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P4‐268: APP endocytosis is required for synaptic‐dependent release of amyloid‐beta in vivo
Author(s) -
Cirrito John R.,
Stewart Floy R.,
Mennerick Steven,
Holtzman David M.
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.2008.05.2337
Subject(s) - endocytosis , microdialysis , in vivo , synaptic vesicle , neurotransmission , microbiology and biotechnology , exocytosis , amyloid beta , chemistry , neuroscience , biology , vesicle , biochemistry , extracellular , receptor , peptide , membrane , secretion
shocking protein 90), ubiquitin proteasome system proteins (Ubiquitin carboxyl-terminal hydrolase isozyme L1), mitochondrion proteins (ATP synthase subunit B) and neural transport proteins (dynein heavy chain). Conclusions: Our results imply that the pathological changes in these proteins may contribute to dysfunction of synapse in AD. These data suggest new molecular mechanisms involved in the synaptic dysfunction that characterizes the AD brain.