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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A couple of years ago, I wrote about a wonderful Alzheimer’s disease (AD) resource in Fairfax County, Virginia located about 15 miles south of Washington, DC, the Alzheimer’s Family Day Center (AFDC). Not only are they a day care center for AD patients, but they have excellent programs for caregivers. I recently attended one such program on communicating with Alzheimer’s patients.

Titled “Understanding the Person with Dementia: How to Communicate Effectively,” it was presented by Susan Stone who is with AFDC and does outreach and education. Susan is an excellent communicator herself and interacts with the audience extremely well. I want to share some of her thoughts in this article and I will continue next month.

Because communication is only 7% verbal and the rest nonverbal, it is important to not limit your communication to just words. People with Alzheimer’s prefer not to talk on the phone and initiating phone calls is difficult. They have difficulty keeping up with conversation and may not understand your words. Their attention span is limited and they may have trouble finding the correct word. Furthermore, they may pick up only every three to four words.

For example, the conversation may sound like this:

___ WANT ___  ___  ___ GET ___  ___  ___ TAKE ___  ___  ___ . WE ___  ___  ___ APPOINTMENT ___  ___  ___  ___ WE ___  ___  ___ BEFORE ___  ___  ___ HOME.

NOW ___  ___ HURRY.

Here is the entire message:

I WANT you to GET up now and TAKE a good shower. WE have a doctor’s APPOINTMENT at 11:00 and WE can have LUNCH before we go HOME.

NOW please just HURRY!

Getting angry and adding a sharp tone of voice is not going to make this message any easier for the AD person to decipher. Here are some suggestions Susan offered:

  • Restating key words will help.
  • Give one direction at a time.
  • No rushing – time does not mean anything to an AD person.

Here are further suggestions repeating just the key words.

  • Get up. (Offer your hand).
  • Shower.

This is all the person needs to know at this point. They don’t really need to know about the appointment and having lunch is too far in the future to mention it now. You want them to take a shower and all they might remember is having lunch.

More suggestions will be coming next month. I hope this gives some understanding as to why communication is so challenging for those with dementia.

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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/

 

ICAD 2011

Last month the Alzheimer’s Association International Conference (AAIC) — there has been a name change from the International Conference on Alzheimer’s Disease (ICAD) — had their annual meeting in Paris, France with more than 5,000 scientists in attendance. Each year we look forward to hearing about the latest advances in detection and cure for Alzheimer’s disease. The good news is that there’s progress toward earlier detection, but as one of the leading causes of death, the bad news is that there is still no cure.

In my next two posts, I will present a study that caught my interest because it has to do with lifestyle changes that we can make to potentially lower our risk for Alzheimer’s disease. In the United States, the researchers found that there are seven potentially modifiable risk factors:

  1. Physical inactivity
  2. Depression
  3. Smoking
  4. Mid-life hypertension
  5. Mid-life obesity
  6. Low education
  7. Diabetes

To view a summary of the Alzheimer’s disease research presented, click here.

Next year the conference will be held in Vancouver, British Columbia, Canada, July 14 -19, 2012.

 

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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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Prolonged stress does ugly things and now, possibly lead to Alzheimer’s disease (AD). Researchers at the Munich-based University of Minho in Braga, Portugal, have shown that stress, and the hormones released during stress, can accelerate the development of Alzheimer disease-like biochemical and behavioral pathology. Protein deposits in nerve cells are a typical feature of Alzheimer’s disease: the excessive alteration of the tau protein through the addition of phosphate groups — a process known as hyperphosphorylation — causes the protein in the cells to aggregate into clumps. Nerve cells die as a result and those in the hippocampus and the prefrontal cortex are important for learning, memory, and higher cognitive functions.

In this study, rats subjected to stress such as overcrowding and placement on a vibrating platform for one hour daily for one month showed increased hyperphosphorylation of tau protein in the hippocampus and prefrontal cortex. The animals that showed these changes in tau had deficient memories showing problems in the hippocampus area and impaired behavioral flexibility showing deficiency in the prefrontal cortex.

Less than 10 percent of Alzheimer cases are genetic. Previous studies have shown that stress leads to the formation of beta-amyloid, another protein implicated in Alzheimer’s disease. According to Osborne Almeida from the Max Planck Institute of Psychiatry, their findings indicate that stress hormones and stress can cause changes in the tau protein like those that arise in Alzheimer’s disease. The next step will be to see if results obtained in animals are applicable to the development of non-familial forms of Alzheimer’s disease.

Related Article: Stress Significantly Hastens Progression of Alzheimer’s Disease

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Researchers at the Research Institute of the McGill University Health Centre (MUHC) have discovered a new blood test to diagnose Alzheimer’s disease (AD) which was published in the May issue of the Journal of Alzheimer’s Disease.  They have found a distinctive biochemical diagnosis in AD patients according to senior author Dr. Vassilios Papadopoulos.

Papadopoulos reports that post-mortem analysis of brain tissue has been the only definitive tool for AD. Now this clinical study shows that a non-invasive blood test based on a chemical process may be able to diagnose Alzheimer’s disease at an early stage and could be differentiated from other types of dementia.

