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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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.

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Memory and Focus

Many people have problems with memory and focus as they age.  Whether the problems are the beginning stages of dementia or just a lack of focus, the following exercise can help to ensure that aging has less power to rob you of precious memories.  In addition, this exercise provides a possible solution for insomnia.

1.  Focus on the events of the day in order from arising in the morning until you go to sleep. The good news is that you will fall asleep long before you reach the end of the day.

2.  During the process, visualize each step of the day.  The process should include all activities, conversations, thoughts and individuals met during the day.  It might be seen as a video recording of the day played back only in your brain.  Focus on details.

3.  Initially, the mind video will be playing in fast forward.  It will be difficult to pick out the small details such as thinking over your today list or looking in the mirror while brushing one’s teeth.  In addition, scenes may jump out of sequence from morning to afternoon and then back to getting out of bed.  However, your goal is to play the video in sequence.

4.  As you continue the exercise several days in a row, you should begin to see some differences.  That which was once a just big chunk of time will begin to develop into fully visualized scenes, which include people, conversations, room decor, signs and thoughts.  Details will become clearer.

5.  It should become a daily challenge to remember more of the day.  You will become more aware of the things you normally would have done without much thought.  Since you know you must recall, your focus changes.  You are using brain cells not previously harnessed.  While the nighttime exercises may be a cure for insomnia, the daytime exercises help you to focus, improve your memory, and lower the chances of developing dementia.

By improving one’s daytime focus and recalling events of the day, it is possible for people to avoid memory loss and dementia.  Additionally, these activities can help with insomnia.

The ideas in this article are adapted from a blog on how to become a better chess player, but certainly seem appropriate for anyone concerned with dementia and having problems with memory and focus.

http://www.mychessblog.com/one-simple-mental-exercise-to-improve-your-mind-power/

 

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.

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Possible New Drug for Alzheimer’s Disease

Taken orally, E64d, a type of cysteine pro-tease inhibitor, has shown to reduce the buildup of β-amyloid (Aβ) present in animal model brains used in Alzheimer’s disease studies. This action resulted in significant improvement in memory loss. The findings were discovered by a group of researchers from the American Life Science Pharmaceuticals-San Diego, University of California-San Diego and the Medical University of South Carolina. Their findings will be published in the Journal of Alzheimer’s Disease in the September issue.

Dr. Vivian Y.H. Hook praises the discovery since according to her, E64d has been proven safe for human consumption and that the results of the research has excellent potential for use in the treatment of Alzheimer’s disease.

It is known that there is a co-relation in the increase in the levels of Aβ peptides, amyloid plaques and the onset of loss of memory. Aβ peptides are separated from the APP or amyloid precursor protein by the β-secretase. The peptides later develop plaques in the regions of the brain associated with memory.

E64d reduces the level of Aβ by blocking the β-secretase from taking apart the amyloid precursor chain. However, researchers also discovered that it also increases BACE1 activity, a protease known as the principal β-secretase. E64d seems to decrease Aβ in the lower brain by blocking the β-secretase activities of Cathepsin B, another protease.

According to Hook, the study shows that Cathepsin B may be used for the inhibition of the production of Aβ and the resulting improvement of memory function. The finding is important since inhibition of β-secretase and Cathepsin-B is possible without the inhibition of BACE1.

The research involved the use of young and old mice with transgenic Alzheimer’s. Young mice fed with E64d avoided memory loss while old mice showed improved memory.

The study is not new — it actually used a previous work where Cathepsin B was also utilized for memory enhancement. In that study published in 2008, though, Cathepsin B inhibitors were directly administered into brains of mice with AD. The recent study shows that oral administration was effective and could pave the way for future human clinical trials.

The study is co-authored by Dr. Gregory Hook of San Diego’s American Life Science Pharmaceuticals and Dr. Mark Kindy of the Medical University of South Carolina, the Ralph H. Johnson VA Medical Center, and Applied Neurotechnology, Inc. in Charleston, SD. The recent study also received some support from the National Institutes of Health and the Alzheimer’s Drug Development Foundation’s National Institute on Aging.

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Statins for Treatment of Alzheimer’s Disease

Alzheimer’s disease (AD) is a disease of the brain and the most common form of dementia that causes problems with daily living, memory, thinking, and behavior.  While statistics vary, as many as 5.1 million Americans suffer from Alzheimer’s.  This estimate counts for as many as 70 percent of dementia cases in adults 60 or older.  While there are several recommendations for AD prevention, including reducing cholesterol, researchers have yet to find a cure for this form of dementia.  Although cholesterol lowering drugs such as statins can slow down the process of Alzheimer’s development, there is a large debate on whether these drugs are effective for reducing damage in patients with Alzheimer’s. How do statins work and how are they used in the treatment of Alzheimer’s disease?

