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COMMENT Was this the right drug at the wrong time? Or another "wrong" drug? (See Golde et al., 2018). This is a critical question for the field to answer. There is evidence that this antibody reduces the amyloid PET ligand signal in many trial ...
COMMENT These are fascinating studies. They remind us there is a lot we do not know about the biology of AD. They reinforce that we need to solve the mystery of how Aβ talks to tau. They also show that kinetics matter. There has been some literature (e.g. Wogulis ...
COMMENT Chad was a great friend and colleague. I first met him when I was a young faculty member at Mayo Clinic in Florida, and Chad was a postdoctoral fellow. He was later promoted to a research track assistant professor and I soon thereafter became his chair. ...
COMMENT Our consortium RNAseq data is available at synapse.org, along with other groups’ data. This data and RNAseq data from Ben Barres and colleagues at Stanford is consistent and pretty unequivocal. In humans, Lag3 RNA levels are ~500- to 1000-fold lower in ...
COMMENT My heart goes out to Dale's family, friends, and colleagues. Like all of the others posting comments here, I am saddened to hear this news. In the early days of Athena, there was a great but yet friendly competition between Athena, the Younkin lab, ...
COMMENT These data look quite interesting and the binding rather compelling. But I would caution that LAG3 is an immune checkpoint molecule whose expression in mice is thought to be largely restricted to T-cells and, in the brain, largely microglial cells. In ...
COMMENT Bart De Strooper’s essay in Cell is a thoughtful evaluation of a “failed” γ-secretase inhibitor (GSI) trial with semagacestat. I agree that the clinical trials with this compound could have been conducted in ways that would provide more guidance for ...
COMMENT It is likely that innate immune activation can have positive or negative effects on proteostasis and behavioral and neurodegenerative phenotypes. That balance between positive and negative effects would contextually depend on the nature, timing, duration, ...
COMMENT My take is that this is fundamentally sound but that some GSMs clearly interact with substrate. Ultimately, I think the truth will be that there will be flavors of GSMs that interact with substrate, substrate and presenilin/γ-secretase, and combinations ...
COMMENT I remain agnostic as to what studies of in vitro toxicity tell us about pathogenic mechanisms in Alzheimer's disease. I think the data is unequivocal that dumping protein aggregates on neurons in culture is harmful, but it has been challenging to ...
COMMENT The recent follow-up to the AN1792 study by Holmes et al. is a thought-provoking study that reinforces but certainly does not prove speculation by many in the field, including myself (Golde, 2006; Golde, 2003), that therapeutic targeting of Aβ may have ...
COMMENT With respect to Dr. Davies's comments, I think first and foremost we have to consider the fact that presenilin mutations are not the sole genetic cause of AD. The recent finding that APP gene duplications (in the absence of overt trisomy 21) cause AD ...
COMMENT I think we in this field have to be careful with overinterpreting phenomena in our APP mouse models. Transgenic mouse models expressing AD-associated mutant forms of the amyloid-β precursor protein (APP), or both mutant APP and mutant presenilin-1 (PS1), ...
COMMENT This is a very interesting story, but assumes a widespread underlying premise that is incorrect. Namely that dopaminergic substantia nigra neurons are selectivley damaged in Parkinson Disease. It is true that dopaminergic SN neurons are selectively ...
COMMENT It is important to clarify the statement "Flurbiprofen is the only approved NSAID still in the running for an AD therapy, though the one discussed here is a version trademarked by Myriad Pharmaceuticals. " The drug under investigation is R ...
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