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P3‐050: An Affibody to Monomeric Aβ as a Novel Therapeutic Approach for Alzheimer's Disease Pathology
Author(s) -
Boutajangout Allal,
Lindberg Hanna,
Awwad Abdulaziz,
Paul Arun,
Baitalmal Rabaa,
Gudmundsdotter Lindvi,
Wahlberg Elisabeth,
Hard Torleif,
Lofblom John,
Stahl Stefan,
Wisniewski Thomas
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.06.1708
Subject(s) - senile plaques , genetically modified mouse , astrogliosis , medicine , alzheimer's disease , hippocampus , transgene , effector , pathology , antibody , immunology , disease , chemistry , biochemistry , central nervous system , gene
Germany), a high throughput surface plasmon resonance imaging analytical biosensor. cSNK-BSAwas immobilized on a sensorchip and serial samples of all mice injected. In a subsequent experiment, the Ig isotype/subclass distribution of serial samples of 20 mice were evaluated: diluted plasma were injected, followed by injections of goat anti-mouse IgA, IgM, IgG, IgG1, IgG2a, IgG2ab, IgG2c and IgG3. Results:Adjuvant-treated mice had no detectable antibodies to cSNK, whilst all cSNK-immunized mice generated high levels of anti-cSNK antibodies commencing at 4 weeks post-vaccination, age month 4. Peak antibody levels were attained at 8 weeks post-vaccination, age month 5, after which levels varied and declined slightly but remained substantially higher than levels at month 4. Ig isotype/ subclass analysis revealed that anti-cSNK antibodies are overwhelmingly of the IgG isotype and predominantly of the IgG1 subclass. Conclusions: Immunization of APP/ PS1 mice with the cSNK tripeptide induces high and sustained levels of anti-cSNK antibodies that demonstrated binding to AbO. Anti-cSNK antibodies are predominantly of the IgG1 isotype, this being indicative of a Th2 immune response.