Biotech Values

[Kadaicher1]

Jellybean, I thought the APP signal to the DR6 was to cull a cell that was malfunctioning and dying. Trophic factor(food) deprivation preceeds the DR6 signal. That is neural pruning. That is perhaps not how most cells die in Alzheimer's. Thats not to say that excessive pruning couldn't trigger excitotoxicity. But how is cutting off the Bace going to stop the trophic-factor deprivation. Am I missing something here? Just from what I have read in that abstract it looks like maybe chopping into the process to cleave the APP may even have an adverse effect.
http://www.sciencedaily.com/articles/e/excitotoxicity.htm
Excitoxicity is seen as a cause of neuron death over various neurodegenerative diseases.
http://www.alscenter.org/living_with_als/causes/excitotoxicity.html
Blocking the glutumate receptors was seen as a way to stop excitotoxicity. Strong argonists of the NMDA glutamate receptors proved to have severe side effects, but a weak argonist was tolerated and LLY developed Memantine in '68 and it is still in use in many forms.
http://en.wikipedia.org/wiki/Memantine
A recent trial in Huntington's, which is another neurodegenerative disease where excitotoxicity is thought to be the final damage, Memanine caused some cognition gains, but increased movement disorder.
http://hddrugworks.org/index.php?option=com_content&task=view&id=141&Itemid=88
Prana's PBT2 will be the next drug to go against Huntingtons with a 6 month trial due to start shortly. A totally different MOA to anything so far and thought to protect against exitotoxicity through its interaction with intracellular metals.
Assoc Professor Kevin Barnham at the Mental Health Research Institute(Melbourne) was recently awarded $419,000 to further research PBT2's effect on excitotoxicity.
http://www.pranabio.com/downloads/Media%20Releases/Media%20Releases%202011/Oct%2027%20Aust%20Fed%20Gov%20Grant%20to%20study%20role%20of%20PBT2%20in%20preventing%20ecitotoxicity.pdf

In saying all the above there is another aspect.
[ In late 2010, for example, a team led by Mathias Jucker at the University of Tübingen, Germany, reported that they could, in essence, transmit Alzheimer's-type brain pathology in a prion-like manner by injecting Alzheimer's brain matter into the bodies of mice (Eisele, Y. S. et al. Science 330, 980–982, 2010). Such findings have contributed to a major rethink of the cause of Alzheimer's disease]

It is contageous just as is mad cow disease.

That was the same experiment Stanley Prusiner performed when defending his Prion work in the 90s.
http://www.slate.com/articles/news_and_politics/hey_wait_a_minute/1997/10/nobel_gas.html

A prion is just a little fragment of protein that can reproduce. Maybe like that little protein fragment that hits the DR6.

Exitotoxicity is assosciated with various conditions, including traumatic brain injury and stroke. Kevin Barnham's work may prove to be very important.