When I tell my story, I'm often challenged with this question: Do I really have Alzheimer's disease? Someone asserted in a comment on the Amazon listing for Beating the Dementia Monster that I couldn't possibly, although the person wasn't a "verified purchaser" and likely hadn't read the book. I've even gotten the question from medical professionals. This is a good question because my case is unusual.
But why is it unusual? As we explain in Beating the Dementia Monster, my experience is actually consistent with research in which lifestyles were actually changed and the results measured. This is notable in the highly respected FINGER study. The FINGER study has invigorated researchers around the world, and there are many efforts underway to replicate and expand on its results. The US version of this effort is the US POINTER study now underway.
My initial neurological evaluation was in 2015, first in my home town, and then at Harborview Medical Center in Seattle. Alzheimer's disease is normally diagnosed through a process that may begin with a screening test, like the "mini mental status exam," and interviews with family members who may have been observing the patient over a period of time. If these indicate a problem, intensive cognitive tests are administered (about 3-4 hours worth), and the process usually ends with a biomarker test. The biomarker test looks for a physiological connection to changes in memory and cognition. In my case, MRI biomarker examination found that my brain was atrophying in a manner consistent with Alzheimer's disease. (Since 2015, I have now had seven MRIs of my brain.) While Alzheimer's disease is only diagnosed definitively in the autopsy, the technology for narrowing the cause of a case of dementia has been getting better and better.
MRIs are considered a little less reliable than a PET scan for assessing Alzheimer's disease. Until recently, the insurance company wouldn't pay for a PET scan because the results wouldn't change the plan of treatment for a given case of cognitive impairment. While the MRI can measure atrophy of the brain, PET scans can do several other things depending on the type. Their original value was in determining where in the brain glucose is being metabolized -- and where it's not. Alzheimer's disease interferes with the metabolism of glucose, and so there are characteristic changes in patterns of glucose metabolism in the disease. More recently, new PET scans can measure the load of amyloid plaques and tau tangles. The plaques and tangles are what make Alzheimer's disease Alzheimer's disease.
While I have ups and downs in my memory and cognition, I have been doing really well, all things considered. But my balance is still terrible, and balance problems interfere with almost anything I want to do. My balance problems began to intensify in early 2020, and have been getting increasingly worse. Maybe I should accept this by virtue of now being 72, but I don't recall either of my grandfathers having balance and gait problems like mine when they were my age. (My Dad died earlier.) It's a good bet that my balance and gait problems are being caused or aggravated by Alzheimer's disease -- if that's what I have.
To further refine their diagnosis, my neurologists in Seattle decided I needed a PET scan. So Amy and I drove over to Seattle a couple of weeks ago, and I spent 45 minutes or so inside another machine. (Before returning home, we also had a chance to see our granddaughters.) I got the results of the scan a day or so later and then spent more than an hour on the phone with my neurologist. The radiologist's report said that there was normal metabolism of glucose throughout the brain. This is not consistent with Alzheimer's disease and brings into question the conclusion about whether Alzheimer's disease caused my cognitive decline.
But the steep cognitive decline I experienced in 2015 and the atrophy of my brain are consistent with Alzheimer's disease. And then the improvements I experienced after my lifestyle changes which work on the disease mechanisms are consistent with recent research. My question to my neurologist was, have the lifestyle changes so disrupted the disease process that glucose metabolism is now normal ... are the changes obscuring the biomarker evidence of Alzheimer's disease to be found in the PET scan? She wasn't sure. And I haven't seen any research that would address this.
But it seems to me to be very logical. The principal consequence of exercise and intermittent fasting are to promote production of the "brain derived neurotrophic factor" which we said repairs brain cells and prompts stem cells to form new neurons. Researchers seem to believe that this is the primary way that lifestyle changes attack Alzheimer's disease. To have experienced the remarkable improvement in memory and cognition that I have, and to have sustained it over these past seven years, suggests to me that the entire disease mechanism must be impeded to some extent by the suite of lifestyle changes. The disease mechanisms would include the impaired metabolism of glucose. So, it seems to me that I shouldn't be surprised to see normal metabolism of glucose in my PET scan, even in the face of Alzheimer's disease.
The PET scan also showed that the metabolism of glucose was less in my cerebellum than other parts of my brain. The cerebellum has a lot to do with balance and gait. The metabolism wasn't much less, but it still suggested to me that the problem with my balance is centered there. But I'm not a neurologist or a radiologist, and my neurologist didn't go there with that observation. She has some other ideas she wants to pursue. We'll see how these turn out.
I've been missing for a couple of weeks. It took several days for the trip to Seattle for the PET scan, including time to visit with our children. After that we spent almost a week in California to attend the wedding of my nephew and to see Big Sur. It was a great trip. As it turns out, there was no big news in Alzheimer's research during that time, so I don't think our readers missed too much.
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