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. 2009 Oct 13;117(1):85–96. doi: 10.1007/s00702-009-0314-x

Table 1.

Demographic data of the human specimen, semi-quantitative plaque load assessment, vessel pathology (congophilic angiopathy, CAA) and Braak staging

Sex Age Plaque load CAA Braak stage
2-48 4G8 Aβ[N]
Control 1 M 74 + + (+) III
Control 2 F 82 I
Control 3 F 73 I
Control 4 F 79 ++ ++ + II
Control 5 M 70 ++ +++ + 0
Control 6 F 73 ++ ++ (+) 0
AD 1 M 72 + ++ (+) VI
AD 2 M 70 +++ +++ +++ V
AD 3 M 78 + ++ (+) IV
AD 4 M 60 +++ +++ + VI
AD 5 M 93 + + + IV
AD 6 M 64 +/++ ++ + VI
AD 7 F 77 ++ +++ + VI
AD 8 F 81 ++ +++ + IV
AD 9 F 78 +++ +++ + IV
AD 10 F 64 (+) ++ III
AD 11 F 88 +++ +++ IV
AD 12 M 81 +++ +++ +++ IV
AD 13 F 84 +++ +++ IV
AD 14 F 84 +++ +++ (+) IV
FAD APP arc M 64 +++ +++ +/++ n.a.
FAD APP swe F 61 +++ +++ +++ n.a.
FAD PS1 P264L M 54 +++ +++ (+) VI

The three familial AD (FAD) patients harbored an APP Swedish mutation (APP swe), an APP arctic mutation (APP arc), and a Presenilin-1 mutation (FAD P264L). Most but not all cases also showed CAA. Antibodies: 4G8 (Aβ 17-24), 2-48 (pGlu Aβ) and Aβ[N] (specific for Aβ at position 1)