A very interesting evolution is taking place in the a-beta42 hypothesis of Alzheimer’s Disease. The link is to a very interesting paper in the latest Nature Neuroscience, but the gist is that rather than polymers of a-beta being the cause of the memory loss, it’s small single molecules or oligomers of a-beta that are acting through binding to the nicotinic receptor to down regulate NMDA receptors–hence a loss of LTP and the ability to store new memories. This finding also seems to suggest a variety of potential new therapeutic targets, but also raises the question of what a-beta might be doing to NMDA glutamate receptors under non-pathological conditions.
Might a-beta be involved in neuroprotection against glutamate toxicity?
I’d be happy to chat about this with folks when I get back to Krasnow.
In the meantime, a gorgeous view of the Lab across Eel Pond this morning.
Jim
Discoverers and Discoveries 