When talking about Alzheimer’s, medical professionals often refer to amyloid plaques. The common belief is that these are the underlying cause of the disease – and that if you get rid of them, you’ll be cured.
But that theory has been proven wrong, over and over again.
First off, every time they’ve developed a drug to reduce levels of these proteins, it hasn’t work. Instead, these experimental drugs seem to make matters worse.
Second, autopsies show that elderly people who never had memory loss – and even had superior thinking skills late into life – have highly dense plaques in their brains. But they never showed a single symptom of Alzheimer’s.
What’s the difference between people with amyloid plaques who develop Alzheimer’s, and those who don’t?
Why do people like Rupert Murdoch, George Burns and Betty White live to nearly 100 years of age with clear thinking skills, while others succumb to clouded minds in earlier years?
For decades I have believed that Alzheimer’s is a disease that stems from inflammatory conditions. Things like viruses, bacterial infections, blood sugar and insulin imbalances, hypertension, stress and a lot of other inflammatory responses can impact brain health.
When these conditions occur, amyloid proteins go to work to protect your brain from harm.
However, as high levels of inflammation continue, they put those protective amyloid proteins through the wringer. Eventually the proteins become misfolded and damaged. Unfortunately, this leads to the development of amyloid plaques. At the same time, levels of the protective amyloid proteins decline.
In other words, it’s not the plaques that damage your brain; it’s the underlying inflammatory factors!
Untangling the Amyloid Theory of Alzheimer’s
Studies agree with me, and a study published in this month’s issue of the popular medical journal Brain adds even further details.
The authors made the confirmation while studying the effect of monoclonal antibody treatments on the brain.
During the study, they noticed the treatments were unintentionally increasing levels of the protective amyloid beta 42 (Aβ42). They also realized that the higher levels of Aβ42 slowed development of cognitive impairment and mental decline, even among people with high levels of amyloid plaques.
According to the lead author, “Even in those with genetic forms of Alzheimer’s disease, higher baseline Aβ42 levels predict a lower progression to dementia.”
This means that as long as you are able to maintain high levels of Aβ42, you may be able to slow cognitive decline, dementia and Alzheimer’s, even if you already have high levels of amyloid plaques.
This is because the Aβ42 is still actively defending the brain against things like elevated sugar levels, excess insulin, bacterial and viral infections, stress, hypertension and other inflammatory conditions.
However, the more exposure to these conditions, the greater the chances are that Aβ42 will drop very low until, eventually, it transforms into amyloid plaques and ceases to function.
Knock Inflammation out of Your Brain
If Alzheimer’s is driven by inflammation, the key, then, is to drive inflammation out of your brain to keep those Aβ42 levels from declining.
Diabetes, high blood and obesity often go hand-in-hand and are three of the most controllable risk factors for cognitive decline. In fact, because risk factors are so similar, some experts unofficially refer to Alzheimer’s disease as type 3 diabetes.
That being said, some of the first steps you can take to help maintain higher levels of Aβ42 are to:
Control diabetes and other metabolic syndromes. High blood sugar is a potential cause of Alzheimer’s because the sugar binds with what we know of as hemoglobin A1C to form what is called advanced glycation end products… AGES; misfolded proteins that add fuel on the fire of potential chronic systemic inflammation.
And the more hemoglobin A1C you have, the more misfolded proteins you’ll have – especially in your brain. So you can see why Alzheimer’s is often called type 3 diabetes.
Reduce central obesity. Visceral fat, which accumulates around the belly, is highly inflamed in obese patients. It produces large quantities of inflammatory cytokines which play a central role in the brain’s inflammatory response that results in Alzheimer’s disease.
Obese individuals with central obesity have about a 3.5 times increased risk of dementia. Even people who are at a healthy weight have an estimated two times higher risk if they are carrying around extra belly fat.
Address high blood pressure. Older people with high blood pressure are more likely to have biomarkers of Alzheimer’s in their spinal fluid. This includes a reduction in the levels of brain protective Aβ42.
Other things like stress, poor sleep habits and a lack of physical activity all take their toll, too. So it is up to you to improve your lifestyle if you want to maintain high levels mental acuity as you age.
SOURCES:
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