DementiaToday.com - It's been one hundred years since Alzheimer's
disease was first described, and yet our best treatments in
development for the disease are still highly toxic drugs. But new
research from Rockefeller University, published in the online edition
of Proceedings of the National Academy of Sciences, has identified a
therapeutic target, called casein kinase 1, that may be the key to
halting the course of the disease. The findings, based on studies in
mammalian cells, show that chemicals that block casein kinase 1 don't
interfere with a closely connected essential pathway.

Alzheimer's disease is caused by a build-up of a small protein called
beta-amyloid, which is formed when a larger protein is broken into
pieces. But the enzyme that produces beta-amyloid is also responsible
for cleavage of another protein called Notch. The problem with current
drugs is that they block these enzymes to stop production of beta-
amyloid, and in doing so they also block the cleavage of Notch --
which plays an important role in the development of healthy brain
cells.

The new research, based on studies by lead author Marc Flajolet and
from the Nobel Prize winning laboratory of Paul Greengard, director of
the Fisher Center for Alzheimer's Disease Research at Rockefeller, has
identified another protein, casein kinase 1, that controls the
regulation of these enzymes. When the researchers block casein kinase
1, production of beta-amyloid proteins goes down, but Notch signaling
is not affected.

"Studies of brain tissue from Alzheimer's patients have shown an
increase in casein kinase 1 expression," says Greengard, Vincent Astor
Professor and head of the Laboratory of Molecular and Cellular
Neuroscience. "We found that the key enzymes involved in beta-amyloid
production - called BACE and gamma-secretase - were targets of casein
kinase 1, so we investigated what role it might be playing." ...cont.

http://www.dementiatoday.com/article-2996209.htm

Tim Silva