Scientists Identify 1 Cause Of Damage In Alzheimer's Disease And Find A Way To Stop It
November 12, 2010
Adapted from the University of California - San Diego
Researchers suspect that a protein superstructure called amyloid beta is responsible for
much of the neural damage of Alzheimer's disease.
A new study at the University of California, San Diego, shows that amyloid beta disrupts
one of the brain's anti-oxidant proteins and demonstrates a way to protect that protein,
and perhaps others, from amyloid's harmful effects.
"Amyloid seems to cause damage to cells," said chemistry professor Jerry Yang. "We have
reported in a very detailed way one potential interaction of how amyloid can cause disease,
and we found a way to stop it." His group's report of their results will appear in the Journal
of Biological Chemistry in December.
Their study focused on catalase, an enzyme that mops up excess oxidants, because
catalase normally helps to prevent the kind of damage seen in the brains of patients with
Alzheimer's disease and previous work had found catalase proteins deposited within
Lila Habib, a bioengineering graduate student and the first author of the report, added
amyloid to cultured neural cells and looked at its effects.
"We were able to determine that amyloid beta and this anti-oxidant enzyme, catalase,
interact, and that this interaction harmed catalase so it wasn't able to perform its
physiological function: to degrade hydrogen peroxide into oxygen and water," she said.
When Habib coated the amyloid with a small molecule designed to prevent its interaction
with other proteins, she was able to restore the activity of catalase and return hydrogen
peroxide to normal levels within the cells.
The coating Habib used to probe the interaction between amyloid and catalase is a
candidate drug —one of a class of molecules that Yang's lab has developed.
"Not only are we learning more about the disease, but we are also developing a potential
strategy for treatment," said Yang, who is currently testing the new approach in a mouse
model of the disease.
View all news updates for Alzheimer's disease
Disclaimer: The information provided in this section is a public service of the BrightFocus Foundation, and should not in any way substitute for the advice of a qualified healthcare professional, and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. BrightFocus Foundation does not endorse any medical product or therapy.
Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.