Alzheimer’s Disease affects more than just the patient.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Most of us are familiar with Alzheimer’s disease (AD). Someone in our family has had it (or has it), or someone we know has/had AD. It progresses in stages, with severity getting worse over time. Initially, there are no symptoms; then mild cognitive impairment becomes visible. Mile, moderate, and severe symptoms follow.

I published a book, Understanding the Causes of Alzheimer’s Disease (https://tinyurl.com/h2x8dw54), earlier this year that was a compilation of over 40 articles I had written, mostly during our pandemic vacation. I research the human body at the cellular level, looking for cause-and-effect relationships. Treat a cause and fix a problem. Treat symptoms, and you will always be treating symptoms. Most prescription medications treat symptoms.

Vascular Dementia (VD)

https://www.mayoclinic.org/diseases-conditions/vascular-dementia/symptoms-causes/syc-20378793 Vascular dementia (VD) depends on the area of the brain where blood flow is impaired. VD affects the speed of thinking and problem-solving. AD involves memory loss. Patients with VD show signs of confusion, trouble concentrating, reduced ability to organize thoughts and actions, difficulty deciding what to do next, restlessness, an unsteady gait, and may lead to depression.

Many times, VD becomes apparent after a stroke or a series of mini-strokes. VD can develop quickly or gradually, like AD. Sometimes, AD and VD occur together. As cell functions become less efficient and non-functional, AD begins its journey through the brain. AD has many causes; however, most opinions focus on beta-amyloid plaques and tau protein tangles. Another unique cause of AD has been uncovered. Iron!

Ferroptosis

https://onlinelibrary.wiley.com/doi/10.1002/ana.26770 Iron can cause the degradation of microglia, the brain’s immune cells that continually pass through the brain responding to invaders and damage. This study involved post-mortem human brain tissue of patients known to have had AD and VD. Microglia swarms to attack any invading pathogens. Sometimes, the myelin, a protective sheath around the neuron, is damaged. Ferroptosis occurs when too much iron is present, causing cell damage and microglia death.

Plaques and tangles have been the primary cause of research over time. The discovery of cascading deaths of microglia resulting from over-saturation of iron is a new breakthrough in the causes of AD.

Causes of Cell Death

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9170779/#:~:text=However%2C%20it%20could%20be%20inhibited,reactive%20oxygen%20species%20(ROS). Typically, we see cell death is caused by apoptosis (expected end of cell life), autophagy (a cellular clean-up function that removes damaged and non-functioning cells and senescence that causes cell death due to age when the cell is no longer capable of dividing and growing.

We would expect normal cell death for the brain’s immune cells, the microglia, but it is not happening normally. Another input into the death cycle is occurring – ferroptosis. Usually, a healthy body maintains stability by removing damaged and aged cells – around 150 billion dead cells are removed daily.

A delicate balance exists between removing dead/damaged/aged cells and the healthy cells next to them. When the processes run amok – cancer, coronary-vascular disease, obesity, etc. – the body’s balance is in jeopardy. Adding ferroptosis to the overall equation of cellular death in the brain is one of those processes running amok.

Causes of Ferroptosis

https://rupress.org/jem/article/218/6/e20210518/212093/Ferroptosis-in-infection-inflammation-and Ferroptosis has both biological and chemical causes. Normal physiological responses are not occurring as they should, and the body’s immune system is also dysregulated. This results in extra iron accumulation in the neuron sheath. The actual description of the excessive accumulation of lipid peroxides and increased inflammation due to reactive oxygen species (ROS) is more detailed than I think is needed for this discussion. It is well documented. Ferroptosis can occur outside the brain – testes, kidneys, and heart. Neurodegenerative diseases, diabetes, arteriosclerosis, and other disease processes in the body can open the door to increased risk of ferroptosis.

Inhibiting Ferroptosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6602333/ Two inducers of ferroptosis are erastin and glutamate. Simply removing them is insufficient to stop the ferroptosis process enough to make a significant difference. Substituting a form of glutathione or an antioxidant, ferrostatis-1, the cells dying from ferroptosis are reversed, and promotion to full recovery is initiated. There are a few other ferroptosis inhibitors (aminooxy acetic acid, deferoxamine, dopamine, vitamin C, etc.), but they are not as effective at preventing and reversing cell death due to ferroptosis.

Conclusion

I thought this research was interesting from several angles. There are several pathways for most diseases, especially AD. You may stop the progression of one cause, and other causes will eventually win out. My brother-in-law developed AD late in life and could not tell you what year it was. However, after a couple of months of phosphatidylserine supplementation, he could tell you what he had for breakfast, what was on television last night, and what he wanted to watch on TV later tonight. He lived a good year without symptoms. Eventually, another AD pathway took over, and the progression of AD began again. Phosphatidylserine is one of four phospholipids the body makes daily. As we age, we produce less of it. Supplementation is easy.

I listed several causes of AD in my book listed above. Subsequent research has found several more causes of AD, and I will update my book accordingly. What am I doing to prevent/delay AD? Attack the first level of the problem – chronic, low-level cellular inflammation. Antioxidants are critical to stop the initiation of disease processes.

A simple CRP (c-reactive protein) blood test tells us the overall body’s level of inflammation. I always insist that it is added to my annual physical. Most of the time, my CRP levels are below 0.5 mg/Dl. My last reading was a bit over 2.0 mg/Dl – still in the normal range but higher than in recent years. You can get a home kit to test your CRP; I believe it is generally reliable for inflammation. You are responsible for your health.

Live Long and Enjoy Life!Red O’Laughlinwww.RedOLaughlin.com

 

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