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amyloid plaques
Red meat could trigger Alzheimer's disease
According to a recent research, eating too much red meat could trigger Alzheimer's disease.
Scientists found that a build-up of iron – abundant in red meat – could cause oxidant damage, to which the brain is particularly vulnerable.
Researchers say this could in turn increase the risk of Alzheimer's.
Prof. George Bartzokis of UCLA said that more studies have suggested the disease is caused by one of two proteins, one called tau, the other beta-amyloid.
As we age, most scientists say, these proteins either disrupt signaling between neurons or simply kill them.
He and colleagues looked at two areas of the brain in patients with Alzheimer's and they compared the hippocampus, which is known to be damaged early in the disease, and the thalamus, an area that is generally not affected until the late stages.
Using brain-imaging techniques, they found that iron is increased in the hippocampus and is associated with tissue damage in that area. But increased iron was not found in the thalamus.
Prof. George Bartzokis said that most research had focused on the buildup of the proteins tau or beta-amyloid that cause the plaques associated with the disease.
Eating too much red meat could increase the risk of Alzheimer's
But he believes the breakdown occurs further "upstream", and it is the protein's destruction of myelin, the fatty tissue which enables nerve signals to be sent along fibres, which disrupts communication and promotes the build-up of the plaques.
These amyloid plaques in turn destroy more and more myelin, disrupting brain signaling and leading to cell death and the classic clinical signs of Alzheimer's.
He points out that myelin is produced by cells called oligodendrocytes.
These cells, along with myelin itself, have the highest levels of iron of any cells in the brain, George Bartzokis says.
He adds that although iron is essential for cell function, too much of it can promote oxidative damage, to which the brain is especially vulnerable.
Hypothesizing that elevated iron in the tissues could cause tissue breakdown, he targeted the vulnerable hippocampus, a key area of the brain involved in the formation of memories, and compared it to the thalamus, which is relatively spared by Alzheimer's until the very late stages of disease.
They found increased iron levels in patients with Alzheimer's.
Prof. George Bartzokis said: "It is difficult to measure iron in tissue when the tissue is already damaged."
But the MRI technology we used in this study allowed us to determine that the increase in iron is occurring together with the tissue damage.
"We found that the amount of iron is increased in the hippocampus and is associated with tissue damage in patients with Alzheimer's but not in the healthy older individuals – or in the thalamus.
"So the results suggest that iron accumulation may indeed contribute to the cause of Alzheimer's disease."
The link to iron could mean that dietary changes and surgical interventions could lower the chances of the developing the disease, he said.
He explained: "The accumulation of iron in the brain may be influenced by modifying environmental factors, such as how much red meat and iron dietary supplements we consume and, in women, having hysterectomies before menopause."
Prof. George Bartzokis said drugs are already being developed to remove iron from tissue and the new study may allow doctors to determine who is most in need of such treatments.
Alzheimer's brain destructive plaques have been cleared in mice tests
US scientists have discovered how to rapidly clear the destructive plaques found in the brains of Alzheimer's patients while they were testing a cancer drug on mice.
The study, published in the journal Science, reported the plaques were broken down at "unprecedented" speed.
Tests also showed an improvement in some brain function.
Researchers said the results were promising, but warned that successful drugs in mice often failed to work in people.
The exact cause of Alzheimer's remains unknown, but one of the leading theories involves the formation of clumps of a protein called beta-amyloid. These damage and kill brain cells, eventually resulting in memory problems and the inability to think clearly.
Clearing protein plaques is a major focus of Alzheimer's research and drugs are already being tested in human clinical trials.
In the body, the role of removing beta-amyloid falls to apolipoprotein E – or ApoE. However, people have different versions of the protein. Having the ApoE4 genetic variant is one of the biggest risk factors for developing the disease.
Alzheimer's plaques (in brown) form around brain cells (in blue) and shrink parts of the brain
Scientists at the Case Western Reserve University in Ohio were investigating ways of boosting levels of ApoE, which in theory should reduce levels of beta-amyloid.
They tested bexarotene, which has been approved for use to treat cancers in the skin, on mice with an illness similar to Alzheimer's.
After one dose in young mice, the levels of beta-amyloid in the brain were "rapidly lowered" within six hours and a 25% reduction was sustained for 70 hours.
In older mice with established amyloid plaques, seven days of treatment halved the number of plaques in the brain.
The study said there were improvements in brain function after treatment, in nest building, maze performance and remembering electrical shocks.
Researcher Paige Cramer said: "This is an unprecedented finding. Previously, the best existing treatment for Alzheimer's disease in mice required several months to reduce plaque in the brain."
The research is at a very early stage, and drugs often do not make the leap from animal experiment to human treatment.
Fellow researcher Prof. Gary Landreth said the study was "particularly exciting and rewarding" and held the "potential promise of a therapy for Alzheimer's disease".
However, he stressed that the drug had been tested in only three "mouse models" which simulate the early stages of the disease and are not Alzheimer's.
Prof. Gary Landreth warned people not to "try this at home", as the drug had not been proven to work in Alzheimer's patients and there was no indication of what any dose should be.
"We need to be clear, the drug works quite well in mouse models of the disease. Our next objective is to ascertain if it acts similarly in humans," he said.
Prof. Gary Landreth's group is preparing to start trials in a small group of people to see if there is a similar effect in humans.
Alzheimer's disease is likely to become more common as people live longer.
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