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P4‐252: REGULATION OF SORLA IN GENERAL AND IN ALZHEIMER'S DISEASE
Author(s) -
Poulsen Annemarie,
Zole Egija,
Ivarsen Anne Kathrine,
Friis Jenny B.,
Vorum Henrik,
Andersen Olav
Publication year - 2014
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.2014.07.023
Subject(s) - promoter , biology , transcription factor , genetics , gene expression , transcription (linguistics) , gene , microbiology and biotechnology , linguistics , philosophy
all experimental models of NPC disease examined in this study; b) BACE1 alteration upon NPC1 dysfunction causes altered metabolism of the major BACE1 substrates Sez6 and Sez6L1; c) Sez6/Sez6L1 induction in hippocampi of NPC mice implicates their potential role in the NPC phenotype. Overall, altered BACE1 levels and processing of its substrates may contribute to the NPC phenotype and BACE1 may represent a novel target for an early intervention in NPC disease.