Alzheimers disease! Pretty scary diagnosis. If a doctor tells us we have a particular disease, does that mean we really have it?
If we really do have it, what does it say about the cause? Well, nothing.
All too often, when a collection of symptoms is matched with a name, the thought processes stop. Neither the patient nor the doctor gives it another thought.
The physician just looks in his Physicians’ Desk Reference to find the right pill to prescribe. The patient obediently takes the pills and hopes the symptoms go away.
In a perfect world, the diagnosis should be the starting flag for the start of the thought processes.
A sign of the times is that diagnoses for dementia and Alzheimers have been increasing rapidly for many years. Alzheimer's disease is now the number six cause of death in the U.S. claiming 83,494 lives in 2010; up from 71,599 lives in 2005. This is an increase of 16.6% in five years and moved Alzheimer's disease from 7th place to 6th place.
Neurologists say that age is highest risk factor for dementia and one in nine people over age 65 have Alzheimer's disease. By age 85 about 38% are diagnosed with Alzheimer's disease.
Yet neurologists also claim that the only way to tell for sure if someone has Alzheimer's disease is to perform an autopsy. So if the latter is true, how do we know that those estimates above for people over 65 and over 85 are true. We don't!
Alzheimers disease is the number one neurological disease in the U.S. It not only destroys the individual, it also devastates the family.
Dementia and Alzheimers disease are often used interchangeably but Alzheimer's is just one type of dementia. In general, dementia is a name given to describe a progressive mental deterioration.
In 1901, Dr. Alois Alzheimer was working at an asylum in Frankfurt, Germany and he observed and worked with a 51 year old woman named Mrs. Auguste Deter.
Mrs. Deter would have the honor of becoming the person defined by Alzheimers disease.
On one occasion she was asked to write her name; she wrote "Mrs." and then paused. After a couple of minutes, she said, "I have lost myself".
That one phrase has come to epitomize what Alzheimers disease
It's amazing that as far back as 1906, Dr. Alzheimer identified the characteristic plaques and tangles of the disease from the autopsy on Mrs. Deter's brain.
Alzheimers disease is generally divided into two types depending on when it manifests; early onset occurs before age 65 and late onset after age 65.
Many think Alzheimer's is genetic in nature and, in fact, some cases are. Genetic forms of the disease have been identified but they only account for less than 10% of the diagnosed cases.
Do you ever wonder what it's like to have Alzheimer's Disease or what it is like to be a caregiver for someone with AD? If so, consider the book shown in the image, Alzheimer's From the Inside Out by Richard Taylor. It is the true story of a man's fight with this dreaded disease. Click on the cover to take a look.
Before going any further, this seems like a good spot to give a plug to an incredibly informative site covering ongoing research into Alzheimers Disease.
The symptomatic behavioral changes in Alzheimer's disease are different in each stage; early stage, middle stage and late stage. It's a pretty subjective thing since it is mostly a matter of degree of severity as the disease progresses through each stage.
Photo: PET scan of normal brain
In early stage, one would see some slight memory loss, especially of the short term variety. There may be decreased personal initiative reflected in hygiene, hobbies, losing an attachment to life and possibly depression. Increased episodes of faulty judgment might be observed by close family members.
By middle stage, memory loss will have become more severe and there will a greater inability to process information; for example the sufferer may not be able to understand jokes or get the point of a story.
Mood disturbances will become more frequent such as a severe anxiety, especially at night. There may be long periods of sleeplessness.
In the late stage the hippocampus will have degenerated to the point that the patient will "lose themselves" and no longer know who they are. The "story of their life" stored in memory will have been lost.
Photo: PET scan of advanced Alzheimer's brain
Psychiatric problems will become severe including periods of mania that may last for several weeks, then stop abruptly and switch to a new mania.
For example there may be a phase of hyper sexuality where the patient wants constant sex, then after some period of time, switch to an insatiable desire to eat. Severe language difficulties will be the norm with an inability to speak.
