7 RESULTS
COMMENT This is very interesting work. Ye et al. provide strong evidence that approaches that aim to restore axonal trafficking and lysosomal degradation of BACE1 may represent a potential therapeutic target for AD. It has been known for many years that BACE1 ...
COMMENT This is a very interesting paper. The authors show with a variety of elegant experiments that BACE1, but not APP, endocytosis is regulated by ARF6, most likely via a clathrin-independent pathway. ARF6 is mainly found at the cell membrane and regulates ...
COMMENT This is very interesting work. The identification of over 60 BACE1 substrates using an unbiased and quantitative proteomic method sheds light on the role of β-secretase in conditions where BACE1 levels are increased. Levels of BACE1 are normally very low ...
COMMENT The recent report by Kukar et al. provides compelling evidence that some GSMs can modulate γ-secretase activity by binding the APP-CTF. The authors propose that the binding of GSMs to the APP-CTF induces conformational changes in the PS1/γ-secretase when ...
COMMENT Small and colleagues (1) had previously shown that VPS26 and VPS35 are decreased in AD brains and that siRNA-mediated depletion of VPS26 and VPS35 produces an increase in Aβ levels in vitro. In this interesting paper, Muhammad and colleagues report that ...
COMMENT I have been working on the regulation of BACE activity together with Rudy Tanzi, and presented our new data at the ICAD meeting. Our data show that GGA3 regulates BACE by modulating BACE degradation in the lysosome. We have found that caspase-3 degrades ...
COMMENT Seminal studies of LeBlanc (1995) have shown that primary neurons committed to undergo apoptosis by serum-deprivation produced increased amount of Abeta. These findings have been confirmed in cerebellar granule cells (Galli et al., 1998), in retinoic acid ...