Statins are prescription drugs that are used to lower blood cholesterol levels by blocking chemicals in the liver that produce cholesterol.  While many may ask how a cholesterol lowering medication could treat Alzheimer’s, many studies have proven that statins have a positive effect in the body for those who suffer from the disease.  High cholesterol levels are recognized as one of the common risk factors that leads to the development of Alzheimer’s.  By lowering these levels early, Alzheimer’s development can be slowed.

In addition to eliminating one of the most common risk factors, statins are known to protect nerve cells against damage in the brain.  The nerve cell damage that is caused by Alzheimer’s is what leads to memory loss and difficulty comprehending.  By reducing cell damage in the brain, studies published by the Journal of Alzheimer’s Disease, have proven that Lovastatin prevents the death of cells in the brain to keep the brain responsive.  Laboratory studies at the University of Groningen have shown that the neuroprotective mechanism slows the progression of the disease.

While there is skepticism relating to Alzheimer’s and statins, studies have shown that if statins are administered in the early stages of Alzheimer’s, patients will not advance through the disease as quickly.  While statins are not a cure or a way to prevent the disease entirely, they are a protective measure that could have a beneficial effect.

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Center for Molecular and Behavioral Neuroscience

The Center for Neuroscience at Rutgers University – Newark publishes a wonderful newsletter, Memory Loss and the Brain. In the Winter 2010 issue, one of the articles is on Parkinson’s disease. Although Parkinson’s is known as a movement disorder which affects how they walk  — slowly with a stiff gait — as well as possibly producing tremors, it also affects memory, learning, and behavior. Alzheimer’s disease and Parkinson’s disease have similarities such as:

  • Both develop slowly over many years
  • Both tend to develop later in life
  • Both are currently incurable
  • Both affect the brain

As a neurological disorder, Parkinson’s disease affects the part of the brain that controls muscle movement. The neurons that make dopamine, a chemical that helps your body coordinate movements, die. As a neurotransmitter, dopamine is essential for the central nervous system to function. Medications are prescribed that increase the amount and effectiveness of dopamine in the brain. However, medications can cause serious cognitive side effects and even possibly addictions such as gambling and overeating.

Unlike Parkinson’s, the cause of Alzheimer’s disease is not as specific. It may be a composite of causes. Medications are available as mentioned in a previous post, but they only work temporarily to slow down the disease and they don’t address the underlying causes. It is difficult to develop effective treatments when the exact cause is not known.

In both cases, lifestyle choice might make a difference. There is growing evidence that aerobic exercise improves memory and various other brain functions … even modest exercise. Click here to see an amazing video of a Parkinson’s patient riding the bicycle. Besides exercise, a healthy diet — one low in “lousy” cholesterol (LDL) and high in fruits, vegetables, and fatty fish — can help possibly prevent dementia. Mental activities that you enjoy and challenge you is possibly another preventive.

We all hope that cures for Alzheimer’s disease and Parkinson’s disease will be found. In the meantime, we can only do what the evidence tells us might possibly help.

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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?

In my previous post, I talked about using the Alzheimer’s Association as our benchmark for determining the stages of Alzheimer’s disease. In Stage 1 there is no evidence of Alzheimer’s disease as determined by a medical interview.

Stage 2 of Alzheimer’s disease shows very mild cognitive decline. At this point, it could be just the normal “senior moments” or it could be the earliest sign of Alzheimer’s disease. According to the Alzheimer’s Association:

Individuals may feel as if they have memory loss and lapses, especially in forgetting familiar words or names or the location of keys, eyeglasses or other everyday objects. But these problems are not evident during a medical examination or apparent to friends, family or co-workers.

Personally, it seems as though most of my conversations with my senior friends which lasts longer than a few minutes are sporadically sprinkled with “senior moments.” As far as I know, these are not friends that have any particular problems like coping with grief, abuse and addiction, anxiety disorders, or sleep problems that could affect their memory.

One day my husband and I were taking a walk in the neighborhood and it took us half the length of the walk to remember the the names of a family that used to live in our cul-de-sac. That family has since moved into a bigger house down the street. The next time we took the same walk, we had forgotten their names again and this time we never did come up with all of the names. Generally, between the two of us, we do manage to come up with all of their names. Thank goodness for a neighborhood directory. Perhaps we won’t forget on the next walk. We laugh about it, but at the same time, that thought of Alzheimer’s disease always crosses my mind.

How about you? If you’re in that situation, does Alzheimer’s disease ever cross your mind?

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.”