Alzheimer’s disease is the sixth leading cause of death in the U.S.  This disease kills more people than breast and prostate cancer combined.  It is a pathological disorder that prevents a person from performing normal day-to-day activities like following a recipe; tracking monthly bills; unlocking the front door; operating an oven; or remembering how to play a favorite card game.  Alzheimer’s disease is a form of dementia that attacks certain regions of the brain that control thought, memory, language and judgment.

There are over 16.1 million people who care for loved ones suffering from this disease.  Oftentimes, the caregiver takes a leave of absence from their primary occupation to provide care that becomes more and more demanding as the disease progresses.  Eventually, the behavior patterns and cognitive abilities degrade to a point that requires 24 hour care that exceeds capability to provide Alzheimer assistance.  If cost were not a limiting factor, what if the primary caregiver had the option to have a team of subordinate caregivers (trained and excellent at what they do) come in as needed and provide services that support a higher quality of life for the person suffering from the disease; provide relief for the primary caregiver; and create a happier living environment for the entire family watching their loved one get progressively worse as the disease deteriorates their brain?

That’s the purpose of this article.  To share a few insightful facts about this disease and expose the best kept secret about adding living benefits to life insurance to cover Alzheimer care cost for patients stricken with Alzheimer’s disease.

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How does this disease attack the brain?

By the time a person shows symptoms of this disease, their brain has suffered irreversible damage and has lost close to 70 percent of the essential neurons in the memory regions of the brain.  There is evidence that the disease may start 10 to 15 years before the clinical symptoms appear.  The attack on the brain is gradual over a period of time while subtle changes happen that are barely noticeable at first.

To understand the warzone, first let’s understand the basic building block components in the brain.

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The neuron is the basic working unit of the brain.  It is a specialized cell that transmits information to other nerve cells, muscle, or gland cells.   Dendrites extend from the neuron cell body and receive messages from other neuronsSynapses are the contact points where one neuron communicates with another.  Alzheimer’s disease (AD) develops when clusters of protein build up between nerve cells in the brain and disrupt the signaling between synapses.  These protein clusters are called amyloid plaque.  The disease strikes first in the hippocampus, which is the file cabinet that stores long term memory.  This attack interferes with a person’s ability to process and retrieve memories.  In a normal brain, these clusters breakdown and get eliminated.

The second defect occurs with the neurofibrillaries called tau (sounds like cow).  Strands of tau breakdown and become twisted together.  When this happens, the nutrient railroad derails critical nutrients required to keep neurons alive.  When neurons die off, the brain loses ability to send and receive important messages to other cells.

These two defects:  amyloid plaque accumulation and tau deformation describe how the disease attacks the brain causing pathological breakdown.

AD also attacks the cerebral cortex which is the wrinkled outer layer of the brain which helps a person speak, read and move.  The cortex shrivels up and slows production of neurotransmitters that help neurons communicate.  When neurons can’t communicate, they die off and as a result, the person suffering the disease can’t remember common things.

What causes a person to develop Alzheimer’s disease?

Doctors have been treating AD for decades, but they are still unsure of the exact causal path for AD.  The medical community believes the disease is triggered mostly be genetics and a number of lifestyle factors:

  1. Family history.  Individuals that have a certain genetic disposition, presence of the APOE e4 gene, increases odds by fifteen-fold for developing the disease.
  2. Body weight.  Obesity doubles a person’s risk of developing amyloid plaque.
  3. Binge drinking. 5 or more drinks in 2 hours (for men) and 4 or more drinks (for women) increases the risk for AD.  However,  < 3 glasses of wine/day lowers the risk of developing AD.
  4. High blood pressure/ Type 2 Diabetes / smoking / depression / physical inactivity all increase the risk for developing AD.
  5. Traumatic brain injury causing loss of consciousness > 30 minutes increases the risk for AD and other forms of dementia.  Injury causing loss of consciousness > 24 hours raises risk for developing AD by 4.5 times.  However, these indicators do not prove that everyone who suffers brain injury develops AD.
  6. Ethnicity.  African Americans have higher rates of dementia than whites.  AD is a pathologic disease within a broader category called dementia.
  7. Age.  Prevalence of AD between ages 65 – 70 is 1.5%; 3.5% above 75 years; 6.8% above age 80; and 44.5% at age 100.

What are some common warning signs for Alzheimer’s disease?

 

Disclaimer:  The statements below are only common traits observed in patients suffering from this disease.  These statements do not imply that EVERYONE displaying these traits has AD.

  1. Memory loss that disrupts daily life, i.e. forgetting important dates and appointments made.
  2. Challenges solving problems or planning, i.e. difficulty following a recipe or tracking monthly bills.
  3. Difficulty doing familiar tasks, i.e. unlocking the front door; operating an oven; playing a favorite card game; putting the dog leash in the linen closet instead of hanging it where it belongs; storing peanut butter in the oven instead of the pantry; leaving water running; leaving fire on the stove; leaving refrigerator open or using the clothing closet as a toilet.
  4. Withdrawal from work and social activities, i.e. tracking scoring in a favorite sport—in football a touchdown adds 6 points, field goal adds 3 points and a goal kick adds extra point.
  5. Confusion with time and space, i.e. getting lost in one’s own neighborhood or forgetting what day it is or the month and date.
  6. Trouble understanding visual images and spatial relationships.
  7. Problems with words and speaking, i.e. constantly repeating a thought; forgetting words and describing a situation in lieu of using the word or name for a particular object or activity.

Senior Alzheimer care

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Scientist use PET scans to detect increased levels of amyloid plaque accumulation in the brain to identify individuals who are vulnerable to develop AD.

Current treatment procedures focus on correcting clinical symptoms of the disease, which in most cases is far too late.  The disease can be compared to a locomotive that does not stop progressing towards deeper brain deterioration.

US Food and Drug Administration has approved several drugs to treat the symptoms of AD:

Donepezil, Galantamine and Rivastigmine are cholinesterase inhibitors designed to preserve acetylcholine which is a neurotransmitter that helps people remember important facts and make sound judgments.  Certain brain cells release acetylcholine which acts like a postal worker delivering messages to other cells in the body.  These drugs are designed to increase the levels of acetylcholine in the brain.  AD heavily damages cells that produce this neurotransmitter.

Although these drugs help a person to sustain memory and make sound judgments, they don’t stop the disease and progressive damage to nerve cells.  At present, there is no cure for Alzheimer’s disease.

Because there is no cure, the treatment has to focus on the early stage development of the disease and protecting the brain from degradation on 2 levels:  amyloid plaque buildup and neurofibrillary tau entanglement.  To find a cure for Alzheimer’s disease, scientist must determine the root cause(s) and the mechanisms that cause these 2 defects to progress.

Four drugs are being tested for effectiveness to remove amyloid beta proteins from the brain: Crenezumab, gantenerumab, solanezumab, (beta secretase inhibitors).  These anti-bodies are designed to bind with clumps of amyloid beta protein and remove them from the brain.    The hope is that at least one of these drugs can effectively slow-down or stop plaque formation in the brain.

It’s likely that a combination of treatment strategies will be required to stop this disease in its tracks, similar to how a cocktail of drug therapies are required to treat HIV, cancer and heart disease—which all  are complex diseases.

How do I get help covering home Alzheimer care?

Contact our office for a free consultation to understand how adding living benefits to life insurance can cover the cost for home Alzheimer care. Call Michael at 510 304 8750 to schedule an appointment.

 

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