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. Author manuscript; available in PMC: 2014 Feb 26.
Published in final edited form as: J Epidemiol Community Health. 2010 Jan;64(1):49–56. doi: 10.1136/jech.2008.083295

Table 2.

Genotype distributions of Apoprotein E, lipoprotein lipase and vascular endothelial growth of the Normative Aging participants between November 2000 and December 2007 in Boston, Massachusetts, USA

Polymorphism N (%)
APOE-T530C (rs7412) Wild 491 (85.1)
Heterozygous 83 (14.4)
Homozygous 3 (0.5)
APOE-G219T (rs405509) Wild 162 (28.7)
Heterozygous 272 (48.1)
Homozygous 131 (23.2)
APOE-T392C (rs429358) Wild 435 (76.9)
Heterozygous 120 (21.2)
Homozygous 11 (1.9)
APOE-G113C (rs440446) Wild 220 (39.8)
Heterozygous 247 (44.7)
Homozygous 86 (15.6)
APOE-A491T (rs449647) Wild 353 (63.2)
Heterozygous 182 (32.6)
Homozygous 24 (4.3)
APOE-T427C (rs769446) Wild 486 (85.1)
Heterozygous 75 (13.1)
Homozygous 10 (1.8)
LPL-N291S (rs268) Wild Type 555 (97.2)
Heterozygous 15 (2.6)
Homozygous 1 (0.2)
LPL-S447X (rs328) Wild Type 460 (83.3)
Heterozygous 86 (15.6)
Homozygous 6 (1.1)
LPL-D9N (rs1801177) Wild Type 537 (97.8)
Heterozygous 12 (2.3)
Homozygous 0 (0.0)
VEGF-G634C (rs2010963) Wild Type 233 (42.5)
Heterozygous 245 (44.7)
Homozygous 70 (12.8)
APOE haplotype E3/E3 358 (63.8)
E3/E2 72 (12.8)
E3/E4 109 (19.4)
Other 22 (3.9)
*

The sum of the subjects in each genotype may not add up to the total number of subjects due to missing genotyping data. Missing genotyping is due to a variable number of samples for each locus for which genotyping was not successful.