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P1‐034: A role for lithium in rescuing amyloid beta pathology in an inducible drosophila model of Alzheimer's disease
Author(s) -
Adesakin Oyinkan A.,
Kerr Fiona,
Partridge Linda
Publication year - 2015
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.2015.06.230
Subject(s) - biology , lithium (medication) , neurodegeneration , amyloid (mycology) , amyloid precursor protein , pathogenesis , microbiology and biotechnology , pathology , neuroscience , disease , alzheimer's disease , immunology , medicine , endocrinology , botany
promotes tau exon 10 inclusion. PP1 interacts with SC35 and suppresses its function in promotion of tau exon 10 inclusion. Among three PP1s, PP1a is the most effective isoform to modulate SC35’s function. This study suggests that decreased activity of PP1 in Alzheimer’s disease brain may cause dysregulation of tau exon 10 splicing through SC35, leading to the imbalance in 3R-tau and 4R-tau expression, which may initiate or accelerate tau pathology and neurofibrillary degeneration.