Takaomi Saido on The off-rate of monomers dissociating from amyloid-β protofibrils.
COMMENT This is a very important study. What would the kinetics be if the authors used amyloid protofibrils and filbrils isolated from human brains? 0 saido
331254 RESULTS
COMMENT This is a very important study. What would the kinetics be if the authors used amyloid protofibrils and filbrils isolated from human brains? 0 saido
COMMENT A very elegant study done in mice, rats, and monkeys showing that clearance of Aβ from the brain is most likely not because of a sink effect between this organ and the periphery. 0 j.goetz
COMMENT This is an interesting paper that supports our findings in mouse models and cell lines that soluble tau is toxic, as evidenced by the trapping of the kinesin adapter protein JIP1 in the soma under conditions where tau levels (irrespective of a pathogenic
MUTATIONS MAPT 44073889 GRCh37/hg19 rs1052553 A G g.109929A> G g.107103A> G Exon 9 Point, Silent Coding Unknown. This variant segregates with the H2 haplotype, which may be associated with decreased tau levels in the brain. Not applicable. A227A Frontotempora
PAPER Gordon RY, Kapralova MV, Godukhin OV, Arkhipov VI
PAPER Molino I, Colucci L, Fasanaro AM, Traini E, Amenta F
Huntington's patientRaleigh, United States
COMMENT This paper beautifully shows that by using a unique method of AAV-mediated gene delivery via the choroid plexus and ependyma, relatively small increases in expression of human ApoE4 are achieved that increase Aβ deposition and toxicity, while ApoE2 has th
COMMENT In this interesting study, the authors demonstrate that the ApoE4 gene variant increases amyloid plaque load, promotes synaptic loss and neuritic dystrophy in close proximity to the plaques, and delays Aβ clearance. In contrast, ApoE2 expression decreases
COMMENT Although the association of ApoE with AD risk and age of onset is indisputable, whether ApoE is a tractable therapeutic target remains an open question. Brad Hyman’s group has recently published a paper that adds considerable strength to the therapeutic p
COMMENT In this elegantly performed study, Hudry and colleagues addressed a few important gaps in the literature on ApoE and its links to amyloid pathology and Alzheimer’s disease. By using a still-unexplored strategy of adding the three different human ApoE isof
PAPER El-Azab MF, Baldowski BR, Mysona BA, Shanab AY, Mohamed IN, Abdelsaid MA, Matragoon S, Bollinger KE, Saul A, El-Remessy AB
PAPER Vantaggiato C, Clementi E, Bassi MT
PAPER Han J, Pollak J, Yang T, Siddiqui MR, Doyle KP, Taravosh-Lahn K, Cekanaviciute E, Han A, Goodman JZ, Jones B, Jing D, Massa SM, Longo FM, Buckwalter MS
PAPER Simmons DA, Belichenko NP, Yang T, Condon C, Monbureau M, Shamloo M, Jing D, Massa SM, Longo FM
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