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P3‐048: The Effect of S‐Adenosylmethionine on Ameliorating Aβ Induced Neural Injury
Author(s) -
Li Liang
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.2016.06.1706
Subject(s) - neuroprotection , oxidative stress , glutathione , astrocyte , chemistry , pharmacology , microglia , neurotrophic factors , apoptosis , microbiology and biotechnology , biology , biochemistry , endocrinology , inflammation , central nervous system , immunology , enzyme , receptor
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.