Alzheimer’s Disease Prevention

Continuing education online courses in Alzheimer’s Disease Prevention

N15. End of Life Care: Alzheimer’s Disease Prevention, 3 CE-hours, $21

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Professor Rudolf Klimes, PhD, welcomes you to this online course. Keep going.

START the course here. TAKE the exam at the end. PAY after the exam.

Course Description: Alzheimer’s disease (AD) is the most common form of dementia among older people. It involves the parts of the brain that control thought, memory, and language.

Objectives: At the end of this course, you will 1) describe the physiological changes resulting in plaque formation, 2) describe the symptoms of the disease, and 3) analyze interventions that may slow or prevent the disease.

Course Format: Online linked resources and lectures that you can use anytime 24/7. One multi-choice test.

Course Developers and Instructors: R. Klimes, PhD, MPH (John Hopkins U), author of articles on Alzheimer’s Disease Prevention and overall wellness.

Course Time: About 3 hours for online study, test taking with course evaluation feedback and certificate printing.

 

Course Test: Click here for the self-correcting test that requires 75% for a passing grade.

N15. Alzheimer’s Disease Prevention, 3 CE course hours

Disclaimer: This course is for general background information for nurses and other health professionals. It was compiled mainly from existing research and university documents. It is a continuing education course and should not be used as an authoritative document for prevention. 

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Questions for Self-study

Do the following for self-study. Do not submit the answers. AD stands for Alzheimer’s Disease.

 F AD is the most common form of dementia in old people.

T   F AD was discovered by a doctor who examined brain tissues.

T   F  AD affects only old people.

T   F   AD can be now be fully prevented.

Introduction

Dementia is a brain disorder that seriously affects a person’s ability to carry out daily activities. Alzheimer’s disease (AD) is the most common form of dementia among older people. It involves the parts of the brain that control thought, memory, and language. Every day scientists learn more, but right now the causes of AD are still unknown, and there is no cure.

Scientists think that up to 4 million Americans suffer from AD. The disease usually begins after age 60, and risk goes up with age. While younger people also may get AD, it is much less common. About 3 percent of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. It is important to note, however, that AD is not a normal part of aging.

AD is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness.  Source: http://www.alzheimers.org/

AD begins slowly. At first, the only symptom may be mild forgetfulness. People with AD may have trouble remembering recent events, activities, or the names of familiar people or things. Simple math problems may become hard to solve. Such difficulties may be a bother, but usually they are not serious enough to cause alarm.

However, as the disease goes on, symptoms are more easily noticed and become serious enough to cause people with AD or their family members to seek medical help. For example, people in the later stages of AD may forget how to do simple tasks, like brushing their teeth or combing their hair. They can no longer think clearly. They begin to have problems speaking, understanding, reading, or writing. Later on, people with AD may become anxious or aggressive, or wander away from home. Eventually, patients need total care.

Read about Alzheimer’s symptoms, diagnosis treatment and Basic Facts: http://www.alzheimers-research.co.uk/  and AD overview: http://www.lef.org/protocols/prtcl-006.shtml

Active Lifestyle and AD Prevention: http://www.alzheimersupport.com/library/showarticle.cfm?ID=1425

AD Deaths Annually: 44,536 (1999)

Age-Adjusted Death Rate: 16.5 deaths per 100,000 population (1999)

Cause of Death Rank Among Americans: 8th (1999)

Source: National Vital Statistics Reports, Vol. 49, No. 8

1. A-BETA (Amyloid beta) Formation

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One of the proteins found in the out layer of brain cells is APP. The ends of these proteins are sometimes cut off by enzymes, namely the beta and gamma secretase, and the resulting fragment is the A-beta. That A-beta can accumulate to form into clusters or plaque and cause problems. The A-beta  needs to be cleaned out of the brain before it forms cluster. Or some way needs to be found to inhibit the secretase. Anything that will do that will contribute to the prevention of Alzheimer’s. A life of regular exercise may, in part, contribute to that.

The 42-43 amino acid amyloid beta (A-beta, A4) protein described by Glenner and Wong is now known to be a major component of both diffuse and neuritic senile plaques (SP). These extracellular structures may be found in the brains of nondemented persons with or without a history of head injury (including boxers), and in individuals afflicted with a variety of neurodegenerative disorders: Alzheimer’s disease (AD), Down’s syndrome (trisomy 21), Creutzfeldt-Jakob disease (CJD) and others.

Source: http://www.adrc.wustl.edu/adrc/abeta_SP.html

Research articles on A-Beta: http://www.math.ubc.ca/~ais/website/refs/amyloidrefs.html

 

2. FIBRIL Formation

As we saw above, the left-over protein parts called A-betas are the problem. When healthy, they are helical like coiled springs. When cut off, they sometimes loose their coil, flatten out, and then cluster together to form beta-sheet structures and these, when stuck together, are fibrils.  Two drugs that may block the A-beta sheets from forming are under development. If that happens, Alzheimer’s would be prevented.

