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. 2017 Jun 19;28(4):451–462. doi: 10.1111/bpa.12532

Figure 2.

Figure 2

TBI increases the levels of Aβ oligomers and protofibrils in surgically resected brain tissue. A. Individual oligomer Aβ levels in patient samples detected with the mAb82E1 sandwich ELISA. The absence of a bar indicates that the value was below the limit of detection. B. Dot‐plot of individual and median Aβ oligomer levels in TBI, Alzheimer's disease (AD) and in the control group (CTRL) consisting of idiopathic iNPH patients and non‐injured, NI individuals. Oligomers were significantly elevated (*) by TBI in comparison to the control group. C. Individual Aβ protofibril levels in patient samples detected with the mAb158 sandwich ELISA. D. Dot‐plot of individual and median Aβ protofibril levels in TBI, AD and in the control group. Aβ protofibril levels were significantly elevated (*) by TBI in comparison to the control group. (A,C) Each bar represents a mean value and standard deviation (SD) from two ELISA experiments performed on two different occasions. E,F. There was a significant positive correlation between Aβ1–42 (E), Aβx‐42 (F), and Aβ protofibril levels in TBI patients. Aβ = Amyloid β, # = TBI patients with Amyloid β aggregates, * = Significant difference (P < 0.05), Strep‐HRP = Streptavidin‐Horseradish Peroxidase; TMB = Tetramethylbenzidine.