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.
US scientists have found that a lifetime of too much copper in our diets may be contributing to Alzheimer’s disease.
However, research is divided, with other studies suggesting copper may actually protect the brain.
The latest study in Proceedings of the National Academy of Sciences showed high levels of copper left the brain struggling to get rid of a protein thought to cause the dementia.
Copper is a vital part of our diet and necessary for a healthy body.
Tap water coming through copper pipes, red meat and shellfish as well as fruit and vegetables are all sources of dietary copper.
The study on mice, by a team at the University of Rochester in New York, suggested that copper interfered with the brain’s shielding – the blood brain barrier.
Mice that were fed more copper in their water had a greater build-up of the metal in the blood vessels in the brain.
A lifetime of too much copper in our diets may be contributing to Alzheimer’s disease
The team said this interfered with the way the barrier functioned and made it harder for the brain to get rid of a protein called beta amyloid.
One of the hallmarks of Alzheimer’s disease is the formation of plaques of amyloid in the dying brain.
Lead researcher Dr. Rashid Deane said: “It is clear that, over time, copper’s cumulative effect is to impair the systems by which amyloid beta is removed from the brain.”
He said that copper also led to more protein being produced: “It’s a double whammy of increased production and decreased clearance of amyloid protein.
“Copper is a very essential metal ion and you don’t want a deficiency and many nutritious foods also contain copper.”
However, he said taking supplements may be “going overboard a bit”.
Commenting on the latest findings, Chris Exley, professor of bioinorganic chemistry at Keele University in the UK, said there was “no true consensus” on the role of copper in Alzheimer’s disease.
His research on human brains reached the opposite conclusion: “In our most recent work we found evidence of lower total brain copper with ageing and Alzheimer’s. We also found that lower brain copper correlated with higher deposition of beta amyloid in brain tissue.
“He said at the moment we would expect copper to be protective and beneficial in neurodegeneration, not the instigator, but we don’t know.
“The exposure levels used mean that if copper is acting in the way they think it does in this study then it must be doing so in everyone.”
A new study has revealed that some of the earliest signs of Alzheimer’s disease have been found in the brain, more than two decades before the first symptoms usually appear.
Treating the disease early is thought to be vital in order to prevent damage to memory and thinking.
A study, published in the Lancet Neurology, found differences in the brains of people destined to develop an early form of Alzheimer’s.
Experts said the US study may give doctors more time to treat people.
Alzheimer’s disease starts long before anyone would notice; previous studies have shown an effect on the brain 10-15 years before symptoms.
It is only after enough brain cells have died that the signs of dementia begin to appear – some regions of the brain will have lost up to 20% of their brain cells before the disease becomes noticeable.
However, doctors fear so much of the brain will have degenerated by this time that it will be too late to treat patients. The failure of recent trials to prevent further cognitive decline in patients with mild to moderate Alzheimer’s disease has been partly put down to timing.
A team at the Banner Alzheimer’s Institute in Arizona looked at a group of patients who have familial Alzheimer’s. A genetic mutation means they nearly always get the disease in their 40s. Alzheimer’s normally becomes apparent after the age of 75.
Brain scans of 20 people with the mutation, aged between 18 and 26, already showed differences compared with those from 24 people who were not destined to develop early Alzheimer’s.
The fluid which bathes the brain and spinal cord also had higher levels of a protein called beta-amyloid.
The researchers said differences could be detected “more than two decades before” symptoms would appear in these high-risk patients.
Dr. Eric Reiman, one of the scientists involved, said: “These findings suggest that brain changes begin many years before the clinical onset of Alzheimer’s disease.
“They raise new questions about the earliest brain changes involved in the predisposition to Alzheimer’s and the extent to which they could be targeted by future prevention therapies.”
Prof. Nick Fox, from the Institute of Neurology at University College London, said some of his patients had lost a fifth of some parts of their brain by the time they arrived at the clinic.
He said: “I don’t think this pushes us forwards in terms of early diagnosis, we already have markers of the disease.
“The key thing this does is open up the window of early intervention before people take a clinical and cognitive hit.”
However, he said this raised the question of how early people would need to be treated – if drugs could be found.
A bad sleep may be an early sign of Alzheimer’s if a study in mice also applies to people, say researchers.
Clumps of protein, called plaques, in the brain are thought to be a key component of the illness.
A study, published in the journal Science Translational Medicine, showed that when plaques first developed, the mice started having disrupted sleep.
The hunt for early hints that someone is developing Alzheimer’s is thought to be crucial for treating the disease.
A bad sleep may be an early sign of Alzheimer's if a study in mice also applies to people
People do not show problems with their memory or clarity of thought until very late on in the disease. At this point, parts of the brain will have been destroyed, meaning treatment will be very difficult or maybe even impossible.
It is why researchers want to start early, years before the first symptoms.
One large area of research is in plaques of beta amyloid which form on the brain.
Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people. However, the protein forms permanent plaques in Alzheimer’s disease.
Experiments at Washington University showed that nocturnal mice slept for 40 minutes during every hour of daylight. However, as soon brain plaques started to form the mice were sleeping for only 30 minutes.
One of the researchers, Prof. David Holtzman, said: “If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of [the disease].”
“If these sleep problems exist, we don’t yet know exactly what form they take, reduced sleep overall or trouble staying asleep or something else entirely.”
However, findings in mice do not always apply to people are there are many reasons for disrupted sleep.
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.