Exercise and Alzheimer’s Disease

As revealed in the Journal of Biological Chemistry “Paper of the Week,” Ayae Kinoshita, a researcher at the Kyoto University Graduate School of Medicine in Japan, exercise is of great significance in fighting against Alzheimer’s disease. Alzheimer’s disease mostly occurs in individuals who are above 65 years of age and is one of the common causes of dementia. This disease is attributed to a number of factors that include the lack of regular exercise as well as an unhealthy diet that includes excess fats.

The research done by Kinoshita included a comparative analysis of voluntary exercise, diet control, and a combination of exercise and diet control in a mouse model with Alzheimer’s disease. Results indicated that regular exercise was of more benefit in reducing formation of β-amyloid—typical characteristic of Alzheimer’s disease — compared to diet control. In addition, exercise triumphed over diet control in restoration of memory loss induced by a fat-rich diet in the mice models. On the basis of this research, the Kyoto University expert recommends that the first priority should be given to exercise in the prevention of Alzheimer’s disease.


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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).

According to an article published in Translational Neuroscience, a study done at the Mount Sinai School of Medicine found that patients with Alzheimer’s disease (AD) have lower glucose utilization in the brain than those with normal cognitive function. The decreased levels could possibly be detected 20 years prior to the first symptoms of AD. With this knowledge comes the possibility of developing new therapies of preventing the start of Alzheimer’s.

In the article reported at NeuroScienceNews.com (http://tinyurl.com/3ompjp6), the study used mice modified to develop Alzheimer’s disease. The research team found that when β-amyloid, an abnormal protein linked to Alzheimer’s disease, starts to become detectable in the brain in its soluble toxic form, the mitochondria, or “power plants” of the cell where glucose is converted into energy, became impaired. Within the equivalent of about 20 human years, mice with decreased energy metabolism developed signs of Alzheimer’s disease such as cognitive defects and impairment of the synaptic terminal, the area of brain cells important in memory formation.

“This evidence in mice validates that the diagnosis of probable Alzheimer’s disease may be the end result of impairment in brain cell energy production,” said the study’s lead author, Giulio M. Pasinetti, MD, PhD, The Saunder Family Professor in Neurology, and Professor of Psychiatry, Geriatrics, and Adult Development at Mount Sinai School of Medicine. “Identifying that mitochondrial impairment is evident years earlier than cognitive defects is a major breakthrough.”

“This new evidence could revolutionize the way we design interventions,” said Merina T. Varghese, MD, co-author of the study and Postdoctoral Fellow in Neurology at Mount Sinai School of Medicine. “This study sets the stage for the development of potential novel preventions or therapies to apply in humans, even when they have normal cognitive function, to prevent the eventual onset of Alzheimer’s disease.”

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A new gene called MTHFD1L has been discovered by a team of researchers led by Margaret Pericak-Vance, Ph.D., director of the John P. Hussman Institute for Human Genomics (HIHG) at the University of Miami Miller School of Medicine. It appears to increase the risk of late-onset Alzheimer’s disease (AD) which accounts for 95% of Alzheimer’s cases. This gene might explain about 5 percent of the inherited AD. The study found that individuals with a particular variation in the gene MTHFD1L may be almost twice as likely to develop AD as those people without the variation.

So far, we believe that:

  • 60 to 80% of Alzheimer’s disease is attributable to genetic and environmental factors
  • 40% of that genetic effect is attributable to the ApoE4 variant

The importance of this study is that high levels of homocysteine are a strong risk factor for late-onset Alzheimer’s disease and the MTHFD1L gene is associated with the metabolism of folate and the raised homocysteine level. Look for foods rich in folate to increase your homocysteine level. Click here for suggestions. If you go for a physical on a regular basis, be sure to have your doctor include the homocysteine test in your blood work.

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In my last post, I talked about the possible shift in the cause of Alzheimer’s disease (AD) from sticky plaques to free-floating clumps of amyloid beta protein (oligomers). It’s possible that the sticky plaques may actually be protecting the toxic clumps and not the cause as was previously thought. Sam Gandy, MD, of the Alzheimer’s Disease Research Center at Mount Sinai School of Medicine in New York, has been working with specially engineered mice with AD where he found clumps of oligomers in their brains and no plaques.

According to Rudolph Tanzi, Ph.D., Director, Genetics and Aging Research Unit at the Massachusetts General Hospital, oligomers “should be enemy number one.” As the body ages, too many of these protein clumps create a damaging buildup in the brain and the brain may try to remove the offending oligomers by forming plaques.

