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P1–083: Exploring the effects of memantine on the production of beta‐amyloid protein species in cells transfected with wild‐type and mutant APP linked to familial Alzheimer's disease
Author(s) -
Tokuda Takahiko,
Oshima Yoichi,
Makino Mitsuhiro,
ItoTakahashi Kaori,
Uraki Fuminori,
Satoh Eri,
Taguchi Katsutoshi,
Watanabe Yoshihisa,
Tanaka Masaki,
Waragai Masaaki,
Nakagawa Masanori
Publication year - 2013
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.2013.05.304
Subject(s) - memantine , nmda receptor , amyloid precursor protein , transfection , pharmacology , neurotoxicity , mutant , wild type , chemistry , antagonist , microbiology and biotechnology , alzheimer's disease , medicine , biochemistry , receptor , biology , disease , gene , toxicity
a novel mechanism involving Nilotinib-induced enhancement of autophagic degradation of amyloid proteins to halt progression of AD pathology. This approach contrasts with previous studies and clinical trials using immunobased therapy to target extracellular plaques that leave neurons vulnerable to intracellular amyloid accumulation, thus leading to decreased plaque load without cognitive improvement. Intracellular A b in AD may lead to extracellular A b plaques, and these studies show that targeting intracellular b -amyloid and Tau not only decreases plaque load, but also prevents amyloid-induced cell death and cognitive deterioration.