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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)