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P2‐327: Curcuminoids improve transcription of GNT III and clearance of amyloid‐β (Aβ)
Author(s) -
Fiala Milan,
Liu Philip T.,
Goldenson Benjamin,
Zaghi Justin,
Taniguchi Naoyuki,
Cashman John
Publication year - 2008
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.2008.05.1404
Subject(s) - phagocytosis , downregulation and upregulation , innate immune system , receptor , flow cytometry , chemistry , amyloid beta , microglia , microbiology and biotechnology , pharmacology , inflammation , biology , immunology , biochemistry , gene , peptide
of Abeta oligomers. The current investigation tested if ICV introduction of anti-ADDL antibody would overcome the transient nature of the anti-Abeta antibody and would produce long-lasting preventive effects in the TgCRND8 transgenic mouse model of AD. Methods: Cerebral amyloid load was quantitated by immunocytochemistry and ELISA. Synaptic degeneration was evaluated by immunocytochemistry. Results: Results show that anti-ADDL antibody persistently reduced cerebral amyloid by 3-fold as evaluated by immunocytochemistry and ELISA; further, a significant reduction in synaptic degeneration ( 55%), as evaluated by immunocytochemistry of a 25-kDa presynaptic molecular marker SNAP-25 critical to calcium mediated synaptic vesicular exocytosis involved in EPSP and long term potentiation (LTP), was maintained up to 8 weeks post injection. Conclusions: The data indicate that passive immunization with antiADDL antibody may be an improved strategy to prevent early synaptic deficits in AD and to delay AD-like pathology and suggest the value in developing simpler means for introducing these antibodies into the brain.