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Abstract Details

Galectin 3 binding protein suppresses Aß production by modulating ß-cleavage of amyloid precursor protein
Aging, Dementia, and Behavioral Neurology
P4 - Poster Session 4 (5:30 PM-6:30 PM)
10-006
To establish a target for unique therapeutic strategies and disease-modifying drugs in AD.
Alzheimer’s disease (AD) is the most common type of dementia, and the accumulation of amyloid-β peptides (Aβ) is associated with AD pathogenesis. Aβ is produced from amyloid precursor protein (APP) via sequential cleavages by β- and γsecretases. Therefore, modification of APP processing has been a target for novel therapeutic options in AD; however, no effective treatment is currently established.
In order to identify endogenous factors that modulate Aβ production, we performed a transcriptome analysis on neuronal cells derived from human induced pluripotent stem cells because these cells changed the Aβ production during neuronal differentiation.
We found that phosphatidylinositol-glycan-specific phospholipase D (GPLD1) gene expression is associated with these changes in Aβ production. Overexpression of GPLD1 in HEK293 cells increased the secretion of galectin 3 binding protein (GAL3BP), which suppressed Aβ production in neuroglioma H4 cells, a model of AD. Mechanistically, GAL3BP suppresses Aβ production via direct interaction with APP that suppresses the processing by βsecretase activity. Furthermore, we show that extracellularly added GAL3BP is taken up by cells via endocytosis and is localized in close proximity to APP in endosomes where amyloidogenic APP processing takes place.
Taken together, our data indicate that GAL3BP may be a target for unique therapeutic strategies and disease-modifying drugs in AD.
Authors/Disclosures

PRESENTER 		No disclosure on file
No disclosure on file
No disclosure on file
Hisatomo Kowa, MD, PhD (Kobe Univ Graduate School of Health Sciences) No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file