Posted by: miriamjang | March 24, 2011

Alzheimer’s disease: Healthy diet could slow or reverse early effects

Patients in the early to moderate stages of Alzheimer’s Disease could have their cognitive impairment slowed or even reversed by switching to a healthier diet, according to researchers at Temple University.
In a previous study [http://www.temple.edu/newsroom/2009_2010/12/stories/alzheimers.htm], researchers led by Domenico Praticò, an associate professor of pharmacology in Temple’s School of Medicine, demonstrated that a diet rich in methionine could increase the risk of developing Alzheimer’s Disease. Methionine is an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds.
“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,” said Praticò.
As in the previous study, the researchers fed one group of mice a diet high in methionine and another group a regular, healthy diet. After three months, they split the group receiving the methionine-rich diet into two, with one group continuing the amino-heavy diet while the second switched to the healthy diet for an additional two months.
“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,” said Praticò. “This improvement was associated with less amyloid plaques — another sign of the disease — in their brains.
Pratico said that the cognitive impairment that had been observed in the mice after three months on the methionine-rich diet was completely reversed after two months on the healthier diet, and they were now able to function normally.
“We believe this finding shows that, even if you suffer from the early effects of MCI or Alzheimer’s, switching to a healthier diet that is lower in methionine could be helpful in that memory capacity could be improved,” he said.
Pratico stressed that this was not a drug therapy for curing MCI or Alzheimer’s, but that it did demonstrate that a lifestyle change such as diet can improve some of the impairments that have already occurred in the brain.
“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,” he said.
Pratico also emphasized that the researchers believe that in addition to switching to a healthy diet, patients diagnosed with MCI or Alzheimer’s also need a regiment of physical as well as mental exercises.
“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.
###
The study, ”
improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer’s disease,” is being published in the Journal of the Federation of American Societies for Experimental Biology (http://www.fasebj.org/). It was funded by a grant from the National Institutes of Health.
Copies of this study are available to working journalists and may be obtained by contacting Preston M. Moretz in Temple’s Office of University Communications at pmoretz@temple.edu.

Published online before print June 2, 2010 as doi: 10.1096/fj.10-161828.
Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer’s disease
Jia-Min Zhuo and Domenico Praticò
E-mail contact: praticod@temple.edu
Hyperhomocysteine (HHcy) is a risk factor for developing Alzheimer’s disease (AD). Previously, we showed that diet-induced HHcy accelerated the AD-like phenotype of a transgenic mouse model, i.e., Tg2576. In the present work, we tested whether an HHcy-lowering strategy in this model would be beneficial. Tg2576 mice received methionine-rich or regular chow diet for 5 mo. Next, while the chow control group was kept on the same regimen, the other mice were randomized into two groups: one was kept on the methionine-rich diet (Met On), the other switched to chow (Met Off). Compared with controls, 5 mo on the methionine-rich diet resulted in HHcy (plasma Hcy level, treated: 12.7±1.2 μM vs. control: 3.1±0.4 μM) and significant behavioral impairments (% freezing, treated: 2.4±1.4% vs. control: 19.9±6.9%). At the end of the study, while the Met On group kept Hcy level elevated, the Met Off group had these values indistinguishable from the controls. The reduction in Hcy levels resulted in a significant improvement of the fear-conditioning performance, and an amelioration of the brain amyloidosis. Our results demonstrate that lowering HHcy in a transgenic AD-mouse model is beneficial since it significantly improves behavior deficits and brain amyloidosis. Our findings provide new biological insights for future clinical trials aimed at lowering this modifiable risk factor in human AD.—Zhuo, J.-M., Praticò, D. Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer’s disease.

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