7 RESULTS
COMMENT While previous studies support the notion that repression of TDP-43 cryptic exons is compromised in neurodegenerative disease exhibiting TDP-43 pathology (Ling et al., 2015; Sun et al., 2017), including ALS, identification of direct targets of such a ...
COMMENT This is a good study that raises the potential side effects of current BACE inhibitors (which do not discriminate BACE1 versus BACE2) due to impact on substrates of BACE2, particularly under pathological conditions. As it is not clear whether this ...
COMMENT If it’s true that accumulation of APP-βCTFs in the brain is toxic in AD, it would suggest that lowering the activity of γ-secretase alone may not be sufficient to deal with both problems of accumulation of Aβ and that of APP-βCTFs. Simultaneous reduction ...
COMMENT The identification by Thathiah and coworkers of the orphan G protein-coupled receptor 3 (GPR3) as a regulator of amyloid-β production is very interesting. Particularly intriguing is the idea that this protein apparently affects formation and cell-surface ...
COMMENT Despite accumulating evidence supporting the view that misfolding and aggregation of SOD1 is central to the pathogenesis of SOD1-linked ALS, and that perturbation of steps of maturation of SOD1 under non-physiological conditions promotes fibrillation of ...
COMMENT Previous studies showed that the deletion of BACE1 abolished the production of Aβ and BACE1 knockout mice are apparently normal. In this current paper, Ohno et al tested whether cognitive deficits occurring in the mutant APP mice (Tg2576) can be ...
COMMENT While there may be some evidence that cathepsins might share some BACE1-like properties, our BACE1 KO neurons/mice clearly demonstrated that it is unlikely there exist other BACE1 homologues as far as processing AbPP is concerned. Moreover, there is no ...
