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Wednesday, January 22, 2014

More Data on DHA and AD


Dear Readers,

As many of you are aware, there is growing evidence that dietary changes can affect the brain’s structure and even functioning. For example, higher adherence to a Mediterranean-type diet has been shown to be associated with decreased cognitive decline. The typical dietary pattern of the Mediterranean-type diet is characterized by a high intake of vegetables, fruits and nuts, legumes, ?sh and monounsaturated fatty acids; relatively low intakes of meat and dairy products; and moderate consumption of alcohol. In fact, higher consumption of olive oil, very rich in monounsaturated fatty, is considered the hallmark of the traditional Mediterranean-type diet.

One particular form of omega-3 fatty acid, called DHA, which is the most abundant fatty acid in the brain, has been of particular interest in regards to AD. In 2006, researchers at the USDA Human Nutrition Research Center on Aging at Tufts University found individuals with the highest DHA levels had a 47% reduction in all-cause dementia and a 39% lower risk of developing AD. In that study, which was a nine-year prospective, follow-up cohort study researchers analyzed completed dietary questionnaires and measured DHA blood levels of 899 study subjects who were participating in the Framingham Heart Study.

Neuropsychological testing revealed that all study participants were dementia-free at baseline. Thereafter, subjects had their cognitive function tested every two years using the Mini-Mental State Examination (MMSE). Those who experienced a decline of three or more points on the MMSE from the most recent exam were called back for a neurological and neuropsychological examination. The study population was 36.5% male and had an average age of 76 years. Plasma samples were measured for plasma DHA. In addition, a subgroup of 488 patients completed dietary questionnaires.

During the study period, 99 of 899 subjects developed dementia, including 71 cases of AD. Researchers divided individuals into quartiles according to their blood DHA levels. Those in the upper quartile experienced a significantly lower risk of all-cause dementia and AD compared with participants with levels in the lower three quartiles.

However, there are two ways to measure blood DHA: to directly measure it in the plasma fraction of blood, or to measure it within the red blood cells. It turns out that red blood cell DHA reflects dietary DHA intake up to 120 days, whereas plasma concentrations reflect intake over only the last few days.

Last year, researchers looked at red blood cell DHA levels and found that lower red blood cell DHA levels are associated with smaller brain volumes even in persons free of clinical dementia. The MRI finding of lower brain volume represents a change equivalent to approximately two years of structural brain aging.

For the latest study, Pottala and colleagues looked at the omega-3 fatty acids levels in the red blood cells of 1,111 women who participated in the Women's Health Initiative Memory Study. The women had MRI scans eight years after the study began to measure their brain volume. They were an average of 78 years old. Those with the highest levels of omega-3 fatty acids in their red blood cells had a 2.7% larger volume in the hippocampus portion of the brain compared with those with the lowest levels of omega-3 fatty acid and those with the highest levels of omega-3 fatty acids in their blood had 0.7% larger overall brain volume compared with those with the lowest levels.

What do these results mean? More data is accumulating that high dietary omega-3 acid levels may reduce the risk of AD in healthy individuals and also reduce the atrophy or shrinkage rate of the brain, including that of the hippocampus. Of course, one must consult with their doctor or pharmacist before purchasing or taking any supplement, as they can interact with medications. But we remain excited about the possibility that diet may influence AD risk.


Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 4:17 PM 0 Comments

Wednesday, January 15, 2014

Potential Early Biomarker of AD


Dear Readers,

Many readers are familiar with Apolipoprotein E, and its effects on AD risk. Now, another protein called apolipoprotein J, also called ‘clusterin’ has been implicated in AD. Apolipoprotein J, turns up repeatedly in large genome-wide association studies of Alzheimer’s disease. The protein is known to be involved in the clearance of cellular debris and prior studies have suggested that people who already have Alzheimer's disease have more Apo J in their blood. In fact, Apo J levels in blood correlate with faster cognitive decline in individuals with Alzheimer's disease.

Now, researchers led by Rahul Desikan at the University of California, San Diego, found that a combination of low beta-amyloid and high Apo J in the cerebrospinal fluid (CSF) of people without dementia identifies those who have the earliest signs of brain atrophy as judged by MRI imaging. The specific atrophy seen in AD is shrinkage of the part of the brain called the entorhinal cortex, and this is exactly what was observed.

The entorhinal cortex is a hub in a widespread network for memory and navigation, and connects the hippocampus with the rest of the brain. The entorhinal cortex is the first area of the brain that degenerates in AD, and is the entry way of information into the hippocampus which consolidates short term memory into long term memory. As such, atrophy and dysfunction of the entorhinal cortex, as well as that of the hippocampus, is thought to serve as the basis for the extensive memory loss observed in AD.

What do the findings of this paper mean? Apo J may be a potential early biomarker of AD. It also helps explain the mechanism by which beta-amyloid causes degeneration, by its known interactions with Apo J. More work is needed, but this paper has certainly brought Apo J into the spotlight.



Thanks for reading,


Michael Rafii, MD, PhD
Director, Memory Disorders Clinic
Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California San Diego
 
Author: Michael Rafii MD, PhD at 2:14 PM 0 Comments

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The Alzheimer's Disease Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a major initiative for Alzheimer's disease (AD) clinical studies in the Federal government, addressing treatments for both cognitive and behavioral symptoms. This is part of the NIA Division of Neuroscience's effort to facilitate the discovery, development and testing of new drugs for the treatment of AD and also is part of the Alzheimer's Disease Prevention Initiative.

The ADCS was developed in response to a perceived need to advance research in the development of drugs that might be useful for treating patients with Alzheimer's disease (AD), particularly drugs that might not be developed by industry.