hCG2024499 X
rs2293277 C10orf3 X
rs2295715 hCG2041216 X
rs2295716 SEMA4G X
rs2295772 SEC31L2 X
rs2295774 SEC31L2 X
rs2295778 HIF1AN X
rs2295874 TACC2 X
rs2295876 TACC2 X
rs2295879 TACC2 X
rs2296136 hCG24072 X
rs2296436 HPS1 X
rs2296441 C10orf33 X
rs2296467 MSRB X
rs2296545 C10orf59 X
rs2296690 PYCS X
rs2297145 hCG25239 X X X
rs2297151 YME1L1 X X X
rs2297452 ZMYND17 X
rs2297492 C10orf25 X
rs2297882 C10orf97 X
rs2297991 GPAM hCG2041212 X
rs2298075 SEC31L2 X
rs2298122 DRD1IP X
rs2304804 ANKRD22 X
rs2305204 PNLIPRP1 X
rs2305386 PKD2L1 X
rs2306264 JMJD1C X
rs2308327 MGMT X
rs2339402 TMEM23 X
rs2339507 TMEM23 X
rs236212 NA X
rs2368184 ABI1 X
rs2370771 hCG2041958 X
rs237596 NA X
rs2388486 GATA3 hCG2041865 X
rs2393989 C10orf74 X
rs2394341 CTNNA3 hCG1810898 X
rs2394522 VPS26 X
rs2394641 hCG2041592 X
rs2394800 CDH23 X
rs2394848 CHST3 X
rs2395335 C10orf11 hCG2040332 X
rs2395373 C10orf11 X X X
rs2395576 C10orf56 X
rs2420367 HTR7 X
rs2421013 C10orf87 X
rs2421131 hCG2040007 X
rs2422324 PDE6C X
rs2429485 hCG1642042 X
rs2435381 GALNACT-2 X
rs2437257 MRC1 X
rs2441743 CTNNA3 X
rs2452505 PHYHIPL X
rs2456664 CTNNA3 X
rs2456751 CTNNA3 X
rs2462712 hCG23635 X
rs2474329 hCG1729712 X
rs2474519 C10orf9 X
rs2474571 hCG25655 X
rs2475298 SEC23IP X
rs2478568 SLC39A12 X
rs2478577 MRC1 X
rs2484180 hCG1642042 X
rs2487068 SLC29A3 X
rs2487999 OBFC1 X
rs2488142 NA X
rs2492651 NA X
rs2501578 ADD3 X
rs2503084 hCG1730556 PBEF1 X
rs2505323 hCG1642042 X X X
rs2505327 hCG1642042 X
rs2515641 CYP2E1 X
rs2531670 NA X
rs2531685 hCG2036773 KIAA1598 X
rs2616652 hCG2040450 X
rs2620918 CTNNA3 X
rs2645227 hCG2041853 X
rs266089 CXCL12 X
rs2663056 NA X
rs2675694 LDB3 OPN4 X
rs2675705 hCG1643076 X
rs2694791 GFRA1 X
rs2704482 COL13A1 X
rs2719995 KCNMA1 X
rs2735343 PTEN X
rs2738222 hCG25651 X
rs2758988 C10orf11 X
rs2761286 FER1L3 X
rs276222 KIAA1754 X
rs276229 KIAA1754 X
rs2764343 PLCE1 X
rs2764345 PLCE1 X
rs2766628 hCG2040450 X
rs2778979 PLXDC2 X
rs2787140 hCG1659888 X
rs2794981 PFKFB3 X
rs2797567 hCG39531 X
rs2798000 PLCE1 X
rs2804535 VDAC2 X
rs2805910 PRG1 X
rs2805915 PRG1 X
rs2808096 ARHGAP12 X
rs2812968 hCG1729643 X
rs2817698 SLIT1 X
rs2839668 GAD2 MYO3A X
rs284596 FAM13C1 X
rs284624 FAM13C1 X
rs284856 C10orf26 X
rs2855025 PRG1 X
rs2862507 hCG1642531 X
rs2894016 CTNNA3 X
rs2894087 NET-7 X
