This still won't likely change the attack on cholesteol since statins are huge money makers.
http://www.biosciencetechnology.com/news/2016/01/atherosclerosis-alzheimers-disease-blood-vessels-study-suggests?
In atherosclerosis, plaque builds up on the inner walls of arteries
that deliver blood to the body. Studying mice and tissue samples from
the arteries of patients, researchers at Washington University School of
Medicine in St. Louis suggest this accumulation is driven, at least in
part, by processes similar to the plaque formation implicated in brain
diseases such as Alzheimer’s and Parkinson’s.
The study is published in the journal Science Signaling.
A look behind the scenes in the process of plaque accumulating in
arteries, the new study is the first to show that another buildup is
taking place. Immune cells attempting to counteract plaque formation
begin to accumulate misshapen proteins. This buildup of protein junk
inside the cells interferes with their ability to do their jobs.
Protein buildup is widely studied in the brain — accumulation of
proteins such as amyloid beta and tau are hallmarks of Alzheimer’s,
Parkinson’s and other degenerative neurological disorders. But until
now, the process of misshapen protein buildup within cells has not been
implicated in atherosclerosis.
“In an attempt to fix the damage characteristic of atherosclerosis,
immune cells called macrophages go into the lining of the arteries,”
said senior author Babak Razani, M.D., Ph.D., assistant professor of
medicine. “The macrophage is like a firefighter going into a burning
building. But in this case, the firefighter is overcome by the
conditions. So another firefighter goes in to save the first and is
likewise overcome. And another goes in, and the process continues to
build on itself and worsen.”
The researchers showed that this protein buildup inside macrophages
results from problems with the waste-disposal functions of the cell.
They identified a protein called p62 that is responsible for
sequestering waste and delivering it to cellular incinerators called
lysosomes. To mimic atherosclerosis, the researchers exposed the cells
to types of fats known to lead to the condition. The researchers noted
that during atherosclerosis, the macrophages’ incinerators become
dysfunctional. And when cells stop being able to dispose of waste, p62
builds up. In a surprise finding, when p62 is missing and no longer
gathers the waste in one place, atherosclerosis in mice becomes even
worse.
Razani and his colleagues, including the study’s first author, Ismail
Sergin, Ph.D., a research assistant, also found these protein
aggregates and high amounts of p62 in atherosclerotic plaque samples
taken from patients, suggesting these processes are at work in people
with plaque building up in the arteries.
“That p62 sequesters waste in brain cells was known, and its buildup
is a marker for a dysfunctional waste-disposal system,” Razani said.
“But this is the first evidence that its function in macrophages is
playing a role in atherosclerosis.”
The study demonstrates that p62’s role in gathering up the misfolded
proteins is protective against atherosclerosis, even if the cell can’t
actually dispose of the waste it gathers.
“If p62 is missing, the proteins don’t aggregate,” Razani said. “It’s
tempting to think this might be good for the cell, but we showed this
is actually worse. It causes more damage than if the waste were
corralled into a large ‘trash bin.’ You can imagine a situation where
lots of trash is being generated and see that it would be better to keep
it all in one place, rather than have it strewn across the floor. You
might have difficulty removing the trash to the dumpster, but at least
it’s contained.”
In atherosclerosis, and perhaps in the brain disorders characterized
by protein accumulation, such evidence suggests it would be better to
focus on ways to fix the cells’ waste-disposal system for getting rid of
the large protein aggregates, rather than on ways to stop the
aggregates from forming.
Source: Washington University in St. Louis
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