Fig. 1.

Abnormalities occur in selective synaptic proteins in preclinical/asymptomatic AD and AD brain. (A-D) Immunohistochemical localization (brown labeling) of the presynaptic vesicle protein synaptophysin in human control (A,C) and AD (B,D) CA1 region of hippocampus with cresyl violet counterstaining. In controls, the neuropil of CA1 is highly enriched in synaptophysin immunoreactivity (A) which can be seen as discrete small particle-like boutons that decorate the surfaces of dendrites (arrow) of CA1 pyramidal neurons (asterisk). In the AD brain, the CA1 region is severely depleted of synaptophysin immunoreactivity (B) and the labeling of synaptophysin-positive presynaptic terminals on dendrites (arrow) of CA1 neurons (asterisk) and in the surrounding neuropil is reduced markedly. Scale bars = 10 μm. (E) Graph showing the results of immunoblot experiments of synaptophysin protein levels in different brain regions of control, preclinical/asymptomatic AD (pAD), and definite AD cases. A representative blot for synaptophysin (Syn) is shown with β-tubulin immunoreactivity serving as a protein loading control. Significant differences in synaptophysin levels from control are indicated by single asterisk (p < 0.05) or double asterisk (p < 0.0001). For more about this study see Sze et al., 1997. (F) Graph showing the result of immunoblot experiments of different presynaptic vesicle exocytosis proteins (synaptobrevin, Rab3A, synaptotagmin, synapsin I, and SV2) and presynaptic plasma membrane proteins (SNAP25 and syntaxin) in CA1 hippocampus of control, preclinical/asymptomatic AD, and definite AD cases. Significant differences in protein levels from control are indicated by single asterisk (p < 0.05), double asterisk (p < 0.01) or triple asterisk (p < 0.005). For more about this study see Sze et al., 2000 [25]. (Colours are visible in the electronic version of the article at www.iospress.nl.)