Overeating and Memory Loss

A recent study shows that overeating more than 2,100 calories a day nearly doubled the risk of memory loss or mild cognitive impairment (MCI). The study concerned those over 70 years old and will be presented at the American Academy of Neurology’s 64th Annual Meeting in New Orleans April 21 to April 28, 2012. According to study author Yonas E. Geda, MD, MSc, with the Mayo Clinic in Scottsdale, Arizona and a member of the American Academy of Neurology, “We observed a dose-response pattern which simply means the higher the amount of calories consumed each day, the higher the risk of MCI.”

According to Wikipedia, MCI is a brain-function syndrome involving the onset and evolution of cognitive impairments beyond those expected based on the age and education of the individual, but which are not significant enough to interfere with their daily activities. It is often found to be a transitional stage between normal aging and dementia.

For this investigation, they turned to the Mayo Clinic Study on Aging, an ongoing, population-based cohort study in Olmsted County, Minnesota. The analysis involved 1233 nondemented participants aged from 70 to 89 years; 1070 patients were cognitively normal, and 163 had MCI.

The subjects noted the amount of calories they ate or drank in a food questionnaire. They were divided into three equal groups based on their daily caloric consumption.

  • One-third consumed between 600 and 1,526 calories per day.
  • One-third consumed between 1,526 and 2,143 calories per day.
  • One-third consumed between 2,143 and 6,000 calories per day.

The analyses were adjusted for history of stroke, diabetes, amount of education, and other factors that can affect risk of memory loss. The risk for the highest calorie group was nearly double that of the lower calorie group. There was no noticeable difference in risk for the middle group.

According to Geda, the findings should be considered preliminary. However, consuming in moderation is a good idea for other medical reasons as well.

The co-authors of the study include Ronald C. Petersen, MD, Fellow of the American Academy of Neurology, and other investigators of the Mayo Clinic Study of Aging in Rochester, Minn.

Enhanced by Zemanta

Scientists are looking at a biomaker that may possibly aid in the identification of individuals with mild memory problems who will eventually develop Alzheimer’s disease. The finding, which was published in the online version of Neurology, the journal of the American Academy of Neurology. It is believed that the new biomarker may prove to be more accurate compared to already established biomarkers.

According to the study author Robert Perneczky, MD, of the Technical University Munich in Germany, identifying individuals who will have Alzheimer’s disease earlier will be an important development. Once treatments that can be used for the prevention of the disease are available, it will become easier to treat and even prevent memory loss.

Fifty eight people with mild cognitive impairment (MCI) participated in the study. It is estimated that as many as 15% of the people who have MCI will develop Alzheimer’s every year.

Cerebrospinal fluid was taken from each participant and tested for certain proteins. Participants were then studied for about three years. Of the participants, 21 developed Alzheimer’s, 27 remained with MCI while 8 people regained normal cognitive skills. Researchers discovered that participants who later developed Alzheimer’s had significantly high levels of sAPPβ or soluble amyloid precursor protein beta in their cerebrospinal fluid.

Based on their findings, the researchers discovered that the person’s age, a protein called tau, and sAPPβ were excellent predictors of future cases of Alzheimer’s. Using these factors as a basis, it was easier to predict if an individual ran the risk of developing the disease. The accuracy for this prediction is pegged at about 80%.

A protein amyloid known as Aβ1-42 or amyloid beta1-42 was once considered one of the biomarkers significant to Alzheimer’s disease. However, it was not used as one of the predictive factors in the study.

The results, Perneczky said, suggest that sAPPβ could be useful as a biomarker and that it may even be better than Aβ1-42 for use in diagnosing Alzheimer’s earlier. The reason for this may be that Aβ1-42 can only indicate events at a later stage – events that already point to the accumulation of amyloid plaques in the brain. Since sAPPβ can be used as a critical initial step in determining if the disease will develop, it is likely to provide a more accurate indication on important pathological events.

Enhanced by Zemanta

As a person advances in age, the brain can lose up to 10% of its original weight. The brain compensates for the loss of the cells through redundancy and plasticity mechanisms. Sylvie Belleville, Ph.D., Research Director of the Institut universitaire de geriatrie de Montreal, has discovered that elderly individuals who have a high risk of suffering from Alzheimer’s disease may find hope in the brain’s plasticity mechanism.

