TABLE 6.

Associations between dietary DHA and cortical thickness in the AD signature in the studied population¹

Variable	Model	APOE-ε4 in the model	Estimate (95% CI)	P	R 2
DHA	Unadjusted	—	0.003 (−0.026, 0.031)	0.858	<0.001
	Adjusted2	Carrier/noncarrier3	−0.003 (−0.032, 0.026)	0.859	0.096
		Number of alleles4	−0.003 (−0.032, 0.026)	0.842	0.096
		Homozygote/nonhomozygote5	−0.003 (−0.032, 0.026)	0.848	0.099
DHA × APOE-ε4	Unadjusted	Carrier/noncarrier3	0.055 (−0.002, 0.113)	0.060	0.013
	Adjusted6		0.033 (−0.024, 0.089)	0.257	0.100
	Unadjusted	Number of alleles4	0.048 (0.010, 0.086)	0.014	0.019
	Adjusted6		0.035 (−0.002, 0.072)	0.067	0.105
	Unadjusted	Homozygote/nonhomozygote5	0.084 (0.012, 0.155)	0.022	0.016
	Adjusted6		0.071 (0.002, 0.141)	0.045	0.110

¹ n = 339. Data are presented for 1 g/d of DHA, obtained by multiple linear regression analyses. Cortical thickness in the AD signature was rank-transformed. ALA, α-linolenic acid.

²Including APOE-ε4, gender, age, BMI, hypercholesterolemia, hypertension, self-reported energy intake, and ALA intake as covariates.

³Distributed into n = 217 carriers and n = 122 noncarriers.

⁴Distributed into n = 122 with 0 alleles, n = 156 with 1 allele, and n = 61 with 2 alleles.

⁵Distributed into n = 61 homozygotes and n = 278 nonhomozygotes.

⁶Including gender, age, BMI, hypercholesterolemia, hypertension, self-reported energy intake, and ALA intake as covariates.