When I hit the middle stage, just shoot me.
Unless you're really into neurology and anatomy of the brain, you can probably skip the next few paragraphs, since we are going to dive deep into a lot of medical jargon pertinent to brain structure.
So here goes and by the way, much of this was paraphrased from notes on Dr. Jeanette Norden's course, "Understanding the Brain".
Dr. Norden is a neuroscientist and Professor of Cell and Developmental Biology at Vanderbilt University and has presented her course on DVD available from The Great Courses. Click the link below to see what the course offers and buy it if it resonates with you.
Extreme destruction of neurons in the central nervous system, particularly in the neocortex is a hallmark of Alzheimers disease.
However, loss of neurons in varying degrees throughout the brain is typical of this disease and will affect the entorhinal cortex and hippocampus, amygdala, nucleus basalis of Meynert, nucleus locus coeruleus and raphe nuclei.
How about a quick description of each of these areas?
The neocortex is the outer layer of the cerebral hemispheres. It is involved in higher functions such as sensory perception (sight, touch, smell, etc.), generation of motor commands (movement), spatial reasoning (position), conscious thought and language.
With Alzheimers disease, neuron loss in the neocortex is massive, primarily in higher-order association areas of the frontal, parietal and temporal lobes. That's pretty much the whole brain except for the occipital lobe in the rear part of the brain.
The typical Alzheimers patient will lose 1000 neurons per day and eventually will reach a point where they can see and hear but just can't think anymore.
The Entorhinal Cortex is a crucial memory center in the brain. It forms the main input to the hippocampus and is responsible for the pre-processing of the input signals. The entorhinal cortex/hippocampus system plays an important role in memory consolidation and memory optimization in sleep.
The entorhinal cortex is one of the first areas to be affected in Alzheimer's disease, and one of the first symptoms is an impaired sense of direction.
The hippocampus is a brain structure that plays a major role in short term memory and spatial navigation. Humans and other mammals have two hippocampi, one in each side of the brain.
In Alzheimers disease the hippocampus is one of the first regions of the brain to suffer damage; memory problems and disorientation appear among the first symptoms.
Among other things, damage to the hippocampus can result from oxygen starvation. This would suggest an impaired blood flow to the area. People with extensive hippocampal damage would likely be unable to form or retain new memories.
The Amygdala (amygdalae since there are two of them) are almond-shaped groups of neurons located deep within the medial temporal lobes of the brain.
They perform a primary role in the processing and memory of emotional reactions. Damage to the amydgalae prevents an Alzheimers disease patient from experiencing emotion in a normal way.
Nucleus basalis of Meynert
The basal nucleus of Meynert is a group of nerve cells that project to the neocortex and are rich in the neurotransmitter acetylcholine and the enzyme choline acetyltransferase, necessary for the production of
In Alzheimers disease (and Parkinson's too) the nucleus undergoes degeneration. A decrease in acetylcholine production is seen in Alzheimer's disease leading to a general decrease of mental capacity and learning.
In every case where this nucleus degenerates, dementia occurs.
Nucleus Locus Coeruleus (blue nucleus)
The Nucleus Locus Coeruleus is a very small nucleus in the brain stem which uses norephinephrine as a neurotransmitter. It has massive widespread projections to the neocortex and is vital to the regulation of blood flow in the brain, extraction of oxygen and glucose for the brain, selective attention, ability to focus, and in the sleep-wake cycle.
The Raphe Nuclei are a moderate-size cluster of nuclei found in the brain stem. Their main function is to release serotonin to the rest of the brain.
Those are the major brain nuclei and structures that are affected by dementia and Alzheimers disease. Note that all of them have some role in memory, thought processes, emotion, movement, and spatial perception; all of which are classic impairments of Alzheimers patients.
All of these structures project directly to the cortex without going through the thalamus as with most other brain nuclei.