Brain plasticity, according to Belleville, is the brain’s ability to modify itself and reorganize in order to adapt. The traditional view is that the brain’s plasticity declines with age, but a study headed by Belleville and published online through Brain: A Journal of Neurology shows that this is not true at all, even at the onset of Alzheimer’s disease.

The new findings are promising in the field of Alzheimer’s treatment and have the potential of encouraging new research into methods, therapies, treatments and medications that can improve the brain’s plasticity, thereby reducing the number and severity of Alzheimer’s disease in patients.

The study also shows that, at least hypothetically, cells known to promote the function of certain brain processes can take over using programs designed to train and enhance memories. For Belleville, the study simply validated that hypothesis. In the study, it was noted that subjects with MCI (mild cognitive impairment) who underwent memory tests after training had increased their correct answers by 33%. MCI is known to significantly increase an individual’s risk of developing dementia.

The program used a variety of strategies to train the subjects, such as encoding, retrieval and mnemonics. There were 30 participants in the study – half of them with MCI. The other group comprised of healthy adults. Using MRI, the subjects’ brain activities were monitored and analyzed at different times during the study – six weeks before training, one week before training and one week post-training. A comparison of brain activity using MRI showed activation in the brain areas that were known to work when used in memory exercises. Activation decreased in participants with MCI as expected but after training, brain activity increased not just in the memory areas but also in those associated with spatial, skill and object memory and language processing. This shows promise in future Alzheimer’s treatment and research.

Source: UdeMNouvelles

Enhanced by Zemanta

Vitamin B12 Deficiency and Cognitive Impairment

In my last post, I wrote about omega-3 fatty acid, a common supplement easily obtained. Vitamin B-12 is another supplement that may support brain health. According to the Oxford Project to Investigate Memory and Aging (OPTIMA), coordinated out of the University of Oxford, providing supplemental B vitamins to older adults with mild cognitive impairment (MCI) could slow age-related brain atrophy. Higher homocysteine (Hcy) levels appear to be linked with a faster rate of brain atrophy and cognitive decline, and using B vitamin supplements to lower those levels could preserve mental well-being.

The researchers concluded that the accelerated rate of brain atrophy in older adults with MCI can be slowed by intervention with B vitamins. They also stated 16 percent of adults over age 70 have MCI, and half of these develop Alzheimer’s disease, with adults with MCI who have accelerated brain atrophy more likely to develop Alzheimer’s disease. Therefore, they suggested further trials are needed to see if the B vitamin treatment could delay this progression.

Daniel Fabricant, Ph.D., vice president, global government and scientific affairs, Natural Products Association (NPA), commented, “This study is important because it emphasizes the importance of prevention. Also, it noted over time, people don’t sustain their levels of B vitamins and tend to have problems assimilating enough of them, particularly B12, from the diet. This will serve as a keystone for other research and longer term studies that can look at the potential of B vitamins as a preventive tool.” Click here to read the full article.

If you take a multi-vitamin, check to make sure B12 is included. Centrum Silver has 25 mcg which is 417% above the average daily recommended amount. Personally I take one of two vitamins — VitaOne contains 60 mcg of B12 (1,000%) and VitaChe contains 200 mcg of B12 (3,333%). Now I know why it gives me so much energy.

If you don’t take supplements, it may be a good idea to take B-12 supplements to avoid risk of deficiency of the vitamin.

In this, the third of our series of breakthrough tests for Alzheimer’s disease, scientists at the University of California San Diego (UCSD), have developed a fast and accurate method for quantifying subtle, sub-regional brain volume loss using magnetic resonance imaging (MRI). This study promises to improve diagnosis and monitoring of Alzheimer’s disease (AD).

The techniques were applied to the dataset of the multi-institution Alzhiemer’s Disease Neuroimaging Initiative (ADNI). What the scientists at UCSD were able to demonstrate was that the sub-regional brain volume measurements outperform available measures for tracking the severity of AD, including widely used cognitive testing and measures of global brain-volume loss.

