Welcome aboard MadGirl!
There are a whole bunch of powerful BACE1 inhibitors that reduce amyloid levels by an overwhelming amount (some greater than 90%).
I am not totally sure whether I would even want my amyloid levels to be reduced by over 90%, it must be doing something useful.
Yet, those who go onto to develop dementia do not have a slight increase in amyloid levels: many of them are carrying more then 5 years of amyloid buildup!http://www.alzforum.org/therapeutics/verubecestat
I think we have already reached the point of no return with verubecestat.
It simply no longer matters what top line results will be reported for these phase 3 trials.
Given the current evidence with the below APP variant, it can be seen that lowering
amyloid by 40% over a long period of time can have profound anti-dementing effects.
The FDA can do whatever it pleases, I think there will be a fair number of people who will be making friends
with some Chinese chemists if there is some sort of push back to making this a consumer medicine.
The market would be overwhelming.
The clinical dementia market would be tiny by comparison; they could play nice with the dementia community
simply to gain goodwill in the consumer market.
Let's see 100 million at risk Americans, charge them say $1000-$2000 per year... hmm that starts to add up to
some truly serious money.
Or, they could try it the dumb way 100 million at risk Americans, charge them say
$50,000 - $100,000 per year and now you're talking about who can you hit up to buy a round of coffee.
Monopolies do not maximize profit by maximizing price, profit is maximized at the production level where marginal revenue equals marginal cost. Pricing at such a point might not exactly maximize total welfare, though there would still be a whole lot of happy people.
These Mendelian randomization studies are more impressive than clinical trials, where
there can be a nearly endless list of confounders. http://www.nature.com/nature/journal/v4 ... 11283.html
"Researchers found that the A allele of the APP variant (rs63750847-A) was significantly more common in a control group of patients who had lived to at least 85 years of age without a diagnosis of AD than in a group with AD (0.62% vs 0.13%; odds radio [OR], 5.29; P = 4.78 × 10-7), pointing to a protective effect against the disease.
Investigators confirmed the results by sequencing rs63750847-A in predicted carriers who were found to have the correct copy number, and by genotyping the allele in cases and controls.
The rs63750847-A variant occurs with greater frequency among the elderly. The authors estimate that the odds for carriers of this variant reaching age 85 are 1.47-fold the odds for noncarriers."
So reducing amyloid by 40% from normal levels (?) reduced AD risk by over 80%!http://www.medscape.com/viewarticle/767403
Did someone say CRISPR? Oh, I thought I heard let's CRISPR it.
Hmm, I suppose the Nordic sperm bank with the 847-As should be doing a roaring business.
I mean why wait 200,000 for the most adaptive genes to win?