[BostonCard]

FYI, MTL subsequently published a paper disproving his own hypothesis:

https://pubmed.ncbi.nlm.nih.gov/24806669/

However, in two distinct APP transgenic models of AD, we did not observe any alteration in the formation of amyloid plaques, gliosis, synaptic loss, or cognitive behavioral deficits with genetic deletion of DR6, though we did observe a transient reduction in the degree of microglial activation in one model. Our results support the view that DR6 functions with APP to modulate synaptic density in the adult CNS, but do not provide evidence for a role of DR6 in the pathophysiology of AD.

BTW, the RRC at Genentech really is a routine review; there is nothing sinister about the fact that his review went before the RRC.

BC

[BostonCard]

FYI, MTL subsequently published a paper disproving his own hypothesis:

https://pubmed.ncbi.nlm.nih.gov/24806669/

However, in two distinct APP transgenic models of AD, we did not observe any alteration in the formation of amyloid plaques, gliosis, synaptic loss, or cognitive behavioral deficits with genetic deletion of DR6, though we did observe a transient reduction in the degree of microglial activation in one model. Our results support the view that DR6 functions with APP to modulate synaptic density in the adult CNS, but do not provide evidence for a role of DR6 in the pathophysiology of AD.

BTW, the RRC at Genentech really is a routine review; there is nothing sinister about the fact that his review went before the RRC.

BC