rs2894103 hCG1796715 X
rs2894280 COL13A1 X
rs2894347 NA X
rs2901127 HTR7 X
rs290481 TCF7L2 X
rs2915772 PNLIP X
rs2927501 ADAM12 X
rs2946994 CTBP2 X
rs2950354 hCG41428 X
rs2986401 PYCS X
rs2996224 Rab11-FIP2 X X X
rs2997211 MPP7 X
rs2999278 ZNF239 X
rs3006365 hCG2044073 X
rs3006739 C10orf68 X
rs3007 GDF10 X
rs3010503 PNLIP X
rs3013236 DMBT1 X
rs3014185 FAM26A X
rs3026782 RET X
rs303169 LOC387700 X
rs303218 IFIT1 X
rs303426 MAP3K8 X
rs303438 MAP3K8 X
rs303450 MAP3K8 X
rs303465 LIPF X
rs303523 hCG1640331 X
rs303533 NA X
rs303537 NA X
rs305375 hCG1805714 X
rs3071 SCD X
rs3088142 DUSP13 X
rs3101793 hCG1785360 X X X
rs3189030 NRAP X
rs35773 KCNMA1 X
rs35791 KCNMA1 X
rs363282 TRIK X
rs363294 PDZK8 X
rs366107 LIPF X
rs369421 GATA3 hCG2041865 X
rs371210 NA X
rs3730463 POLL X
rs373304 FAM13C1 X
rs3737015 PDLIM1 X
rs3737294 CSPG6 X
rs3739989 TMEM23 X
rs3739998 hCG1643737 X
rs3740015 DHTKD1 X
rs3740094 C10orf10 X
rs3740097 RASSF4 X
rs3740199 ADAM12 X
rs3740211 SEPHS1 X
rs3740215 hCG2041844 X
rs3740329 ZNF11B X
rs3740423 MKI67 X
rs3740462 UNC5B X
rs3740469 SLK X X X
rs3750718 CPN1 X
rs3750805 hCG1776259 TCF7L2 X
rs3750898 DCLRE1A X
rs3758402 RASSF4 X
rs3758490 ZNF365 X
rs3763695 SEC31L2 X
rs3763735 TYSND1 X
rs3763747 SLC16A9 X
rs3763792 CNNM1 X
rs3764990 MIR X
rs3765101 PITRM1 X
rs3765595 RSU1 X
rs3780971 RSU1 X
rs378308 LIPF X
rs3793663 hCG1789661 USP54 X
rs3793706 SEC31L2 X
rs3793771 WNT8B X
rs3802557 hCG1817623 X X X
rs3802656 LIPA X
rs3808909 ARMC4 X
rs3812619 HSGT1 X
rs3814165 hCG24161 X
rs3814568 RASSF4 X
rs3814596 PITRM1 X
rs3816 HPS6 X
rs3816699 PFKP X
rs3818672 hCG2042945 X
rs3818909 ZDHHC16 X
rs3824700 MYO3A X
rs3824754 CYT19 X
rs3829142 hCG2041141 X
rs3829909 hCG1776259 X
rs3850680 SORCS1 X
rs3852407 PLEKHK1 X
rs3858340 BAG3 X
rs3862018 HABP2 X X X
rs3862030 SUFU X
rs3862501 KCNMA1 X
rs3862511 RAI17 X
rs388972 FAM13C1 X
rs3900887 TFAM X
rs390414 LIPF X
rs391260 LIPF X
rs391683 LIPF X
rs3939 ANKRD1 X
rs3952313 SPAG6 X
rs4025981 NEBL X
rs402781 LIPF X
rs405635 LIPF X
rs4065 PLAU X
rs4078488 CH25H X
rs4096395 COL13A1 X
rs412927 LIPF X
rs4144422 RPP30 X
rs4147179 ARHGAP21 X
rs415996 LIPF X
rs416957 LIPF X
rs418276 LIPF X
rs4237438 FRMD4 X
rs4242746 PITRM1 X
rs4323796 ADAMTS14 X
rs436207 FAM13C1 X
rs4400684 JMJD1C X
rs4412676 ADAM12 hCG1644692 X
