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In the Media

article imageStudy: Vitamin B treatment can prevent Alzheimer's disease

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By JohnThomas Didymus
May 21, 2013 in Health
By JohnThomas Didymus.
A new study shows that elderly people at risk could stave off Alzheimer's disease by taking vitamin B supplements. The study shows that Vitamin B with folic acid reduces brain atrophy in areas of the brain associated with Alzheimer's by up to 90 percent.
The study, published in the journal Proceedings of the National Academy of Sciences (PNAS), titled, "Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment," was designed to determine whether consuming high doses of Vitamins B6, B12 and folic acid could stave off development of Alzheimer's. It found that patients who received high doses of B vitamins were protected from brain shrinkage occurring mostly in those areas of the brain linked to development of Alzheimer's.
The research (PDF) was based on data from a two-year trial conducted at Oxford University. It involved 156 patients, 70 years and older, showing signs of mild cognitive impairment (MCI) believed to be a precursor of full blown Alzheimer's. The initial results published in the journal PLOS ONE in 2010 showed that patients with mild cognitive impairment who took high doses of vitamin B suffered 50 percent less whole-brain shrinkage than those who took placebo pills.
The authors explained in the abstract of the new study published in the journal PNAS:
In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjects with high homocysteine levels are warranted to see if progression to dementia can be prevented.
They participants were administered memory and cognitive tests and their brains were scanned using magnetic-resonance imaging. Blood levels of the protein homocysteine were taken at the beginning and end of the study.
The patients had mild memory loss and high levels of homocysteine.
The study showed that those taking high doses of Vitamin B had 90 percent less shrinkage of gray matter than those on placebo pills, a level much higher than the previous study had estimated.
This picture by the National Institute of Health compares a healthy brain to a brain damaged by Alzh...
National Institutes of Health via Wikimedia Commons
This picture by the National Institute of Health compares a healthy brain to a brain damaged by Alzheimer's Disease.
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Bloomberg reports Dr David Smith, professor emeritus of pharmacology at Oxford, who led the study, said: "It’s a big effect, much bigger than we would have dreamt of. I find the specificity of this staggering. We never dreamt it would be so specific."
The Daily Mail reports he said: "Our work shows that a key part of the disease process that leads to Alzheimer’s disease, the atrophy of specific brain regions, might be modified by a safe and simple intervention."
One of the signs of Alzheimer's is a rapidly shrinking brain. Although a rate of loss of gray matter of about 0.5 per cent a year is normal as we get older, it is as high as one per cent in people with mild cognitive impairment and two-and-a half per cent in people with Alzheimer's. Mild cognitive impairment precedes Alzheimer's in some people, according to neuroscientists, but some people with signs of mild cognitive impairment never develop full Alzheimer's.
While the initial study looked at the effect of vitamin B therapy on the whole brain, the new study concentrated on the effect on those areas of the brain that Alzheimer's specifically targets. It showed that areas of the brain that the vitamin B doses protected from damage were those associated with learning and memory and which degenerate in the course of Alzheimer's disease.
The study (PDF) also established a connection between shrinkage and cognitive impairment, that is, slowing down the rate of brain shrinkage through vitamin B therapy was linked to a slowing down in the development of Alzheimer's disease.
Paul Thomspon, professor of neurology and head of the Imaging Genetics Center at UCLA School of Medicine California, said: "I've never seen results from brain scans showing this level of protection."
The study (PDF) found that consuming Vitamins B6, B12 and folic acid can lower levels of homocysteine, an amino acid linked to brain shrinkage, and found in high levels in patients with Alzheimer's disease.
Homocysteine levels are lower in people who do not have Alzheimer's. The amino acid is readily converted into chemicals such as acetylcholine which play a role in memory formation. However, impairment of the process of conversion of homocysteine leads to build up of the substance in the brain. People with Alzheimer's have been found to have low levels of acetylcholine and many drugs developed to fight Alzheimer's work by boosting acetylcholine levels.
Vitamin B appears to boost the conversion of homocysteine to acetylcholine.
The results come at a time that research into drugs to cure or slow down the development of Azheimer's have largely failed. Bloomberg reports that the US Food and Drug Administration has not cleared new drugs for dementia in a decade. According to Bloomberg, a joint US-European Union task force in 2011 found that all treatments for Alzheimer’s in the previous decade failed late-stage trials after huge financial expenditure.
Smith, commenting on the promising results of the vitamin B trials, said: "It’s the first and only disease-modifying treatment that’s worked. We have proved the concept that you can modify the disease."
Vitamin B12 is found most abundantly in animal food products especially meat, liver, fish and milk, while folic acid is found in fruits and vegetables.
Although scientists are excited at the prospects that a simple and cheap regimen of vitamins could achieve what decades of research costing billions of dollars has failed to achieve, some experts have cautioned against drawing firm conclusions too soon. Dr Eric Karran, Director of Research at Alzheimer’s Research UK, said: "It is too early to know whether these effects mean someone is less likely to develop dementia in the long term. It is also not clear from other research in this area whether B vitamins would have any benefit for those who already have dementia. Until further trials have confirmed these findings, we would recommend people think about eating a healthy and balanced diet. Controlling weight and blood pressure, as well as taking exercise, are also ways that we can help to keep our brains healthy as we get older."
Bloomberg reports that Joshua Miller, a professor in the department of nutritional sciences at Rutgers University in New Brunswick, New Jersey, said: "If you have somebody who has outright Alzheimer’s disease, this isn't really going to help them much. If you can catch them at an earlier level, they may be able to benefit from it but only if you have elevated homocysteine."
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More about Alzheimer's, vitamin b, Alzheimer's disease, mild cognitive impairment, MCI
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