Tanzi calls the plaques “brain pearls” and likens them to an oyster forming a pearl around a grain of sand to protect itself. Plaques may serve as traps for the oligomers that are attacking the brain. Some people who never have dementia have brains that are inundated with plaques and their brains may be been exceptionally good at converting the “sand” into “pearls.”

Several drugs are in the early stages of development aimed at the oligomers, with the emphasis on early. So this is the direction that research may be heading. A new drug bapineuzumab recently introduced to reduce plaque in the brain did not show any improvement in the subjects.

But it’s not a simple situation. According to Andrew Dillin, Ph.D., of the Salk Institute for Biological Studies, “I think plaques are a sign that your brain was trying to do something very beneficial for itself in the last stages of the disease. If you go in and take these plaques apart, you’re going to make oligomers, and that could actually be worse.”

We will anxiously wait to see what kinds of new medication are developed and how well they take care of the oligomers.

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Most people did not believe Columbus when he said the world is round. Now in the world of Alzheimer’s disease research, Sam Gandy, M.D., Ph.D., Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer’s Disease Research Center, Mount Sinai School of Medicine, has created quite a stir. He states, “The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer’s pathology. But there has been a longstanding debate over whether plaques are toxic, protective, or inert.”

So instead of the belief that brain cells are being destroyed by the sticky plaques, Gandy and his researchers think that there are free-floating clumps of protein that may be the culprit and that the sticky plaques may actually be protecting the body against these toxic clumps.

According to the Mount Sinai School of Medicine:

Several research groups had previously proposed that rather than plaques, floating clumps of amyloid (called oligomers) are the key components that impede brain cell function in Alzheimer’s patients. To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.

The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers. Moreover, when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before.

This will take research in a new direction. Drugs that target plaques may not be of any help and could even make the disease worse.  Gandy works with specially engineered mice and William Thies, Chief Medical Officer, Alzheimer’s Association, warns us that the leap from mice to men is a long one and until Gandy’s experiments can be duplicated, drug companies will not be investing billios of dollars into creating new medication.

When Andrew Dillin, Ph.D., of the Salk Institute for Biological Studies started pursuing the oligomer theory several years ago, he said the the idea was so controversial that some scientists would walk out of the room when he made his presentations at conferences. Now, many top researchers are convinced.

More about oligomers and plaques in the next post.

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Here are two evils — Alzheimer’s disease and cancer. Which would you choose? Of course, neither. I recently read something that said if you have Alzheimer’s you’re not likely to get cancer and vice versa, if you get cancer, you’re not likely to get Alzheimer’s. So that got me researching — is Alzheimer’s disease protection for cancer?

In December 2009, Neurology published a report by Dr. Catherine M. Roe of Washington University School of Medicine in St. Louis which stated that understanding the link between Alzheimer’s disease and cancer may lead to possible treatments.

Roe and her team studied 3,020 people aged 65 and older. They were followed for an average of five years to see if they developed dementia and an average of eight years for cancer. Here is how the study started:

  • 164 (5.4%) had Alzheimer’s disease
  • 522 (17.3%) had cancer

Here is what they found:

For people who had Alzheimer’s disease at the outset, the risk of future cancer was reduced by 69 percent compared to those who did not have Alzheimer’s disease when the study started.

For white people who had cancer when the study started, their risk of developing Alzheimer’s disease was reduced by 43 percent compared to people who did not have cancer at the start of the study.

This effect, however, did not apply to minority populations. In fact, the opposite effect was observed in minority populations — those who started out with cancer at the beginning of the study were more likely to develop Alzheimer’s disease. However, the sample size of minorities starting off with cancer (29 individuals) was too small for the result to be considered significant.

Overall, the results of this study support previous findings that cancer and brain degenerative diseases such as Parkinson’s and Alzheimer’s disease may share common molecular underpinnings. However, Roe noted in an email to Reuters Health, “Since we found no associations between vascular dementia and cancer, we don’t think that cancer is linked to dementia generally.”

Vascular dementia, the second most common form of dementia after Alzheimer’s disease, is caused by clogged blood vessels and other conditions affecting the blood supply to the brain. Based on the current study, only the degenerative form of dementia, and not the form caused by lack of blood to the brain, appears to be somehow protective against cancer.

To read the full article, click here.