Premium
Specific reactivity of mild/severe Alzheimer’s disease patient’s sera to antibody against Aβ1–40 epitope 17–21
Author(s) -
Bolukbasi Hatip F. F.,
Matsunaga Y.,
Yamada T.
Publication year - 2008
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2007.00959.x
Subject(s) - epitope , monoclonal antibody , antibody , proteinase k , alzheimer's disease , immunology , monoclonal , enzyme , reactivity (psychology) , medicine , chemistry , microbiology and biotechnology , disease , biology , pathology , biochemistry , alternative medicine
Objectives – To detect the reactivity pattern of sera from patients with mild and severe Alzheimer’s disease (AD) to specific antibodies targeting different epitopes in the primary structure of amyloid‐beta (Aβ). Materials and methods – Sera from patients diagnosed with mild or severe AD were used. The reactivity of sera to monoclonal antibodies recognizing 1–7, 5–10, 9–14 and 17–21 epitopes of Aβ1–40 at 36–42°C was determined by an enzyme‐linked immunosorbent assay. Proteinase K digestion of Aβ1–40 was investigated by dot blotting at 36 and 40°C. Results: – Sera of patients with AD displayed reactivity only with monoclonal antibody recognizing the epitope 17–21 (4G8). The reactivity of sera from patients with severe AD was less than that of sera from patients with mild AD at temperatures 36–41°C, with no difference at 42°C. Patients with severe AD displayed lesser digestion with proteinase K. Conclusions – Sera derived from patients with AD could react with monoclonal antibodies directed to 17–21 sequences of Aβ1–40 in a temperature‐dependent manner. The severity of AD is associated with greater Aβ1–40 aggregation and resistance to proteinase K. The present results may be of value in staging and following up of patients with AD.