According to insciences.org, the new research shows that changes in the brain’s memory regions, in particular a region of the entorhinal cortex, offer sensitive measures of the early stages of the disease. According to Anders M. Dale, PhD, professor of neurosciences and radiology at the UC San Diego School of Medicine, who led the study, “Loss of volume in the hippocampus is a consistent finding when using MRI, and is a reliable predictor of cognitive decline. However, we have now developed and validated imaging biomarkers to not only track brain atrophy, but distinguish the early stages of Alzheimer’s disease from changes related to normal aging.”

The study’s co-author, James Brewer, MD, PhD, a neurologist and assistant professor in the Departments of Radiology and Neurosciences at UCSD adds that, “The technique is extremely powerful, because it allows a researcher to examine exactly how much brain-volume loss has occurred in each region of the brain, including cortical regions, where we know the bad proteins of Alzheimer’s disease build up.”

If a picture is worth a thousand words, here are serial MRI brain scans, taken six months apart, that show progression from mild cognitive impairment to Alzheimer’s disease with significant atrophy (blue) and ventricle enlargement (orange/red).

For more information, see “Analyzing Structural Brain Changes in Alzheimer’s Disease” at insciences.org.

Reblog this post [with Zemanta]

UCLA Ronald Reagan Medical Center

As stated in the previous post, today there are no reliable tests to determine conclusively if a person has Alzheimer’s disease (AD). However, there are several breakthrough tests on the horizon that have us hopeful that soon we may have an accurate test to diagnose Alzheimer’s disease. In the last post, I covered what’s happening at the Blanchette Rockefeller Neurosciences Institute (BRNI) at West Virginia University and Inverness Medical Innovations. In this post I will report on the breakthrough test for Alzheimer’s disease at the University of California at Los Angeles (UCLA).

At UCLA, researchers have developed a blood test that would measure the amount of amyloid beta that is being absorbed by immune cells in the blood. If the immune system isn’t adequately clearing amyloid beta, it may indicate Alzheimer’s risk. According to Gen News, the UCLA scientists took blood samples and isolated monocytes including amyloid beta. The monocytes were incubated overnight with amyloid beta, which was labeled with a fluorescent marker. Using flow cytometry, the investigators then measured the amount of amyloid beta ingested by the immune cells.

The 18 Alzheimer’s disease patients in the study showed the least uptake of amyloid beta. The healthy control group, which consisted of 14 university professors, had the highest uptake.

The method was able to distinguish the Alzheimer’s disease patients with adequate sensitivity and specificity and the results were found to be positive in 94% of patients and negative for the entire control group. Additionally, the data was positive in 60% of participants who suffered from mild cognitive impairment.

Milan Fiala, M.D., is the lead author of the UCLA study, which appeared in the May 2009 issue of the Journal of Neuroimmunology.

Reblog this post [with Zemanta]

Depending on the source, some say there are seven (7) stages of Alzheimer’s disease while others say there are three (3). The Alzheimer’s Association says that there are seven (7) stages of Alzheimer’s disease. I will cover each stage of Alzheimer’s in separate posts.

Stage 1, according to the Alzheimer’s Association, is No Impairment (normal function). No evidence is apparent to a health care professional during a medical interview. In my post on What is Alzheimer’s Disease? I mentioned three ways that doctors determine how a diagnosis is made —

  1. Lab tests
  2. Neuropsychological testing (extensive assessment of thinking and memory skills)
  3. Brain scans

Apparently, Stage 1 only involves an interview since there is no evidence or reason for more extensive testing at this point. So why a Stage 1? If Stage 1 is normal functioning with no impairment, then it seems to me in order to determine a Stage 1, it is can only be determined AFTER a person has been diagnosed with Alzheimer’s disease. There is no abnormality in Stage 1. So after a person has been diagnosed, then we can go back and say this person with Alzheimer’s was in Stage 1.

On the other hand, it might be possible to detect a Stage 1 if you lived with someone or you know someone very well … a loved one whom you can detect mild memory loss or mild cognitive impairment or other signs and symptoms such as personality changes, all of which may indicate a future Alzheimer’s diagnosis. Or, if you personally feel that something is not right with your memory,  then you may possibly be in Stage 1 of Alzheimer’s disease, but Stage 1 means that you are still functioning normally. At this point, though, from a medical standpoint, an Alzheimer’s diagnosis is not possible. Other problems such as anxiety disorders, bipolar disorders, sleep problems, depression, or medications could also point to Alzheimer’s disease, but that would be conjecture at this time.

