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P4–022: Effect of APP 319–335 on the expression of β–amyloid associated protein in APP V717I transgenic mice
Author(s) -
Wang Rong,
Min Rong,
Zhao Zhi wei,
Liu Meng Xia,
JI Zhi Juan,
Sheng Shu Li
Publication year - 2006
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.2006.05.1760
Subject(s) - amyloid precursor protein , genetically modified mouse , transgene , mutant , neurodegeneration , amyloid (mycology) , phenotype , microbiology and biotechnology , biology , medicine , pathology , biochemistry , alzheimer's disease , gene , disease
tion of CDK-5 by roscovitine, arrested A secretion and tau hyperphosphorylation. Inhibition of PKC by GF-109203X activates GSK-3 whereas activation of PKC by PDBu inhibits GSK-3. Conclusion: These results together suggest that endogenously overproduced A induces tau hyperphosphorylation through activation of GSK-3, and inactivation of PKC is at least one of the mechanisms involved in GSK-3 activation.
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