There are currently more than 850,000 people in the UK living with dementia, of these between 50 to 75 per cent have Alzheimer’s. If current trends continue, the Alzheimer’s Society estimates that this figure could reach 1,590,000 by 2040.
There are as yet no effective treatments for Alzheimer’s, but a team from the University of Delaware how found new clues that diet could have an impact on the progression of the disease.
In the brains of humans with Alzheimer’s, the build-up of amyloid beta over the years causes toxic effects in cells, resulting in reduced energy, fragmentation of the mitochondria – the cells’ power plants – and oxidative stress.
In C. elegans, tiny soil-dwelling worms often used to study biology and disease thanks to their simple cell structure, a build-up of amyloid beta causes paralysis within 36 hours of them reaching adulthood – an effect that can be easily observed as they stop wriggling.
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The team found that when fed with E. coli containing higher levels of vitamin B12, C. elegans were protected from this paralysing effect.
“The read-out is black or white – the worms are either moving or they are not,” said lead researcher Prof Jessica Tanis. “When we gave vitamin B12 to the worms that were vitamin B12 deficient, paralysis occurred much more slowly, which immediately told us that B12 was beneficial. The worms with B12 also had higher energy levels and lower oxidative stress in their cells.”
After further study, the team discovered that the effect is only seen in the presence of a specific enzyme called methionine. They also found that adding the vitamin to the worms’ diet only helped if they were deficient in B12 to begin with – supplementing healthy animals with B12 had no effect.
“Right now, there is no effective treatment for Alzheimer’s disease,” Tanis said. “There are certain factors that you cannot change – you cannot change the fact that you age, and you cannot change a genetic predisposition to Alzheimer’s disease.
“But one thing you can control is what you eat. If people could change their diet to affect the onset of disease, that would be fantastic. That’s something my lab is excited to continue to explore.”
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The finding has been cautiously welcomed by Dr James Connell, Head of Translational Science at Alzheimer’s Research UK, who was not involved in the research.
“The human brain is incredible, with more connections in it, known as synapses, than astronomers have estimated there are stars in the galaxy. But this complexity makes diseases that cause dementia difficult to study, so using organisms like worms can be a great way for scientists to study disease. Research like this in worms helps understand the impact of a potential treatment and can help accelerate the development of drugs,” he said.
“Extensive research has been carried out into whether vitamin B12 without a pre-existing vitamin deficiency can protect against Alzheimer’s disease, with studies so far suggesting vitamin B12 supplements do not offer extra protection.
“While research in worms can support wider efforts to identify causes of disease and new treatments, clinical trials in people are the only way to find out if potential new approaches will improve people’s symptoms.”