Table 1. Demographic and clinical characteristics of the control and AD continuum groups
VariableControl (n = 150)AD continuum (n = 374)P‐value (group effect)
Preclinical AD (n = 63)MCI‐AD (n = 111)AD dementia (n = 200)
Females, %596060620.940
APOE ε4 carriers, %2158a52a62a<0.0001
Age, years62.4 (11)70.8 (11)a74.3 (9)a73.8 (10)a<0.0001
CSF biomarkers
1–42, pg/ml796 (159)414 (98)a426 (107)a408 (113)a<0.0001
T‐tau, pg/ml218 (81)450 (428)b737 (410)a,c920 (564)a,d,e<0.0001
P‐tau181P, pg/ml43 (12)66 (39)a95 (32)a,d102 (44)a,d<0.0001
  • Aβ, amyloid β‐peptide; AD, Alzheimer's disease; APOE, apolipoprotein E; CSF, cerebrospinal fluid; MCI‐AD, MCI due to AD; P‐tau181P, tau phosphorylated at threonine 181; T‐tau, total tau.

  • Data are expressed as percent (%) or mean (SD), as appropriate. Probability values (P) denote differences between groups.

  • APOE genotype was available in 103 controls (69%), 39 preclinical AD (62%), 89 MCI‐AD (80%), and 148 AD dementia (74%). Only Aβ1–42 values measured by the INNOTEST ELISA are included; Aβ1–42 values from Bonn group (measured with MSD platform) are excluded.

  • Chi‐square statistics were used for the group comparisons of gender and APOE ε4 carrier. One‐way ANOVA was used to compare age and CSF biomarkers between groups. The P‐values indicated in the last column refer to the group effects in these tests. Significant group effects were followed by Bonferroni‐corrected pair‐wise post hoc tests.

  • a P < 0.0001 versus controls.

  • b P = 0.002 versus controls.

  • c P = 0.0001 versus preclinical AD.

  • d P < 0.0001 versus preclinical AD.

  • e P = 0.002 versus MCI‐AD.