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. 2021 Apr 23;26(10):5833–5847. doi: 10.1038/s41380-021-01101-5

Table 1.

Clinical demographic data for subjects used in this study.

Sex (M/F) Age (years) Braak stage ApoE (E/E) Onset Postmortem delay (hr:minutes)
For binding studies
  Control F 50 1 3/3 N/A 4:10
M 62 1 3/3 N/A 7:20
F 71 1 3/2 N/A 7:10
F 77 1 3/3 N/A 2:55
M 78 1 3/3 N/A <17:40
M 79 2 3/3 N/A 9:00
F 84 1 3/3 N/A 6:55
3M/4F 71.5 ± 11.8 1–2 7 E3 0 E4 7.7 ± 4.7
  Alzheimer’s disease F 59 5 4/4 EOAD 4:20
F 66 5 4/3 EOAD 6:30
M 70 4 4/4 EOAD 4:00
M 78 5 4/4 LOAD 6:35
F 81 5 4/3 LOAD 6:15
F 85 4 3/3 LOAD 6:00
2M/4F 73.1 ± 9.8 4–5 1 E3 5 E4 3EOAD/3LOAD 5.5 ± 1.0
For large frozen section autoradiography studies
  Control F 56 N/A N/A N/A N/A
  Sporadic Alzheimer’s diseasea F 79 V 4/4 LOAD 16:00
  AβPPArca M 64 VI 3/3 EOAD 12:00

Bold values show the total number of male and female cases used in the study from control and AD cases as well as the means ± standard deviation of age, Braak stage, ApoE allele forms, and postmortem delay time from these cases.

AβPPArc Arctic amyloid-β protein precursor mutation, ApoE Apolipoprotein E, M Male, F Female, EOAD Early onset alzheimer’s disease, LOAD Late onset alzheimer’s disease, N/A Not applicable/available.

aSporadic Alzheimer’s disease and AβPPArc cases have been also reported and described in our previous publications [39, 40, 70].