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Table 1 Demographics of study participants

From: P-tau subgroups in AD relate to distinct amyloid production and synaptic integrity profiles

  Amyloid-negative CN Preclinical AD Prodromal AD AD dementia
n 112 51 102 188
Age in years, mean ± sd 58.6 ± 7.8abc 63.7 ± 7.9ad 66.9 ± 7.7bdf 65 ± 7.2cf
Sex, female (%) 38 (34%) 24 (47%) 35 (34%) 90 (48%)
APOE ε4 carriership (%) 34 (30%)abc 30 (59%)a 71 (70%)b 115 (61%)c
MMSE, mean ± sd 28.4 ± 1.4bc 28 ± 1.4de 26.4 ± 2bdf 21 ± 4.4cf
Amyloid, pg/ml, mean ± sd 1144 ± 167abc 651 ± 109ae 625 ± 100bf 593 ± 100cf
T-tau, pg/ml, mean ± sd 227 ± 85abc 500 ± 307ae 554 ± 319bf 717 ± 398cf
P-tau, pg/ml, mean ± sd 40.3 ± 14abc 72.1 ± 39ae 75.4 ± 34bf 86.2 ± 36cf
T-tau abnormal (%) 8 (7.1%)abc 31 (61%)ae 73 (72%)b 152 (81%)c
P-tau abnormal (%) 9 (8%)abc 30 (59%)ae 70 (69%)b 147 (78%)c
  1. Abnormal t-tau and p-tau status were based on previously derived cutoffs of 349 and 56 pg/ml (further details are in the “Methods” section). Differences in demographic variables between the diagnostic groups were tested with ANOVA, Wilcoxon rank sum test, or chi-square tests, followed by post hoc t tests, Wilcoxon rank sum tests, or chi-square tests as appropriate. p-values for the post hoc tests were FDR-adjusted to account for the multiple comparisons between the diagnostic groups
  2. CN, cognitively normal
  3. a–fGroups differed at p-value < 0.05
  4. aAmyloid-negative CN vs preclinical AD
  5. bAmyloid-negative CN vs prodromal AD
  6. cAmyloid-negative CN vs AD dementia
  7. dPreclinical AD vs prodromal AD
  8. ePreclinical AD vs AD dementia
  9. fProdromal AD vs AD dementia