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Table 4 Influence of APOE genotype on AD pathology

From: The characterization of AD/PART co-pathology in CJD suggests independent pathogenic mechanisms and no cross-seeding between misfolded Aβ and prion proteins

 

APOE ε4 status, n (%)

p

ε 4-

ε 4+

ABC score

 Not

163 (42.9)

10 (14.3)

< 0.001

 Low

191 (50.3)

49 (70.0)

 Intermediate/ High

26 (6.8)

11 (15.7)

Thal phase

 0

163 (42.9)

10 (14.3)

< 0.001

 1-2

112 (29.5)

21 (30.0)

 3

64 (16.8)

25 (35.7)

 4-5

41 (10.8)

14 (20.0)

CAA

 not CAA

289 (76.1)

33 (47.1)

< 0.001

 CAA

91 (23.9)

37 (52.9)

Braak stage

 0 − +

208 (54.7)

34 (48.6)

0.203

 I-II

134 (35.3)

24 (34.3)

 >III

38 (10.0)

12 (17.1)

 n

380 (84.4)

70 (15.6)