Since the thalamus is believed to both process and relay sensory information selectively to various parts of the cerebral cortex, it may be significant that none of the structures involved in Alzheimer's degeneration go through the thalamus.
Damage to the thalamus can lead to permanent coma which could also explain why Alzheimer's patients don't go into a comatose state.
Did we mention that Alzheimers disease is idiopathic, meaning they don't know what causes it and it is only positively identified at autopsy?
Photo: Healthy neuron; NIH National Institute on Aging
At autopsy, the pathologist will look for abnormal inclusions that include:
Recent speculations from scientists, as reported in the Wall Street Journal of December 28, 2010, are starting to link Alzheimer's disease with a buildup of waste products in the brain which includes the amyloid beta protein and other cellular waste products.
As the thinking goes, waste material is broken down in the brain by lysosomes, one of the cellular components. If the lysosomal system starts to break down, waste products build up and accumulate in the neurons, causing the type of damage seen in autopsied Alzheimers brains.
Encouraging results have been documented in mice with Alzheimers in which degeneration of cognitive processes were prevented. The conclusion is that drugs that focus solely on the amyloid plaques and tangles are too narrow.
Very recent findings reported in the August 19,2013 issue of Proceedings of the National Academy of Sciences, seem to indicate that accumulations of copper may disrupt the normal workings of the lysosomal system in removing waste products from the brain.
While these working hypotheses are far from being proven in humans, it is encouraging that Alzheimer's research is exploring new avenues.
Photo: Neurofibrillary tangle typical of Alzheimer disease
Other common central nervous system abnormalities will include:
So far as medical science is concerned, there is no known cause and no cure for Alzheimers disease. Meds are given mainly to replace lost neurotransmitters, such as acetyl-choline.
Jeff T. Bowles, author of Alzheimer's Treatments that Actually Worked in Small Studies has some different thoughts about how to deal with Alzheimer's that don't depend on drugs. Many have found it to be extremely helpful, others, not so much. Certainly the medical community will find it controversial. Nevertheless, it is worth the read.
There are two classes of drugs currently approved by the FDA for use in treating Alzheimer’s symptoms. The first are the cholinesterase inhibitors, defined as drugs that increase the level of the neurotransmitter acetylcholine in the brain. Acetylcholine plays a key role in memory and learning.
The best that these drugs can do is to delay the worsening of symptoms for 6 to 12 months in about half of the people who take them. Aricept is one such drug and has not shown to slow the disease progression at all. The other two are Exelon (Novartis) and Razadyne (Ortho-McNeil Neurologics).
The other is Namenda (Forest Laboratories) that regulates the activity of glutamate in the brain. Glutamate plays a key role in memory and learning, but an excess can lead to the disruption of nerve cell communication or nerve cell death.
Many medications and even over the counter remedies interfere or compete with nutrients for absorption. As such, over medication, especially of seniors in assisted living facilities, has been shown to produce dementia or Alzheimer's symptoms.
Dr. David Morris of New York's Hebrew Home for the Aged, believed his patients were taking far too many drugs and started weaning them off. His patients' health quickly and surprisingly improved. Too many of the patients diagnosed with Alzheimer's turned out to be old people doped up with too many medications.
There is a naturally occurring amino acid in the body, N-acetyl-cysteine (NAC), that augments and improves the body's normal mechanisms that thwart illness and disease.
A study published in Neurology (October 2001), showed that Alzheimer's patients improved in cognitive tasks after six months of NAC treatments. Where the drugs don't work, maybe more research needs to be done in the area of natural substances.
The medical community and neurologists typically list the following as risk factors for Alzheimer's.
1. Age is listed as the highest risk factor with one in eight people over 65 being diagnosed rising to 50% over age 85.
Do all these people really have Alzheimers disease or do the doctors tend to diagnose their symptoms as Alzheimer's just because they are old? Interesting question.