This blood test is based on the production of a brain hormone called dehydroepiandrosterone (DHEA) which is present at high levels and has a wide range of biological effects. The researchers used a chemical process called oxidation to promote the production of DHEA in blood taken from non-Alzheimer’s patients. However, blood from AD patients did not produce an increase of DHEA.

The researchers were able to accurately and repetitively detect AD with small samples of blood. Although there are many possible therapies in clinical trials, there must first be an accurate diagnosis. Together with clinical findings, the blood test could be used to diagnose AD at a very early stage and the appropriate therapies could be monitored.

Source: MUHC Newsroom

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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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Carmellia sinesis foliage

Green tea is my favorite drink and is in the news again. Now it’s exciting to hear that green tea may help prevent Alzheimer’s disease. The latest news comes out of Newcastle University where Dr. Edward Okello, executive director of the university’s Medicinal Plant Research Group, reports that when green tea is digested by the body, the polyphenol compounds that are in green tea will produce new chemicals that can protect the cells from toxic damage and hence, reduce the risk of Alzheimer’s disease. The digested chemicals also slowed down the rate of cancer growth.

Digestion is the critical component. Because we put foods into our body that we consider “healthy,” it does not mean that out body absorbs the nutrients. At noranagatani.com, I have a post about enzymes. There is also a fascinating book on enzymes written by DiQue Fuller, Ph. D. Click this link or the link to the right — The Healing Power of Enzymes.

In the United States, black tea has been the predominant tea, but green tea is becoming more popular. What is green tea? It is tea whose leaves have been steamed and dried without fermenting and therefore, there’s minimal oxidation during processing. It originates from the leaves of Camellia sinensis. The green tea that I like is the Japanese version. Over the years, they have improved on the quality and taste from the original import from China over 500 years ago. Alibaba.com has a discussion of the difference between Chinese green tea and Japanese green tea in case you are considering green tea in your diet.

The study, “In vitro protective effects of colon-available extract of Camellia sinensis (tea) against hydrogen peroxide and beta-amyloid (A(1-42)) induced cytotoxicity in differentiated PC12 cells,” was published in Phytomedicine. The next step is for the team to test whether the beneficial compounds are produced during digestion after healthy human volunteers consume tea polyphenols. Perhaps, one day, green tea might be the simple answer we’re looking for to help prevent Alzheimer’s disease.

Nancy Nicholson

Today’s poignant blog post is written by Nancy Nicholson, LBSW, author of Help! What Do I Do Now? Caring for Your Loved One with Alzheimer’s. She writes about Alzheimer’s and caregiving on her website: http://nancynicholson.net. Nancy shares with us part of why she wrote the book.

Making Invisible Alzheimer’s Patients Visible

Our friends had stopped by to visit. We didn’t get much company living out on the ranch anyway, but since Dad’s Alzheimer’s disease (AD) diagnosis, visits were even fewer. The guests, who lived only about a mile away, had been friends and co-workers for more than a quarter of a century—she had worked with Mom and he had worked with Dad. Mom welcomed them in, and we all took seats in the living room. There were the “how are you doing?” and “long time no see” exchanges. Then an uncomfortable silence set in. The couple sat facing Mom and me, and the few words they spoke were directed to us. They did not address Dad directly and appeared uneasy and never tried to include him in the conversation. Their visit was short, and, honestly, I believe very uncomfortable for everyone. Dad had seemed excited about the prospect of visitors, but as they drove away, he turned and walked back to the bedroom with shoulders slumped.

This is just one of many experiences that had a profound effect on me while caring for Dad. I was angry at his so-called friends for basically ignoring him. He was still a person and could still participate in conversations even if he was slow to answer or occasionally misunderstood what was said. I had thought that a visit from old friends would be good for him, but at the end, he seemed sad. I could only imagine what he was thinking.

Through the seven years we cared for Dad with this devastating disease, it seemed that often he was invisible to other people. He was treated as if he wasn’t a person, as if he had no value, as if he wasn’t even there anymore. During that time, I resolved that I would make it my vocation to help make life easier for those afflicted with the disease and to help other people to see AD-afflicted patients as human beings with emotions and value. I went on to get my degree in social work and worked in long term care facilities as a social worker. Currently I am a social services consultant to nursing homes. Training staff members is one of my primary duties, and I especially enjoy training people about caring for dementia patients. I want to make them understand that someone with AD is still a person with feelings and a need to be included.

I also see a lack of knowledge among caregivers. Almost everything my family and I learned about caring for Dad came through trial and error. I’ve seen so many “errors” made by well-intentioned, caring family members who simply don’t know how to deal with their loved one. The relationship has totally changed, and they may feel the patient is no longer the person they know and love. That’s why I wrote Help! What Do I Do Now? Caring for Your Loved One with Alzheimer’s. It’s a short guide with lots of examples and tips for specific situations. Most of all, though, I want to encourage family members to continue to relate to their loved one, to remember he is still the same person inside even if the disease has camouflaged that person, and to make the best of the journey they are on together.

Click here to order Help! What Do I Do Now? Caring for Your Loved One with Alzheimer’s from Amazon (print and Kindle) or here to order from Smashwords (ebook format). Bulk orders: support groups or families who need 10 or more copies can order at a discount; click here.

Nancy is also the sister of editor and writer, Lillie Ammann, who writes http://lillieammann.com/blog, and was last cited in this blog here.

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