Souvenaid and Alzheimer’s Disease

Souvenaid, in its second clinical trial, has been proven to help the memory of people who suffer from mild Alzheimer’s disease (AD). Results of the trial were given at the 4th International Conference on Clinical Trials in Alzheimer’s Disease (CTAD) by Philip Scheltens, MD, PhD in San Diego in early November. Scheltens is head of the Alzheimer Center at the VU University Medical Center in Amsterdam.

Souvenaid has a unique mixture of nutrients that work by stimulating the connections between nerves, also known as synapses. Losing these connections is what many experts think is responsible for losing memory in Alzheimer’s patients.  Studies demonstrate that the nutrients in Souvenaid can help grow new synapses in the brain. People taking Souvenaid daily over three months had improved scores on memory tests.

Scheltens is cautiously optimistic about the new findings. More research needs to be done before any conclusions can be drawn, but he thinks it is a step in the right direction.

Souvenir II was completed at  27 centers in six countries in Europe to see if the effects from Souvenir I would last for eight weeks. This study used additional measures to test for recall and also measured brain activity. Of 259 subjects, over 91% finished the study.

Memory was tested at the beginning, at 12 weeks, and at 24 weeks. The composite score was gotten from the Rey Audtiory Verbal Test which tests instant recall, delayed memory, and recognition. The Wechlser Scale which tested verbal association was also used.

Over the 24 weeks, the total scores from the Souvenaid group were much higher than those from the control group. Besides just looking at memory scores, they are attempting to analyze the electroencephalogram and magnetoencephalogram data, which may help figure out the influence  Souveniad has on synapse building in patients with Alzehimer’s disease and dementia.

CTAD is sponsored by the University of California, San Diego School of Medicine and the European Alzheimer’s Disease Consortium (EADC).

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

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Phosphatidylserine Memory Booster

Last month a friend gave me an issue of  Woman’s World magazine. In it was a tiny article, Ward off Alzheimer’s with the new “Memory” Pill! As the author of this Alzheimer’s disease blog, that certainly caught my attention. It’s called phosphatidyl serine (PS) or more commonly spelled as one word in the scientific community, phosphatidylserine. It says, “it’s a supplement proven to prevent age-related memory loss and help your brain function as if it were 12 years younger!” Now, wouldn’t that catch your attention, too? Could we all use a memory booster?

Since it’s such a short article, let me share the rest of it.

PS helps restore the brain’s supply of acetycholine, a neurotransmitter that’s crucial for memory, reports Thom Lobe, M.D., of Beneveda Medical Group in Beverly Hills, California. In one study, folks who took 100 mg., three times a day, scored 30% higher on memory tests after just 12 weeks! Your Rx: 200 mg. to 300 mg. daily in supplement form (find it in health-food stores). Important: Ask your doctor before taking this or any supplement, especially if you also take an anticoagulant drug.

If phosphatidylserine is such an impressive supplement, shouldn’t all Alzheimer’s patients be on it? According to the Mayo Clinic, “Several studies involving phosphatidylserine indicate a benefit — improved cognitive abilities and behaviors. However, improvements in memory lasted only a few months and were seen in people with the least severe symptoms.” They go on to say that earlier studies were based on brain cells of cows. However, because of concerns about mad cow disease, most manufacturers now produce phosphatidylserine supplements from soy or cabbage derivatives. So it’s not really known if the plant-based supplements are equally effective.

WebMD adds that phosphatidylserine is a chemical that the body can make, but it gets most of what it needs from foods. Side effects include insomnia and upset stomach for doses over 300 mg. They warn that there could be drug interactions. Click here for more information and click on Interactions.

So the old adage, if it’s too good to be true, it probably is, appears to be in effect here. Have you ever taken phosphatidylserine? What is your opinion?

Alzheimer’s Research Part 2

Taken from


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.

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What is Alzheimer’s Disease?

Take the Alzheimer's Association's Brain Tour

Brain Tour from Alzheimer's Association (click image)

Just what is Alzheimer’s disease (AD)? Everyone seems to agree that it is the most common form of dementia accounting for at least half of all dementia cases. (See previous post on discussion of dementia). There is also agreement that in advanced Alzheimer’s disease, a person cannot function intellectually and socially. According to the Mayo Clinic, “Alzheimer’s disease is not a part of normal aging, but the risk of the disorder increases with age. About 5 percent of people between the ages of 65 and 74 have Alzheimer’s disease, while nearly half the people over the age of 85 have Alzheimer’s.”

What is happening in the brain that is causing a person not to be able to function intellectually and socially? Take the “Brain Tour” on the left and notice the shrinkage of the brain as well as the tangles. Just looking at those pictures explains the confusion, doesn’t it?

According to the Mayo Clinic, there are currently three major areas that doctors depend on to make a diagnosis:

  1. Lab tests
  2. Neuropsychological testing (extensive assessment of thinking and memory skills)
  3. Brain scans
    • Magnetic resonance imaging (MRI)
    • Computerized tomography (CT)
    • Positron emission tomography (PET)

Although memory assessments should always be conducted by a medical practitioner, here are two quick paper and pencil tests. The first was published by Times Online (UK) called the “Five Minute Alzheimer’s Test.” The second one is on the Web site of a well-known Alzheimer’s drug, but it states, “This screening tool cannot be used to tell if your loved one has a medical problem, only whether he or she should be tested.” It was adapted from Galvin JE, et al. The AD8, a brief informant interview to detect dementia. Neurology 2005:65:559-564.

Once again, do not draw any conclusions from these memory tests. As discussed by Carrie Hill, Ph.D. in “What you Need to Know about Screenings for Memory Problems,” she states:

  1. A memory screening should not be used to make a diagnosis
  2. A memory screening does not replace a diagnostic workup
  3. Memory screenings should only be performed by qualified professionals
  4. Memory screenings should be confidential and provide follow-up resources
  5. Memory screenings can be used to establish a baseline
  6. Opinions differ on the value of memory screenings. Here she talks about the different views of the two leading non-profit Alzheimer’s organizations — Alzheimer’s Foundation of America and Alzheimer’s Association.

In our next blog post next week, we will look at the most recent diagnosis tools. In the meantime, have you done your Sudoku for today?

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