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[P3–038]: ANTI‐AMYLOID ANTIBODIES AS A POTENTIAL THERAPEUTIC FOR ALZHEIMER's DISEASE: NEUROPROTECTIVE ACTIVITY OF SAR228810 AGAINST AMYLOID‐INDUCED NEUROTOXICITY IN VITRO
Author(s) -
Taupin Veronique,
Vaucher Nadine,
Loux Christophe,
Le Parc Josiane,
Michoux François,
Colonna Christine,
Capdevila Cecile,
Ferrari Paul,
Jeannin Pascale,
Cohen Caroline,
Pradier Laurent,
Bertrand Philippe
Publication year - 2017
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.2017.06.1851
Subject(s) - neurotoxicity , neuroprotection , neurite , chemistry , senile plaques , in vitro , amyloid (mycology) , extracellular , pharmacology , intracellular , biochemistry , neuropathology , amyloid beta , alzheimer's disease , peptide , microbiology and biotechnology , biology , toxicity , pathology , medicine , disease , inorganic chemistry , organic chemistry
inhibition of LTP in a dose-dependent manner. Finally, we examined if systemic passive immunization could prevent or reverse the persistent inhibition of LTP measured in vivo 7 days after a single i.c.v. injection of synthetic Aß42. A single systemic injection of MEDI1814, given either prior to i.c.v. treatement with Aß on day 1, or prior to recording synaptic plasticity on day 7, prevented the disruption of LTP. In contrast, neither prenor post-Aß treatment with the control antibody was effective. Conclusions: Intracerebral or systemic administration of a high affinity monoclonal antibody directed to the C-terminus of Aß42 rapidly prevents or reverses synaptic plasticity impairment in the rat hippocampus caused by synthetic or human AD brainderived Ab aggregates.