the whole amyloid thang is a red herring, sister?
http://medicalxpress.com/news/2016-07-cerebrovascular-disease-linked-alzheimer.html
Let's play "Antibodies for Alzheimers!"
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the whole amyloid thang is a red herring, sister?
http://medicalxpress.com/news/2016-07-cerebrovascular-disease-linked-alzheimer.html
I don't know about you, but I'm going to buy a ton of out of the money puts starting in November.
Worst Case - Phase 3 trial doesn't meet its primary endpoint...stock tanks.
Best Case - The trial has a statistically significant, but clinically meaningless endpoint. Stock will not tank, but will drop nicely.
It is a win-win regardless of the outcome. muwhaahahaha.
a P/E of 40 is insane. Somethings gotta give, but I don't touch options, too much price rigging
Mind your microvessels and exosomes!
http://medicalxpress.com/news/2016-07-sac-future-cellular-vessels-likelihood.html
here's some red CCI presented to you by gage risk: sola is not going to produce any clinically significant results and you can get the same bullshit results just by smoking some of that sweet sweet ganja http://www.nature.com/articles/npjamd201612.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
here's some red CCI presented to you by gage risk: sola is not going to produce any clinically significant results and you can get the same bullshit results just by smoking some of that sweet sweet ganja http://www.nature.com/articles/npjamd201612.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
here's some red CCI presented to you by gage risk: sola is not going to produce any clinically significant results and you can get the same results just by smoking some of that sweet sweet ganja http://www.nature.com/articles/npjamd201612.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
join the new alzheimers trial by lighting up today. half of lilly's workforce is already in phase I.
antibiotics for Alzheimer's ! Give it to Elanco
http://medicalxpress.com/news/2016-07-antibiotics-weaken-alzheimer-disease-gut.html
http://medicalxpress.com/news/2016-07-antibiotics-weaken-alzheimer-disease-gut.html
This could be our greatest success, as we are good at selling NOTHING!
"I need a no-drug
One that won't make me sick
One that won't break the bank
One that won't have side effects
One that won't keep me up all night"
Praise the Lord for the Pension Benefit Guarantee Corporation
Because all of John's Horses
And all of John's FDEs
Won't be able to put Humpty Dumpty back together again
Because all of John's Horses
And all of John's FDEs
Won't be able to put Humpty Dumpty back together again
careful with that antibody, Eugene
Human amyloid-beta acts as natural antibiotic in the brain: Alzheimer's-associated amyloid plaques may trap microbes
Date:
May 25, 2016
Source:
Massachusetts General Hospital
Summary:
A new study provides additional evidence that amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection.
Human amyloid-beta acts as natural antibiotic in the brain: Alzheimer's-associated amyloid plaques may trap microbes
Date:
May 25, 2016
Source:
Massachusetts General Hospital
Summary:
A new study provides additional evidence that amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection.
Yet much about its cause and the mechanisms driving its progression remain unknown. Alzheimer's disease typically starts with the death of brain cells, or "neurons," in one part of the brain and then, over time, slowly spreads to other regions. Amyloid fibrils—thin rigid strands of protein aggregates—accumulate in these areas of neuronal death, packing together to form dense plaques.
"Just as there are different strains of a virus, there appear to be different strains of fibrils," explains Makowski. "Remarkably, the different strains have the same chemical makeup but different three-dimensional structures."
http://medicalxpress.com/news/2016-09-critical-insights-alzheimer-disease.html
"Just as there are different strains of a virus, there appear to be different strains of fibrils," explains Makowski. "Remarkably, the different strains have the same chemical makeup but different three-dimensional structures."
http://medicalxpress.com/news/2016-09-critical-insights-alzheimer-disease.html
The whole recent phase 3 trial was based on "data dredging" or "p-value hacking". Let's look at the studied FALSE POSITIVE error rates for p-values. For instance, a p-value of 0.05, that magical value in pharma, leads to a probability of incorrectly rejecting the null hypothesis of AT LEAST 23% and typically can reach levels as high as 50%. A p-value of 0.01 has a false positive error rate of at least 7%.
Remember that reps the next time you start throwing p-values around an office. Sir Ronald Fisher who developed the p-value statistic never ever meant it to be used as a binary accept/reject criterion. The idea that the prior study in Alzheimers showed clinically benefit in a subset of patients was essentially just a little better than a coin flip.
https://www.sciencedaily.com/releases/2016/11/161117151205.htm
The study is published in the journal Science.
Studying human brain tissue, the UNSW and Neuroscience Research Australia research team identified a protein, kinase p38γ, which is lost as AD progresses. When they reintroduced the protein into the brains of mice, it was shown to have a protective effect against memory deficits associated with the disease.
"This study has completely changed our understanding of what happens in the brain during the development of Alzheimer's disease," said lead author UNSW Professor Lars Ittner.
The study is published in the journal Science.
Studying human brain tissue, the UNSW and Neuroscience Research Australia research team identified a protein, kinase p38γ, which is lost as AD progresses. When they reintroduced the protein into the brains of mice, it was shown to have a protective effect against memory deficits associated with the disease.
"This study has completely changed our understanding of what happens in the brain during the development of Alzheimer's disease," said lead author UNSW Professor Lars Ittner.