In my view, a new study published in Neurology should finally put to rest the long-held, but flawed theory that amyloid protein plaques in the brain cause Alzheimer’s disease (AD) and dementia.
Of course, I’ve been questioning that theory for a very long time now. In fact, I first noted a problem with it decades ago when I worked as a hospital pathologist and observed amyloid build-up in virtually every tissue of the body.
Sometimes, there was dysfunction in the organs with a lot of amyloid. And other times, the presence of amyloid didn’t appear to be significant at all. So, at best, amyloid seemed to be an inconsequential side effect of aging—in some people.
Not to mention, a few years ago, autopsy studies began to show that 50 percent of people diagnosed with dementia do not have amyloid in the brain. And half of people who do have amyloid in the brain do not have dementia!
Now, let’s take a closer look at that new study…
Amyloid starts to collect AFTER memory decline
The new study followed nearly 750 older adults over four years, ages 55 to 90, who had participated in the Alzheimer’s Disease Neuroimaging Initiative. First, the participants underwent brain scans to determine their baseline amyloid buildup. (And they received scans each year over the next four years.)
Next, the participants took tests to evaluate their initial memory, language, and attention capacities.
Then, researchers categorized the participants into three initial groups:
- Those who were cognitively normal
- Those with mild cognitive impairment (MCI)
- Those with subtle cognitive difficulties (called SCD) in standard clinical assessments.
It turns out, the initial scans were essentially useless in predicting who would go on to develop MCI—the stage before dementia—and who would not. (None of the participants had AD at the study’s outset.)
On the other hand, the simple clinical functional assessments were highly accurate in predicting who would decline cognitively and develop more serious memory problems. In fact, nearly half of those who exhibited SCD at the initial evaluation went on to develop MCI. Plus, they had a three times higher risk of being diagnosed with MCI than those who didn’t initially show memory impairments.
Now, compared to participants with normal cognitive function at the study’s outset, those with SCD did exhibit a faster buildup of amyloid. But the buildup began only after the onset of cognitive impairment had already begun!
Which means amyloid couldn’t have caused the decline.
The researchers even stated that if amyloid were the cause of dementia, then signs of cognitive decline should not precede accumulation of it.
And this observation aligns with what I noted years ago as a hospital pathologist…that amyloid may accumulate in the brains of some people as a consequence of declining brain function. Or that it could even be an unrelated finding associated with aging in some people.
But it’s certainly NOT the cause of dementia. And trying to thwart amyloid production with prescription drugs—or by some other artificial means—is rather like “trying to lock the barn door after the horses got out.”
Thankfully, there are many safe and effective natural approaches to prevent and even reverse AD and dementia. And you can learn all about them in my comprehensive, online learning tool, my Complete Alzheimer’s Prevention and Repair Protocol. To learn more, or to enroll today, simply click here.
Source:
“Objective subtle cognitive difficulties predict future amyloid accumulation and neurodegeneration,” Neurology, 1/28/20; 94(4). Doi.org/10.1212/WNL0000000000008838