Amyloid-β-protein isoforms in brain of subjects with PS1-linked, βAPP-linked and sporadic Alzheimer disease
✍ Scribed by Akira Tamaoka; Paul E Fraser; Kazuhiro Ishii; Naruhiko Sahara; Kazuharu Ozawa; Masaki Ikeda; Ann M Saunders; Yasuko Komatsuzaki; Robin Sherrington; Georges Levesque; Gang Yu; Ekaterina Rogaeva; Shin'ichi Shoji; Linda E Nee; Daniel A Pollen; Lydia Hendriks; Jean J Martin; Christine Van Broeckhoven; Allen D Roses; Lindsay A Farrer; Peter H St. George-Hyslop; Hiroshi Mori
- Book ID
- 117387101
- Publisher
- Elsevier Science
- Year
- 1998
- Tongue
- English
- Weight
- 127 KB
- Volume
- 56
- Category
- Article
- ISSN
- 0169-328X
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
Both neural and nonneural human tissues from patients with or without Alzheimer's disease (AD) were surveyed to detect the presence of the P-amyloid protein and its precursors. This was accomplished using polyclonal and monoclonal antibodies to epitopes in the 695 amino acid long p-APP (i.e., P-APPm
Amyloid f3 protein (AD) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of AP4,, and AfL,2(431, respectively. In all patients, AP42(
To determine whether the presenilin 1 (PS1), presenilin 2 (PS2) and amyloid beta-protein precursor (APP) mutations linked to familial Alzheimer's disease (FAD) increase the extracellular concentration of amyloid beta-protein (A beta) ending at A beta 42(43) in vivo, we performed a blinded comparison