Amyloid-β1–43 cerebrospinal fluid levels and the interpretation of APP, PSEN1 and PSEN2 mutations

Federica Perrone, Maria Bjerke, Elisabeth Hens, Anne Sieben, Maarten Timmers, Arne De Roeck, Rik Vandenberghe, Kristel Sleegers, , Peter P. De Deyn, Sebastiaan Engelborghs, Julie Van Der Zee, Christine Van Broeckhoven & Rita Cacace
Abstract Background Alzheimer’s disease (AD) mutations in amyloid precursor protein (APP) and presenilins (PSENs) could potentially lead to the production of longer amyloidogenic Aβ peptides. Amongst these, Aβ1–43 is more prone to aggregation and has higher toxic properties than the long-known Aβ1–42. However, a direct effect on Aβ1–43 in biomaterials of individuals carrying genetic mutations in the known AD genes is yet to be determined. Methods N = 1431 AD patients (n = 280 early-onset...
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