rs4417206 PYCS X X X
rs444386 LIPF X
rs4485000 CACNB2 X
rs4548513 CTNNA3 X
rs4581397 hCG1791394 X
rs4595427 JMJD1C X
rs4630205 IFIT4 LIPA X X X
rs4646953 NA X
rs4646957 IDE X
rs4646958 IDE X
rs4691 NDST2 X
rs4745805 hCG2041396 X
rs4746015 COL13A1 X
rs4746332 C10orf11 X
rs4746821 SUPV3L1 X
rs4746946 H2AFY2 X
rs4747194 CDH23 X
rs4747647 hCG1774090 X
rs4747796 hCG1792626 X
rs4750568 hCG2039913 hCG2041288 X
rs4751651 C10orf84 X
rs4751995 PNLIPRP2 X
rs4751996 PNLIPRP2 X
rs4838592 ARHGAP22 X
rs4880241 C10orf39 X
rs4880801 ADARB2 X
rs4917723 BLNK X
rs4917766 NA X
rs4919058 MLR2 X
rs492943 XPNPEP1 X
rs4933617 RPP30 X
rs4933620 RPP30 X X X
rs493392 PARD3 X
rs4935502 PCDH15 X
rs4948550 BICC1 X
rs4948970 hCG17919 X
rs495998 NA X X X
rs498055 hCG1641328 X X X
rs500470 NA X X X
rs5030920 TACR2 X
rs5030949 HK1 X
rs523611 KCNMA1 X
rs526219 PIK3AP1 X
rs527458 KCNMA1 X
rs530872 MRC1 X X X
rs532678 PTEN X
rs533343 NA X X X
rs533383 NA X X X
rs533480 SORBS1 X X X
rs542007 KCNMA1 X X X
rs554765 SORBS1 X
rs558764 hCG1796761 X
rs559198 IFIT5 X
rs566484 PIK3AP1 X
rs569511 PKD2L1 X
rs577537 CRTAC1 X X X
rs5870 ACTR1A X
rs590142 hCG1648219 X
rs591157 C10orf129 X
rs595652 CX40.1 X
rs597371 AMACO X
rs600879 SORCS1 X X X
rs607437 SORCS1 X
rs6163 CYP17A1 X
rs618687 hCG1640833 X
rs621375 KIAA1914 X
rs622491 hCG1640638 X
rs623980 XPNPEP1 X
rs625039 hCG1781727 LBX1 X
rs625859 PIK3AP1 X
rs626394 PARD3 X
rs626859 PARD3 X
rs636555 C10orf79 hCG23142 X
rs646668 KIAA1914 X
rs646767 PKD2L1 X
rs647758 PARD3 X X X
rs6480404 HK1 X
rs6481530 NA X
rs649785 AMACO X
rs650212 PARD3 X
rs6537579 NA X
rs657477 PARD3 X X X
rs6580 FAM26B X X X
rs6585312 TRUB1 X
rs6597731 ADAM12 X
rs6602141 RSU1 X
rs6602160 RSU1 X X X
rs6646 ABLIM1 X
rs6686 SEC61A2 X
rs67179 hCG1783557 X
rs673009 PARD3 X
rs678188 PARD3 X
rs6816 OGDHL X
rs682304 PIK3AP1 X
rs684395 hCG2042948 X
rs687528 PIK3AP1 X
rs6896 ANXA7 X
rs6901 PITRM1 X
rs690763 MRC1 X
rs691196 MRC1 X
rs691773 MRC1 X
rs691863 MRC1 X
rs692126 MRC1 X X X
rs693986 ATRNL1 X
rs7006 DPCD X
rs7013 C10orf10 X
rs701834 LZTS2 X
rs701836 LZTS2 X
rs701846 CPEB3 X
rs701865 PDE6C X
rs702366 ALOX5 X
rs703258 VCL X
rs703460 SORCS3 X
rs703461 SORCS3 X
rs703973 RAI17 X
rs703981 RAI17 X
rs703982 RAI17 X
rs703990 RAI17 X
rs704010 RAI17 X
rs7070570 CTNN3 X
