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P3‐166: RanBP9 promotes mitochondrial dysfunction and calcium deregulation in primary neurons
Author(s) -
Roh SeungEon,
Hong YunHwa,
Liu Tian,
Kim Sang Jeong,
Kang David
Publication year - 2011
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.2011.05.1606
Subject(s) - mitochondrion , calcium , glutamate receptor , membrane potential , calcium in biology , depolarization , biology , microbiology and biotechnology , calcium signaling , chemistry , medicine , endocrinology , receptor , intracellular , biochemistry
soluble As aggregates revealed high levels of high-molecular weight Asoligomers and protofibrils (hiMWAs) in APP23 and APP51/16 mice. Using native (BN-PAGE) and denaturing (SDS-PAGE) protein analysis all types of As-aggregates occurring in APP23 mice were also observed in APP51/16 mice. The major difference between APP23 and APP51/16 mice was that APP23 mice exhibited higher levels of easily denaturable As-aggregates than APP51/16 mice. Conclusions: These results indicate that high levels of soluble, denaturable As-aggregates are related to dendritic and synapse degeneration in APP23 mice whereas low levels of these aggregates, as well as As-plaque deposition, had no effect on the integrity of the neurons in APP51/16 mice. Thus, the concentration of soluble, denaturable As-aggregates is related to its toxicity and acidic neurotransmitters can be discussed to cause denaturation of these aggregates and release of presumably toxic low-molecular weight oligomers. Supported by DFG and AFI.