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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