In healthy neurons, microtubules form structures like train tracks, which guide nutrients and molecules from the bodies of the cells down to the ends of the axon. Tau normally holds together the “railroad ties” or connector pieces of the microtubule tracks. However, in AD tau is changed chemically, and this altered tau twists into paired helical filaments – two threads of tau wound around each other. These filaments aggregate to form neurofibrillary tangles. When this happens, the tau no longer holds the railroad tracks together and the microtubules fall apart. This collapse of the transport system first may result in malfunctions in communication between nerve cells and later may lead to neuronal death that contributes to the development of dementia  Source: http://www.alzheimers.org/pubs/prog00.htm#Amyloid%20Plaques

Tau normally undergoes a process called phosphorylation in which molecules called phosphates are added to the protein. Scientists have found that tau in the tangles that characterize AD and other neurodegenerative diseases is composed of overly and abnormally phosphorylated tau. They speculate that this process causes the tau to aggregate into tangled filaments instead of attaching itself to the microtubules, thereby destabilizing the microtubules. Source: http://www.alzheimers.org/pubs/conv09n4.html

 

 3.PLAQUE Formation and Buildup

The above mentions A-beta fibrils connect with SAP proteins and with each other to form an insoluble plaque that is hard for the body to clean out. With time, this plague replaces many brain cells. Then the brain cannot produce enough of the neuron transmitter acetylcholine, and there is a loss of memory and cognition. Some drugs that will bind with SAP before it can bind with A-beta fibrils are under development. This too will contribute to the prevention of Alzheimer’s.

In AD, plaques develop first in areas of the brain used for memory and other cognitive functions. They consist of largely insoluble (cannot be dissolved) deposits of beta-amyloid – a protein fragment snipped from a larger protein called amyloid precursor protein (APP) – intermingled with portions of neurons and with non-nerve cells such as microglia (cells that surround and digest damaged cells or foreign substances that cause inflammation) and astrocytes (glial cells that serve to support and nourish neurons). Plaques are found in the spaces between the brain’s nerve cells.  Source:

 

4. NEURON Death

At this stage, Alzheimer’s patients have very high levels of the brain chemical glutamate, making brain cells insensitive to glutamate bursts that help in new memory development. Thus the patient cannot remember. One drug that regulates glutamate has been approved in Europe. 

 

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5. Moving toward Prevention

Currently there is no proven way to prevent AD. A vaccine is being developed and early testing is under way. Various studies are under way to clarify the role of some common medications in the prevention of AD. Among these are non-steroidal anti-inflammatory drugs (NSAIDs), antioxidants such as vitamin E, estrogen replacement therapy, and ginkgo biloba. None of these are currently recommended, all of these have side effects, and all can interact with other medications. Consult a healthcare provider before considering or taking them. Source: http://www.nlm.nih.gov/medlineplus/ency/article/000760.htm#prevention

AD is a disease that turns parts of the brain into a sticky mess and thus inhibits its functions. Thus the onset of the disease has to be prevented or stopped early.  Once the brain tissue is destroyed, it cannot be restored. The prevention of DA can take a number of approaches: 1.Prevent particles that may form plaque from forming. 2. Prevent these particles from forming plaque. 3 Flush out of the brain particles that can accumulate and cause plaque. 4. Destroy the particles that may form plaque. 5. Destroy the plaque.

At present, some clinical trials are under way for medications that may do one or more of these things. Lifestyle and other remedies may contribute to the prevention of AD as outlined above.

At this time, there is not enough research that indicates that AD can be prevented or delayed. But there are partial prevention strategies  that may slow the progression of the disease or may have elements of prevention. In England, three drugs have been developed that have been approved there and that deal with some aspects of AD. Some studies have suggested populations that have less AD and thus may practice prevention strategies without knowing it. And some populations have more AD. There are some clinical trials under way, and these may discover areas that may in time uncover prevention strategies and preventive or healing drugs. Here are presented two things individuals may do.

First of all, the practicing Daily Health and a healthy lifestyle may be, to some extend and to some people, preventive of many diseases, including Alzheimer’s.

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Daily Health

Exercise   vigorously  for 30  minutes

Eat 5  servings of fruit and vegetables

Enjoy TobaccoFree & DrugFree living

Embrace faith, hope and love.

Secondly, the following practices are not harmful and may with time prove preventive of AD for some individuals:

  • Drink 8 glasses of water a day. The body needs to replace the water lost in perspiration and excretion to flush out selected particles.
  • Maintain your immune system through, among others, adequate sleep and rest time, in order to give it strength to fight.
  • Use Ginkgo Biloba Herbal Tea as a supplementary hot drink. There is some indication that it may improve memory functions. (Do not use it if you are using blood-thinning medications.)
  • Reduce your stress and tension through meditation and relaxation exercises. Stress hinders the functions of the immune system.
  • Keep mentally active by reading, studying, and mental games. An active brain may be less vulnerable to attack.

 

 6. Alzheimer’s Library

Speak to an Information Specialist at 800-438-4380.

Enter Watch of Clinical Trials: http://www.centerwatch.com/patient/studies/CAT11.html

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TEST

Study this web-site for 3 hours for an approved 3 hours Continuing Education Certificate (0.3 CEUs). Click here for the self-correcting test & online payment, and 2) receive your certificate immediately online. All is online, nothing by post-mail. 

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