Apolipoprotein levels in different <i>APOE ε</i>4 carrier groups.

<p>Statistics details: ANCOVA, Post-hoc: Bon Ferroni Covariates: age, sex.</p>*<p>Compared to non<i>APOE</i> ε4 carrier, p<0.05, **Compared to non<i>APOE</i> ε4 carrier, p<0.0005.</p>§<p>Compared to <i>APOE</i> ε4 heterozygote carrier, p<0.0005.</p>#<p>When heterozygous and homozygous carriers are pooled and compared with non <i>APOE</i> ε4 carriers the ApoH values are statistically significant (n = 156, mean = 158.95±42.78, F = 4.23, p = 0.04). Pooling of data from heterozygous and homozygous carriers makes no difference to the statistical outcomes for any of the other apolipoproteins, though the significant p values all become even slightly lower.</p

Partial correlations between apolipoproteins and lipid profiles.

*<p>p<0.05, **p<0.01, *** p<0.001(FDR corrected p values) Covariates: age, sex.</p

Summary of correlations between apolipoproteins and cognitive impairment, cognitive decline and MRI changes over 2 years.

<p>+ Significantly indicates relationship in direction of pathology.</p

Demographic characteristics of nonconverters and converters at Wave 1.

<p>Demographic characteristics of nonconverters and converters at Wave 1.</p

Logistic regression analyses for the prediction of conversion from CDR 0 at Wave 1 to CDR >0 at Wave 2 from Wave 1 plasma apolipoprotein levels.

<p>Covariates: age, sex, years of education and <i>APOE</i><b>ε</b>4 carrier status. CVD risk index was also included as a covariate in the series of analyses shown on the left side of table.</p>¶<p>CH, cholesterol; TG, triglycerides; HDL, high density lipoprotein; LDL, low density lipoprotein.</p

Participant Wave 1 demographic information and apolipoprotein levels.

<p>Data are presented as mean±SD.</p><p>Covariates in ANCOVA for effects of apolipoproteins: age, sex, years of education, <i>APOE</i><b>ε</b>4 carrier status, hypolipidaemic medications.</p

Potential pathophysiological mechanisms involving apolipoproteins in Alzheimer’s disease.

<p>Literature evidence: *, Katzav, Faust-Socher et al. 2011; George and Erkan 2009. **, Lewis, Cao et al. 2010; Roher, Maarouf et al. 2009; Martins, Berger et al. 2009; Bereczki, Bernat et al. 2008.</p

Baseline characteristics of the study participants^a.

<p><i>APOE</i> = <i>apolipoprotein E</i>; BMI = body mass index; BP = blood pressure; BSIT = Brief Smell Identification Test; eGFR = estimated glomerular filtration rate; GDS = Geriatric Depression Scale; NESB = non-English-speaking background.</p>a<p>Data are presented as No. (%), unless otherwise indicated.</p>b<p>Maximum n for the whole sample is 889; minimum is 820 (homocysteine).</p>c<p>For categorical factors, d is the difference in mean age of those meeting the factor versus those not meeting the factor. For continuous factors, r is the correlation coefficient with age.</p>*<p><i>p</i><.05 for men versus women (t- or χ² tests) or age associations (t- tests or Pearson correlations).</p

Factors associated with cognitive decline.

<p>Interventions modifying factors with a significant population attributable risk might greatly reduce population-wide cognitive decline. Age and sex interactions suggest further benefits by tailoring interventions to particular demographic groups.</p

Baseline factors associated with cognitive decline^a.

<p>BSIT = Brief Smell Identification Test; eGFR = estimated glomerular filtration rate; MCI = mild cognitive impairment.</p>a<p>Includes factors remaining in reduced generalized linear models initially containing all associated with the cognitive measure at <i>p</i><.1 (including age and sex if not already present). Interaction results are adjusted for the independent factors listed, in addition to age (sex interactions) or sex (age interactions). Sex is coded as female = 0 and male = 1.</p