The Right Diet Could Lower The Risk Of Alzheimers Disease

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June 15, 2010

The right diet could lower the risk of Alzheimer’s disease

The right diet could lower the risk of Alzheimer’s disease

An article published online on June 2, 2010 in FASEB Journal reports the discovery of Temple University researchers of the benefit of a low methionine diet in slowing or reversing early to moderate stage Alzheimer's disease in an animal model. Methionine is an essential amino acid that occurs in relatively high amounts in red meat, fish, eggs and other foods. A byproduct of methionine metabolism is homocysteine, another amino acid that has been linked to an increased risk of Alzheimer's disease as well as cardiovascular disease when elevated.

Acting on previous findings of an association between a methionine-rich, homocysteine-elevating diet and an increased risk of Alzheimer's disease in a mouse model, Domenico Praticò and postdoctoral student Jia-Min Zhuo sought to determine the effects of lowering homocysteine in the same strain of transgenic mice. In the current study, the animals were divided to receive a high methionine diet or a healthy (control) diet for 5 months, following which the group receiving the methionine-rich diet was subdivided to receive either the same regimen or the healthy diet for two months. "The question we asked now as a follow-up is if, for whatever reason, you had made bad choices in your diet, is there a chance you can slow down or even reverse the disease or is it too late — that there is nothing you could do," Dr Praticò explained.

Mice on the methionine-rich diet had higher homocysteine levels and significant behavioral impairments at 5 months compared to the control group. While those that remained on the high methionine diet continued to show elevations in homocysteine, those that were switched to the healthy diet experienced reductions in homocysteine to levels similar to those of the control group as well as improvements in fear-conditioning performance and a decrease in brain amyloid levels, which are elevated in Alzheimer's disease.

"At the end of the study, when we looked at these mice, what we found — very surprisingly — was that switching to a more healthy diet reversed the cognitive impairment that had built up over the first three months of eating the methionine-rich diet," Dr Praticò reported. “This improvement was associated with less amyloid plaques — another sign of the disease — in their brains.”

"We believe this finding shows that, even if you suffer from the early effects of mild cognitive impairment or Alzheimer's, switching to a healthier diet that is lower in methionine could be helpful in that memory capacity could be improved," he added. "What it tells us is that the brain has this plasticity to reverse a lot of the bad things that have occurred; the ability to recoup a lot of things such as memory that were apparently lost, but obviously not totally lost."

"This combination won't cure you, but we believe, as we saw in this study, that it will be able to slow down or even possibly reverse the effects on the cognitive impairment," he said.

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Homocysteine reduction

Homocysteine is an intermediary amino acid; its role in the body is complex, but very important. Homocysteine is a necessary byproduct of a healthy metabolism. Homocysteine is produced as part of the methionine cycle, in which methionine is converted to S-adenosylmethionine (SAMe). SAMe is valuable because of its ability to donate methyl groups during chemical reactions throughout the body. Homocysteine is synthesized when SAMe donates its methyl group. In scientific terms, this means the SAMe has been methylated (lost a methyl group). Methylation is crucial to the health of our cells and tissues by regulating gene expression, protein function, and RNA metabolism.

The methionine cycle is responsible for the creation of all the homocysteine in the body. Most of the resulting homocysteine is bound to plasma and considered stored, or inactive. It may be released into the bloodstream as free homocysteine in response to adverse changes in the body's biochemistry. Thus, high levels of homocysteine are linked to specific health problems. There is also evidence that homocysteine itself causes damage to the cells within blood vessels. Homocysteine in the bloodstream is metabolized through two principal pathways. It may be remethylated back into methionine through a process that involves folic acid (folate) and vitamin B12. This is called the remethylation pathway and is responsible for consuming most of the body's free homocysteine. The remethylation pathway creates more SAMe to support healthy methylation. (Some organs, namely the kidney and liver, are able to remethylate homocysteine directly back into SAMe, but only a fraction of homocysteine is processed in this way.)

Alternatively, some of the excess homocysteine may be used to create cysteine, which is then converted into glutathione. Glutathione is an important and powerful antioxidant. The conversion of homocysteine into glutathione may be accelerated when the body is under oxidative stress. This second process is called the transsulfuration pathway because it produces sulfate byproducts that are flushed from the body in urine. The transsulfuration pathway depends on vitamin B6 to work properly.

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