Damn: Myriad Genetics Stops Work on Alzheimer’s Drug

uscitizen

uscitizen

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Myriad Genetics Stops Work on Alzheimer’s Drug

Myriad said the drug, called Flurizan, did not improve thinking ability by a statistically significant amount compared with a placebo. Nor did it improve the ability of patients to carry out daily activities. The company, based in Salt Lake City, said it would discontinue development of the drug.

The failure is significant because Flurizan was one of the first drugs to reach late-stage testing that was seen as working by trying to prevent the buildup of toxic amyloid plaques in the brain. Such plaques are the focus of the leading theory for the cause of Alzheimer’s disease. The drug’s failure might cast some new doubt on that theory as well as on other experimental drugs to block amyloid plaques.

http://www.nytimes.com/2008/07/01/business/01gene.html?partner=MYWAY&ei=5065
 
The latest I've read (and I think it was just last week) is that of the different types of amyloid plaque, one in particular has been discovered to produce the sorts of cognitive deficits that are believed to occur in Alzheimer's, whereas the others had no effect.

It would be wise, then, to discontinue work on a drug that may address all amyloid plaques and focus on the one, less-occurring but potent, that seems to be responsible.

I suspect that the interpretations of this finding may be overly optimistic, though, as plaque occurs in Alzheimer's patients exclusively (I'm reasonably certain, anyway, though it's not my field), and can greatly interfere with synaptic transmission. Perhaps this one type has a permissive effect on the generation of the others?

We're embarking on a new project soon, and I'll be busier than I've ever been with this one as results are being requested in record time. My reading/posting will suffer, unfortunately. :(
 
Thorn said:
The latest I've read (and I think it was just last week) is that of the different types of amyloid plaque, one in particular has been discovered to produce the sorts of cognitive deficits that are believed to occur in Alzheimer's, whereas the others had no effect.

It would be wise, then, to discontinue work on a drug that may address all amyloid plaques and focus on the one, less-occurring but potent, that seems to be responsible.

I suspect that the interpretations of this finding may be overly optimistic, though, as plaque occurs in Alzheimer's patients exclusively (I'm reasonably certain, anyway, though it's not my field), and can greatly interfere with synaptic transmission. Perhaps this one type has a permissive effect on the generation of the others?

We're embarking on a new project soon, and I'll be busier than I've ever been with this one as results are being requested in record time. My reading/posting will suffer, unfortunately. :(
Click to expand...

sounds exciting anyway!
 
Darla said:
Thorn, is it something that Top can make money off of?
Click to expand...

LOL! Only if he has substantial holdings in the company that's funding this work! Oh, and if any of the three drugs we'll be testing show the promise we're hoping at least one might. We won't know 'til it's all done.
 
Thorn said:
LOL! Only if he has substantial holdings in the company that's funding this work! Oh, and if any of the three drugs we'll be testing show the promise we're hoping at least one might. We won't know 'til it's all done.
Click to expand...

And which company might that be? :)
 
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