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P4–092: Regulation of NF–κB and AP–1 by poly(ADP–ribose) polymerase–1 in astrocytes of Alzheimer's disease
Author(s) -
Tanaka Seigo,
Ueda Kunihiro
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.2006.05.1830
Subject(s) - poly adp ribose polymerase , biology , senile plaques , astrocyte , microbiology and biotechnology , electrophoretic mobility shift assay , transcription factor , dna repair , programmed cell death , apoptosis , alzheimer's disease , dna , polymerase , biochemistry , gene , pathology , medicine , endocrinology , disease , central nervous system
APP phosphorylation and other APP metabolites such as C-terminal fragments (C99, C89, C83 and AICD) were unaffected. To investigate other potential mechanisms for the neuroprotective effects of NEP, levels of neuropeptides and neurotrophic factors were ascertained. We found that only levels of neuropeptide Y (NPY) were affected by NEP in APP tg mice. NEP did not affect levels of NT3, NT4, NGF, BDNF or substance P. Conclusions: This indicates that NEP does not interfere with the activity of specific neurotrophic factors. Studies are underway to identify the NPY neuroprotective fragments generated by NEP cleavage. In conclusion, this study suggests that NEP beneficial effects might not only be dependent on reducing A load but also by activating the generation of neuroprotective neuropeptides.