Alzheimers disease is one of the people often ask summers disease and dementia is the umbrella term for lots of different problems, that people have with memory and thinking but also MERS is the most common it’s characterized by memory loss.
Almost always and then other functions of thinking like word-finding ability to do calculations ability to remember how to do procedural things like loading the dishwasher and eventually goes on to real problems doing almost anything.
It affects daily life in a major way and also many other members of the family spouses’ children, in particular, a very common cause of dementia is Alzheimer’s disease.
Am I Getting Alzheimers Disease?
Alzheimer’s 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.
When a collection of symptoms is matched with a name, the thought processes stop. Neither the patient nor the doctor give 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. Alzheimers 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 Alzheimers disease from 7th place to 6th place.
Neurologists say that age is the highest risk factor for dementia and one in nine people over age 65 have Alzheimers disease., By the age of 85, about 38% of patients 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!
Symptoms by Stage
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.
Alzheimer’s disease Early Stage
In the early stage, one would see some slight memory loss, especially of the short term variety. There’s maybe decreased personal initiative reflected in hygiene, hobbies, losing an attachment to life and possibly depression.
The increased episodes of faulty judgment might be observed by close family members.
Alzheimer’s disease Middle Stage
By the 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 frequently such as severe anxiety, especially at night. There may be long periods of sleeplessness.
Alzheimer’s disease Late Stage
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 be lost.
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 hypersexuality 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.
Brain Physiology and Alzheimers Disease
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.
Understanding The Brain
Extreme destruction of neurons in the central nervous system, particularly in the neocortex is a hallmark of Alzheimer’s 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’s 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 Alzheimer’s 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 a great 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 Its first symptoms are 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 every side of the brain.
In Alzheimer’s disease, the hippocampus is one of the first territories 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 basic role in the processing and memory of emotional reactions. Damage to the amygdalae prevents an Alzheimer’s 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 acetylcholine.
In Alzheimer’s disease (and Parkinson’s too) the nucleus undergoes degeneration. Decreasing in acetylcholine production is seen in Alzheimers disease and it leads to a general decrease in 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 norepinephrine 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.
Raphe Nuclei is a gentle-size cluster of nuclei, found in the brain stem. Their main function is to produce serotonin to the rest of the brain.
Those are the major brain nuclei and structures, that are affected by dementia and Alzheimer’s 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 Alzheimer’s 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 a permanent coma which could also explain why Alzheimer’s patients don’t go into a comatose state.
Risk Factors for Alzheimers Disease
The medical community and neurologists typically list the following as risk factors for Alzheimer’s.
No 1 Factor
The age is listed, as the highest risk factor, with one in eight people over 65 being diagnosed and rising with 50% over age 85.
Do all these people have Alzheimer’s disease or do the doctors tend to diagnose their symptoms as Alzheimer’s just because they are old? Interesting question.
No 2 Factor
Next is genetics. An allele is a variant of a “normal” gene and the inheritance of a gene allele labeled “E4/E4” indicates a proclivity for Alzheimer’s. In this case, a normal gene is involve 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.
No 3 Factor
Trauma to the head or concussion can contribute to the onset of Alzheimer’s, most likely due to damage to critical vascular feeds with accompanying oxygen and nutrient starvation.
No 4 Factor
High-fat diet, obesity, and elevated, cholesterol levels are believed to be contributory factors to Alzheimer’s. Maybe, but see number two above.
5. Diabetes, hypertension, and atherosclerosis implicated in Alzheimer’s disease. Now, this makes sense that all are characterized by inflammation.
6. Smoking is a risk factor that seems to make a lot of sense knowing how smoking affects the Cardiovascular System and could by 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 Alzheimer’s diagnosis?
8. Diagnosis of mild cognitive impairment. Could this be one of those misdiagnoses since “everyone knows” that mild cognitive impairment is an early stage symptom of Alzheimes 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 Alzheimer’s disease cases is in lifestyle changes instead of more drugs. Did anyone ever do any research on why animals don’t get Alzheimer’s 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 chances for Alzheimer’s.
Factors Believed to Decrease Alzheimers Risk
1. Inheritance of a gene allele for E2/E2. This is the counterpoint to the inheritance of the allele E4/E4 mentioned above.
2. Taking omega-3 fatty acids is a 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.
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, which 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 one’s risk for AD since the brain’s waste removal system is only active during deep sleep.
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.