"The inability of mutant APP to control p53 activation may help to explain, at least in part, why Alzheimer's-linked APP mutations result in the early onset of neurodegenerative disease," Mucke said. "The next step will be to determine if the APP mutations directly impair the protective function of APP or rather counteract it by increasing a neurotoxic APP breakdown product."
eurekalert.org
"Remarkably, the amyloid-induced disruption of memory circuits was found in the transgenic mice even before they developed AD-like amyloid plaques. This demonstrates that plaque formation is not required for amyloid peptides to impair the communications between nerve cells in the brain,"
So...does this change anything, overweight neuroprotection?
How far up or down the pathway? And who are the players again--
GLIA--block the glial cell activation by beta amyloid
SIBI--APP Processing Modulators, proteases, apoptosis--
with Bristol-Myers Squibb
Glaxo--??
NTII--neuroprotection.
A stretch: Ariad's NF-kB, sorry kids, you just know I
am going to slip that one in whenever I can.
Or how about glial growth factors, yeah, I'll sneak in
CNSI's rhGGF2 just for the hell of it--glial cells in
synapse formation
And stem cells--CTII, you know that story already. Okay
okay, enough of the spam.
Other: cholinergic hypothesis, neurotrophins, ampakines
And some links on AD
for newbies
ggc.org
FAD, presenilin
nih.gov
The Role of the Carboxyl-Terminal fragment of APP in the Neurodegeneration and Cognitive Loss in Alzheimer Disease
alzforum.org
Alzheimer's Disease Genetics, FAQ
alzheimers.org
National Institute on Aging
Progress Report on Alzheimer's Disease, 1998
alzheimers.org
Gliatech drug development
gliatech.com
Sibia Candidates
sibia.com |