If you detect dementia, though, and if you are a future caregiver, you need to remember to most importantly take care of yourself. But it also gives you time to get things in order and prepare for the future. Through our continuous journey, I hope we can learn what to expect (even though each case is unique) and follow the Scout motto: “Be Prepared.”

Alzheimer’s Research Part 2

Taken from Reuters.com

from Reuters.com

In July of this year, Reuters reported that new tests assessing brain changes and body chemistry are showing promise at diagnosing Alzheimer’s disease in its earliest stages. Studies presented at an Alzheimer’s Association meeting in Vienna, Austria included:

  1. Irish researchers found scans measuring brain volume and a combination of memory tests accurately identified nearly 95 percent of people who had progressed from mild cognitive impairment to early Alzheimer’s disease.  Michael Ewers of Trinity College Dublin and colleagues studied 345 participants in the ADNI study with mild cognitive impairment, a precursor to Alzheimer’s. They looked at an array of tests and found three memory tests plus MRI measurements of brain volume in the left hippo campus — a region closely linked to memory — were most predictive of disease progression.
  2. U.S. researchers found that a type of brain scan that measures glucose combined with low scores on memory tests was a strong predictor of disease progression. Susan Landau of the University of California, Berkeley used data on 85 patients and found positron emission tomography scans that measure glucose in the brain and poor memory recall were strong predictors. People who did poorly on these measures were 15 times more likely to progress to Alzheimer’s within two years.
  3. A team at Duke University in North Carolina led by Dr. Allen Roses found that a gene called TOMM40 raises Alzheimer’s risk. The gene predicted the age of Alzheimer’s development within a five- to seven-year window in people over 60. It is closely linked to another Alzheimer’s gene called APOE4. Both APOE4 and TOMM40  account for an estimated 85-90 percent of the genetic effect according to Roses.

As was mentioned in Part 1, there’s progress, but we still have a long ways to go to find an effective test. But even if we were to have a conclusive test, doctors still have very few effective treatments for Alzheimer’s disease. And still, as it has been for a long time, only an autopsy will reveal definitively whether or not a person truly has Alzheimer’s disease.

Alzheimer’s Research Part 1

Although there is still no conclusive test for the determination of Alzheimer’s disease (AD), there is hope and occasionally, new information. Last month, Science Daily reported that:

Elderly people exhibiting memory disturbances that do not affect their normal, daily life suffer from a condition called “mild cognitive impairment” (MCI). Some MCI patients go on to develop Alzheimer’s disease within a few years, whereas other cases remain stable, exhibiting only benign senile forgetfulness. It is crucial to develop simple, blood-based tests enabling early identification of these patients that will progress in order to begin therapy as soon as possible, potentially delaying the onset of dementia.

A group of investigators, led by Professor Massimo Tabaton of the University of Genoa, Italy, have data that sheds light on this issue. The results of their research are published in the October issue of the Journal of Alzheimer’s Disease.

The investigators report that the concentration in blood of amyloid beta “42,” the toxic molecule that is believed to be the main cause of Alzheimer’s disease, is, on average, higher in MCI cases that went on to develop Alzheimer’s disease approximately three years later. The values of amyloid beta in blood vary considerably among the patient groups examined (MCI that develop Alzheimer’s disease; MCI stable; normal subjects). “This variability is likely very important,” Dr. Tabaton noted and went on to add, “but means that this needs further work before we can use this test for a definitive diagnosis.” For example, the scientists are going to set up a test that picks up a variant of amyloid beta potentially more specific of the disease.

There’s progress, but we still have a long ways to go to find an effective test. A conclusive blood test would certainly be ideal. But even if we were to have a conclusive test, doctors still have very few effective treatments for Alzheimer’s disease. And still, as it has been for a long time, only an autopsy will reveal definitively whether or not a person truly had Alzheimer’s.

Click Here to share this page with your friends, website visitors, ezine readers, social followers and other online contacts.