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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Cerebrospinal fluid Presenilin-1 increases at asymptomatic stage in genetically determined Alzheimer’s disease

Fig. 2

The increase in the CSF-PS1 complexes in ADAD. a Representative blot of the PS1 complexes in the CSF samples from eight symptomatic ADAD (syADAD), six presymptomatic mutation carriers (psADAD) and 23 younger NC controls (yNC), eight of which were from the same families a the ADAD subjects but that did not carry mutations (black symbol; see also Table 1). b Densitometric quantification of the accumulative immunoreactivity from the sum of the higher molecular mass PS1 complex (100 + 150 kDa). A quotient was calculated for each sample defined as the sum of (100 + 150 kDa) immunoreactivity relative to the 50 kDa immunoreactivity: (100 + 150 kDa/50 kDa). c Six syADAD and five yNC samples were fractionated on 5–20 % sucrose density gradients to further characterize the PS1 complexes. The fractions (collected from the top of each tube) were immunoblotted under denaturing conditions and probed for PS1, as in (a). β-Galactosidase (G, 16.0S; ~540 kDa), catalase (C, 11.4S; ~232 kDa) and alkaline phosphatase (P, 6.1S; ~140–160 kDa) were used as internal markers. Representative blots are shown. d The “stability” quotient was defined as the sum of the stable immunoreactive bands that sediment close to alkaline phosphatase (~140–160 kDa; fractions 2–7), mainly the 100 and 150 kDa bands, relative to the large unstable complexes that sediment closer to catalase (~232 kDa; fractions 8–12), and resolve mainly as 50 kDa immunoreactive bands in Western blots. The data are the means ± SEM: *Significantly different (p <0.005) from the yNC group as assessed by the Student t or Mann-Whitney U tests

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