2. Next is genetics. An allele is a variant of a "normal" gene and inheritance of a gene allele labeled "E4/E4" indicates a proclivity for Alzheimers. In this case the normal gene is involved in lipid and cholesterol transport.
Another interesting one...the brain is about 60% fat and if it doesn't get the lipids and cholesterol it needs, cognitive problems will result. Statin drugs lower cholesterol, often to the extent that the brain is deprived of the cholesterol it needs.
An interesting read on how statin drugs affected one man’s cognitive abilities is Dr. Duane Graveline's book, "Lipitor: Thief of Memory: Statin Drugs and the Misguided War on Cholesterol." Click on the link above to Amazon.com to order this amazing book.
3. Trauma to the head or concussion can contribute to the onset of Alzheimers, most likely due to damage to critical vascular feeds with accompanying oxygen and nutrient starvation.
4. High fat diet, obesity and elevated cholesterol levels are believed to be contributory factors to Alzheimers. Maybe, but see number two above.
5. Diabetes, hypertension, and atherosclerosis are implicated in Alzheimers disease. This makes perfect sense in that all are characterized by inflammation.
Smoking is seen as a risk factor which seems to make a lot of sense knowing how smoking affects the cardiovascular system and could, over time, restrict blood flow to the brain.
7. History of clinical depression, chronic depression. How about looking for an endocrine imbalance before jumping to an Alzheimers diagnosis?
8. Diagnosis of mild cognitive impairment. Could this be one of those mis-diagnoses since "everyone knows" that mild cognitive impairment is an early stage symptom of Alzheimers disease. Maybe the patient is taking too many statins.
9. Hormone replacement therapy has also been listed as an Alzheimers risk factor. Beats me as to why.
What's interesting is that most of these risk factors exactly match the risk factors for stroke and heart attack.
Maybe the answer to many Alzheimers disease cases is in lifestyle changes instead of more drugs. Did anyone ever do any research on why animals don't get Alzheimers disease...let's see; they don't smoke, they eat natural food, they don't have crazy bosses or drive cars, and they don't watch TV.
See the factors below that are viewed as decreasing ones chances for Alzheimers.
1. Inheritance of a gene allele for E2/E2. This is the counter point to inheritance of the allele E4/E4 mentioned above.
2. Taking omega-3 fatty acids is thought to decrease Alzheimers risk. Now we’re getting somewhere; an essential fatty acid that has incredible whole body benefits for fighting inflammation.
3. Get familiar with virgin coconut oil.
4. Maintaining a normal weight and avoiding obesity and diabetes. Again we are doing something to minimize inflammation.
5. Eating low fat food. Simply wrong! Low fat food is what's behind the obesity epidemic; just learn to eat the right fats.
6. Eat your fruits and veggies; consume high antioxidant foods. Right on, no argument here.
7. Exercise: cutting edge research shows that the hippocampus undergoes mitosis throughout life and exercise promotes mitosis in the hippocampus. In plain language, that means that the hippocampi have the ability to crank out new neurons; maybe the only brain structure that can...we will see.
Let's see, exercise gets the heart pumping, that gets more blood flowing; that means more blood to the brain which means more oxygen and nutrients to the hippocampus. Who would have thought?
8. Get at least eight hours of high quality sleep. There are several recent studies that indicate that insufficient sleep increases ones risk for AD since the brains waste removal system is only active during deep sleep.If you want to know more about this, get to know the glymphatic system.
9. Continuing mental challenge, learning a new language, learning an instrument, etc. Yes, every time we learn something new, we build new neurons and new connections.Go to the page on Brain Fitness to see how that works.
Most of these factors were researched extensively in the 20-year Nun Study. This landmark study focused on nuns living in a convent, leading a very active physical lifestyle, eating their own home grown fruit and vegetables, having no stress, meditating and practicing yoga and keeping mentally fit.
They typically lived past 100 years of age and died peacefully in their sleep with no signs of dementia in their brains at autopsy.
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