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Transcriptional regulation of APP by apoE: To boldly go where no isoform has gone before
Author(s) -
Lee Liying Corinne,
Goh Michele Q. L.,
Koo Edward H.
Publication year - 2017
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.201700062
Subject(s) - apolipoprotein e , gene isoform , dementia , disease , amyloid (mycology) , neuroscience , pathophysiology , alzheimer's disease , amyloid precursor protein , mechanism (biology) , cognitive decline , biology , bioinformatics , psychology , medicine , endocrinology , genetics , philosophy , gene , pathology , epistemology
Alzheimer's disease (AD) is the most common form of dementia that gradually disrupts the brain network to impair memory, language and cognition. While the amyloid hypothesis remains the leading proposed mechanism to explain AD pathophysiology, anti-amyloid therapeutic strategies have yet to translate into useful therapies, suggesting that amyloid β-protein and its precursor, the amyloid precursor protein (APP) are but a part of the disease cascade. Further, risk of AD can be modulated by a number of factors, the most impactful being the ɛ4 isoform of apolipoprotein E (apoE). A recent study reported a novel isoform-dependent transcriptional regulation of APP by apoE. These interesting new results add to the myriad of mechanisms that have been proposed to explain how apoE4 enhances AD risk, highlighting the complexities of not only apoE and AD pathophysiology, but also of disease itself. Also see the video abstract here: https://youtu.be/yd14MBdPkCY.