11173 RESULTS
COMMENT The findings reported by the Rubinsztein group on new targets for Huntington disease also have potential implications for the pathogenesis and treatment of Alzheimer disease. In both diseases, less-than-effective autophagy contributes to intracellular pro
COMMENT Capturing Aβ Using Engineered Affinity Proteins Alzheimer disease (AD) is associated with the amyloid-β protein (Aβ) which assembles into toxic oligomers, protofibrils, and fibrils, and is the major component of amyloid plaques in the AD brain. Substantia
COMMENT This will be exciting to watch and follow up. sambak 0
COMMENT I have a couple of thoughts. First, there is no good evidence, other than correlative, that age-related memory declines in canines are secondary to amyloid accumulation. Rats and mice show age-associated loss of memory without amyloid accumulation. Perhap
COMMENT This new data on curcumin stimulated neurogenesis look pretty good and the dosing at 500nM to get the effect in vitro and via stimulation of MAPK is credible and consistent with other literature. Their in vivo results are the most important demonstration
COMMENT I am glad to see that the FDA is taking a closer look at what constitutes clinically meaningful change in AD trials. My feeling is that the ADAS-Cog is an inadequate instrument for assessing drug efficacy, so it is good to see that the use of standard neu
COMMENT We would like to comment on the interesting article by Wen et al. [1] on triggering BACE1 gene
COMMENT Phenserine is a unique compound including both cholinesterase- and APP synthesis-inhibitory properties. This publication presents several original first-time features: first, it evaluates a new molecule with potential anti-amyloid properties by directly m
COMMENT Congratulations to Howard Fillit, ADDF, and all the contributors for sharing. This is the way towards engaging the wider public in neuroscience, the challenges, and strategies going forward. gerryroberts2 0
COMMENT New diagnostics go hand in hand with new therapies. Are we there yet! Roll on the summer months! gerryroberts2 0
COMMENT Comment by Charles Duyckaerts, Jack-Christophe Cossec, and Marie-Claude Potier Accumulation of the
COMMENT This exciting report led by Troy Rohn at Boise State University and Elizabeth Head at UC Irvine quite convincingly shows a remarkable effect of Bcl-2 overexpression in curbing Aβ and tau pathology in the brain of 3xTg-AD mice. The authors elegantly show t
COMMENT Transthyretin (TTR) interaction with Aβ in the CSF has been known at least since 1994 when Schwarzman and colleagues (Schwarzman et al., 1994) concluded that TTR was the major Aβ binding protein in the CSF, observing a decrease in the aggregation state of
COMMENT These papers report using invertebrate models of human neurodegenerative disease to identify genes that play a role in the cellular toxicity associated with aggregation-prone, disease-relevant proteins. The studies focus on different diseases and use diff
COMMENT In this elegant paper, Rohn and colleagues show that overexpressing the anti-apoptotic protein Bcl-2 prevents the development of Alzheimer-like pathology and cognitive deficits in the 3xTg mouse model of AD. These data strengthen the growing body of evide