rs7072367 CWF19L1 X X X
rs7072645 ADAMTS14 X
rs7073610 CWF19L1 X
rs7074064 BMPR1A X
rs7074242 hCG1641715 X
rs7075141 IDI1 X
rs7075260 hCG1817623 X
rs7075831 BLNK X
rs7075888 hCG40944 X
rs7075964 hCG2023790 XPNPEP1 X
rs7076888 SORBS1 X
rs7077596 hCG2036689 X
rs7079901 RSU1 X
rs7080160 hCG1646572 X
rs7080643 hCG23635 X
rs7081273 ADAMTS14 X
rs7081275 JMJD1C X
rs7081960 CCAR1 X
rs7082044 hCG25652 X
rs7082342 hCG1800341 X
rs7082434 FBXO18 X
rs7082558 HTR7 X
rs7084090 IDE X
rs7084874 CDH23 hCG1745900 X
rs7085991 NA X
rs7086446 hCG2040215 X
rs7089142 PCDH21 X
rs7089312 FLJ22761 hCG2038551 X
rs7089349 hCG39169 X
rs7091896 SIRT1 X
rs7092539 JMJD1C X
rs7093729 RSU1 X
rs7094973 ANKRD2 X X X
rs7097295 hCG20065 X
rs7099478 GRK5 X
rs7099565 TRUB1 X
rs7099777 NA X
rs7100129 NA X
rs7100340 NA X
rs7100382 hCG2042429 X
rs7100623 IDE X
rs7184 MRPL43 X
rs7199 hCG23640 X
rs719909 PANK1 X
rs725529 hCG41574 X
rs726817 C10orf4 X
rs727427 PANK1 X
rs727532 ABLIM1 X
rs728289 PSAP X
rs7304 COMTD1 VDAC2 X
rs731947 hCG2040574 X
rs732102 SORBS1 X
rs735104 NA X
rs736189 ADAMTS14 X
rs736535 MAWBP X
rs736597 VTI1A X
rs7377 PRG1 X
rs740595 hCG2023700 X
rs746472 hCG1811015 X
rs748164 ADAMTS14 X
rs748165 ADAMTS14 X
rs748235 HK1 X
rs749049 PYCS X
rs749304 SORCS3 X
rs749377 ARHGAP22 X
rs750431 ADAMTS14 X
rs751450 CHST3 X
rs752372 KCNMA1 X
rs752974 LZTS2 X
rs753270 RAI17 X
rs755381 KCNIP2 X
rs780157 RAI17 X
rs780631 RSU1 X
rs780668 SLC29A3 X
rs787037 APBB1IP X
rs787041 APBB1IP X
rs787634 FER1L3 X
rs788219 MASTL X
rs788237 MASTL X
rs7895441 NA X
rs7896327 MINPP1 X
rs7897619 IFIT4 LIPA X
rs7897947 NFKB2 X
rs7899065 SORBS1 X
rs7899853 RSU1 X
rs7900095 SORBS1 X
rs7900392 FER1L3 X
rs7900830 PHYH X
rs7900859 hCG2006597 hCG2041102 X
rs7901045 PCDH15 X
rs7902355 DC-TM4F2 X X X
rs7903091 CBARA1 X
rs7903397 SVIL X
rs7903964 CTNNA3 X
rs7905087 PI4KII X
rs7905162 hCG41189 X
rs7905784 MCM10 X
rs7906450 NA X X X
rs7906504 GHITM X
rs7906894 hCG20066 X
rs7908112 RSU1 X
rs7908745 MIR X
rs7909832 hCG23996 PTER X
rs7910154 hCG1783494 X
rs7911748 RSU1 X
rs7912249 SORBS1 X
rs7913176 NHLRC2 X X X
rs7914287 CTNNA3 X
rs7915504 hCG2023773 X
rs7916571 hCG2040007 X X X
rs7916821 MYPN X
rs7918084 hCG1641008 X
rs7918118 GTPBP4 X
rs7923749 NA X
rs792718 NA X
rs805657 SLK X
rs805721 COL17A1 X
rs807023 hCG1647209 X
