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Publication : Oral administration of a fusion protein between the cholera toxin B subunit and the 42-amino acid isoform of amyloid-β peptide produced in silkworm pupae protects against Alzheimer's disease in mice.

First Author  Li S Year  2014
Journal  PLoS One Volume  9
Issue  12 Pages  e113585
PubMed ID  25469702 Mgi Jnum  J:348418
Mgi Id  MGI:6251339 Doi  10.1371/journal.pone.0113585
Citation  Li S, et al. (2014) Oral administration of a fusion protein between the cholera toxin B subunit and the 42-amino acid isoform of amyloid-beta peptide produced in silkworm pupae protects against Alzheimer's disease in mice. PLoS One 9(12):e113585
abstractText  A key molecule in the pathogenesis of Alzheimer's disease (AD) is a 42-amino acid isoform of the amyloid-beta peptide (Abeta42), which is the most toxic element of senile plaques. In this study, to develop an edible, safe, low-cost vaccine for AD, a cholera toxin B subunit (CTB)-Abeta42 fusion protein was successfully expressed in silkworm pupae. We tested the silkworm pupae-derived oral vaccination containing CTB-Abeta42 in a transgenic mouse model of AD. Anti-Abeta42 antibodies were induced in these mice, leading to a decreased Abeta deposition in the brain. We also found that the oral administration of the silk worm pupae vaccine improved the memory and cognition of mice, as assessed using a water maze test. These results suggest that the new edible CTB-Abeta42 silkworm pupae-derived vaccine has potential clinical application in the prevention of AD.
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