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P1‐164: LXR/APOE ACTIVATION VIA INTRANASAL ROUTE PREVENTS COGNITIVE DEFICITS AND FACILITATES AMYLOID BETA CLEARANCE IN A TRANSGENIC AD‐LIKE MOUSE MODEL
Author(s) -
Navas Guimaraes Maria Eugenia,
Bistue Millon Maria Beatriz,
Bruno Martin Alejandro
Publication year - 2019
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.2019.06.719
Subject(s) - genetically modified mouse , liver x receptor , transgene , neuroinflammation , amyloid beta , apolipoprotein e , biodistribution , pharmacology , medicine , neuroscience , endocrinology , in vivo , chemistry , biology , inflammation , disease , nuclear receptor , biochemistry , gene , microbiology and biotechnology , transcription factor
of ILEI. Three mice in a same cage were sacrificed every 3 hours for a day. Brain ILEI level showed phasic alteration; low in daytime and high in nighttime. Fluctuation of CSF ILEI was not synchronized with that of brain ILEI. Microdialysis study using APP–knockin mice revealed that interstitial fluid concentration of ILEI was roughly parallel with a level of physical activity (amount of movement) but not always with that of Ab. Treatment with anesthetics, tetrodotoxin or tetanus toxid obviously decreased both of ILEI and Ab in the interstitial fluid. Conclusions: Our results suggested that presynaptic ILEI and Ab were similarly released into the extracellular space in a synaptic activity–dependent manner.