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O5‐01‐03: LDLR‐related protein 10 (LRP10) alters amyloid precursor protein (APP) trafficking and processing: evidence for a role in Alzheimer's disease
Author(s) -
Brodeur Julie,
Theriault Caroline,
LessardBeaudoin Melissa,
Lavoie Christine
Publication year - 2012
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.2012.05.1971
Subject(s) - endosome , amyloid precursor protein , amyloid precursor protein secretase , microbiology and biotechnology , endocytic cycle , golgi apparatus , alpha secretase , retromer , ldl receptor , immunoprecipitation , p3 peptide , biology , chemistry , intracellular , receptor , alzheimer's disease , endocytosis , biochemistry , medicine , gene , lipoprotein , disease , cholesterol , endoplasmic reticulum
patch clamp recordings indicated that PAK inactivation blunted change in glutamatergic activity in frontal cortex neurons, while decreasing the firing rate and increasing mIPSC of entorhinal cortex neurons from 3xTg-AD mice. Surprisingly, the expression of dnPAK reduced the deposition of Ab and tau in detergent-insoluble fractions from the parieto-temporal cortex, whereas this effect was limited to tau in the frontal cortex. Conclusions: In summary, our results revealed a complex region-dependent impact of PAKonAD neuropathology and neuronal function, but nonetheless substantiate a critical role for PAK in the genesis of neuronal abnormalities underlying the emergence of symptoms in AD.