Fig. 4

Representative Western blots analysis of amyloid precursor protein (APP) forms in platelets obtained from Met239Val-mutated subjects, sporadic AD patients (spAD) and control (C). Proteins transferred into nitrocellulose paper were stained with 22C11, a monoclonal antibody raised against a N-terminal region common to all APP forms. A 130 kDa form and a doublet at 106–110 kDa are present (arrowheads). Immu-noreactive bands were measured by means of computer-assisted imaging. No difference in the ratio between 130- and 106–110 kDa forms was observed in presenilin 2 (PS2)-mutated subjects [mean ± standard deviation (SD): 0.973 ± 0.2, Optical Density (OD)], compared with controls (0.87 ± 0.15; mutation carriers vs. controls: p = 0.78), but it was significantly different from sporadic AD patients (0.35 ± 0.15; p > 0.001 vs. controls and vs. PS2 mutated). The presence of the mutation in the family members is reported.