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. 2014 May 24;137(7):1958–1970. doi: 10.1093/brain/awu119

Figure 3.

Figure 3

PSEN1 and α-synuclein interactions are elevated in axons from the amygdala of patients with dementia with Lewy bodies (DLB) and PSEN1 familial Alzheimer’s disease (PS1 FAD). (A) Representative pseudocolour lifetime images from donor and acceptor immunostained amygdala tissue from dementia with Lewy bodies, PSEN1 familial Alzheimer’s disease, and control cases shows enhanced PSEN1–α-synuclein interactions (shorter lifetime) in tissue from dementia with Lewy bodies and PSEN1 familial Alzheimer’s disease cases compared to healthy controls. (B) Scatter-plot of % Efret (and median and interquartile range) of axon-based region of interest analysis for each case showed a significant increase in α-synuclein-PSEN1 interactions in the axons of cases with dementia with Lewy bodies and with PSEN1–familial Alzheimer’s disease compared with controls (n = 4 cases for each disease group, Kruskal Wallis, Dunns multiple comparisons, **P < 0.01, ***P < 0.001).