8719 RESULTS
COMMENT Apart from the topological problem (i.e., the cellular compartments in which each of the players exist: e.g., does extracellular PrP ever normally come into direct contact with cytoplasmic α-syn?), the biological relevance of these interactions remains ...
COMMENT This comprehensive work extends previous work describing the critical role of cellular prion protein (PrP) as a member of the multiprotein Aβ oligomer receptor complex pioneered by Strittmatter and colleagues (Smith et al., 2019). As in previous published ...
COMMENT Neuronal dysfunction is thought to precede cell death in most, if not all, neurodegenerative diseases. However, it is still unclear what are the molecular events triggering neuronal dysfunction. While protein aggregation is a pathological hallmark in AD, ...
COMMENT Since the Strittmatter group described the interaction between cellular prion protein (PrP C) and Aβ oligomers (Laurén et al., 2009), PrP C has been suggested as a mediator of functional and toxic deficits in Alzheimer’s disease. Later papers have ...
COMMENT Since the identification of Alzheimer’s disease-associated variants in the Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) gene in 2013 (Guerreiro et al., 2013; Jonsson et al., 2013), many labs have focused their attention on understanding TREM2 ...
COMMENT This is an intriguing study highlighting the importance of TREM2-dependent microglial activity in protecting against neurotoxic pathology associated with β-amyloidosis. Unique to this study is their use of PS2APP mice to examine sex- and age-dependent ...
COMMENT That these subjects are younger than expected points to a possible interaction between environmental exposure and age at onset of latent idiopathic disease, which may be unmasked by the specific exposure circumstances in this population. As Gandy ...
COMMENT In our 2014 paper, Scott Small’s lab and ours collaborated to show that R33 (and a related compound, R55, which I think some companies call TPT-260) stabilized retromer in vitro and also increased retromer protein levels in neurons in culture. Treatment ...
COMMENT This work elegantly addresses an important question: Does tau spread through synaptically connected brain regions as Alzheimer's disease progresses? By using detailed functional connectivity maps and, importantly, two independent cohorts of ...
COMMENT In 2014, as a joint effort with the Petsko and Ringe labs, we introduced a class of drugs called “retromer pharmacological chaperones” (Mecozzi et al., 2014). Retromer’s core is a trimer, and one of the most reliable observations from the ever-growing ...
COMMENT CryoEM structures of tau filaments isolated from brain could lead to insights whether this disease is similar to Alzheimer's at the molecular level or not. scheres_235491 0 ...
COMMENT Sean Clouston, Ben Luft, Evie Bromet, and Roberto Lucchini discovered this WTC-related cognitive impairment and began reporting the clinical picture as early as 2016. Roberto recruited Mary Sano, Cheuk Tang, and me to join the group to advise on clinical, ...
COMMENT So far, the data are very preliminary. Some responders/survivors are cognitively impaired. There are subjects who appear to be amyloid-positive or tau-positive, but it is not clear what the overlap is between them. The number of tau and amyloid scans done ...
COMMENT I do not think it is surprising that these individuals, who have a range of post-WTC problems, also have cognitive impairment. What is important is to determine the underlying biology of the impairment. Also, it will be important in future studies to know ...
COMMENT Last October, I attended a workshop on WTC and brain injury Sean Clouston organized. Clouston showed some preliminary brain imaging, and most discussants agreed that findings are not yet definitive for any specific neuropathologic processes. Besides the ...