rs807037 KAZALD1 X
rs807038 KAZALD1 X
rs807042 NA X
rs8139 NT5C2 X
rs814624 LIPF X
rs814626 LIPF X
rs814628 LIPF X
rs816827 KCNMA1 X
rs8181357 FLJ44653 X
rs8187694 ABCC2 X
rs821942 SORCS1 X X X
rs827241 PCBD X
rs829237 TMEM20 X
rs8354 ARL3 X
rs838759 hCG1652542 X
rs8473 MKI67 X
rs860989 KCNMA1 X
rs866255 HERC4 X
rs867407 NA X
rs867629 NA X
rs8677 ANK3 X
rs868750 CHAT X
rs869156 RASSF4 X
rs869801 DOCK1 X
rs870957 RASSF4 X X X
rs874556 FLJ22761 X
rs874885 KCNIP2 X
rs877779 CREM X
rs880348 hCG1788074 X
rs881343 NA X
rs881406 RAI17 X
rs882052 DOCK1 X
rs882845 C10orf10 RASSF4 X
rs882872 hCG1818441 X
rs883604 MAPK8 X
rs884144 NKX2-3 X
rs885822 PRF1 X
rs892691 ALOX5 X
rs894375 CRTAC1 X
rs902991 NEURL X
rs906217 SUPV3L1 X
rs906219 FLJ22761 X
rs912485 PIK3AP1 X
rs914325 CAMK1D X
rs915230 hCG2042179 X
rs915432 CBARA1 X
rs921742 RSU1 X
rs922239 hCG2039963 X
rs923799 hCG1811015 X
rs927099 NRP1 X
rs932512 hCG1655317 X
rs9325593 SNCG X
rs9333269 ITGA8 X
rs934187 ALOX5 X
rs9414761 hCG1820925 hCG41574 X
rs9416746 BICC1 X
rs9419048 C10orf125 Sprn X
rs942077 hCG2036763 X
rs9420822 BTRC X
rs9423590 hCG20066 X
rs942431 PARD3 X
rs942775 STAM X X X
rs942789 RAI17 X
rs943265 TECTB X
rs943542 SORBS1 X
rs945189 NA X
rs947599 C10orf3 X
rs951308 MYST4 X
rs951647 LIPA X
rs952919 GFRA1 X
rs954439 IFIT2 LIPA X
rs955157 C10orf11 hCG2041509 X
rs959629 PAPD1 X
rs962524 MPHOSPH1 X
rs9664986 SVIL X
rs9665610 NA X
rs977096 C10orf35 X
rs980994 NA X
rs985273 ABLIM1 X
rs994174 hCG1650570 X
rs994811 C10orf107 X
rs9971293 GDF2 X
rs998799 PAX2 X
rs999995 KCNMA1 X

Note.— The public gene name or hCG identifier for predicted genes from the Celera database indicates which sample sets were genotyped, and a 60-bp sequence is provided for SNPs without a public “rs” identifier. NA=not applicable.

Web Resources

The URLs for data presented herein are as follows:

  1. Alzheimer Disease Forum, http://www.alzforum.org/res/com/gen/alzgene/chromo.asp?c=10
  2. Entrez Gene, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene
  3. Online Mendelian Inheritance in Man (OMIM), http://www.ncbi.nlm.nih.gov/Omim/ (for AD, APP, PSEN1, PSEN2, LOAD, APOE, GAPD, RPS3A, PYCS, ALDH18A1, ENTPD1, CTNNA3, PLAU, IDE, BCL2, PARP1, SORBS1, and SORCS1)

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