SNAG

I'm reading a book called Anatomy of the Soul, written by a Christian psychiatrist, Curt Thompson, MD.  The book explores several areas of neuroscience, including memory formation.  He discusses a strategy to enhance growth and activation of neurons proposed by Daniel Siegel, clinical professor of psychiatry at the UCLA School of Medicine.  Siegel came up with the acronym SNAG, which stands for "stimulation of neuronal activation of growth." 

So what are the elements of SNAG?  There are three:

• Aerobic activity.  Engage in at least 45 minutes per day, five days per week.
• Focused attention exercise.  This could be some kind of meditation or prayer.
• Novel learning experience.  This is learning something that expands creativity, such as learning a new language or how to play a musical instrument.     

AD and dementia are not a focus of the book, but these three elements are certainly familiar to us.

Viruses and Alzheimer's disease

This week's ALZForums newsletter highlighted an article connecting the herpes virus with AD.  The article reflects the results of a four-year "big data" study of available  information regarding what goes wrong in brains suffering AD.  It found evidence linking viral load (notably herpes) to the molecular, pathological, and clinical manifestations of dementia.  There was a connection between how many herpes viruses were present in the brain with the brain's dementia status.

But, the researchers who made this connection could not determine cause and effect.  Are the viruses driving the disease, or are they opportunistic, taking advantage of the weakened condition of the already diseased brain? 

A couple of points in the article:

• An association between AD and some viruses, especially herpes, has long been recognized.
• The different herpes viruses cause a variety of problems with the nervous system.
• The viruses may be driving the production of amyloid.
• People begin to accumulate these viruses at a young age, but they may only be activated at the time AD pathology begins.  Most people have them hiding in their brains.      

Post Script

During my June 22 visit with my neurologist, she said one more thing worth mentioning.  She said that, while the practice effect can inflate test scores, they still look at it as a positive indicator.  For the practice effect to have influenced test performance, your brain must have successfully encoded the memories. 

It just keeps getting better

On June 11 we traveled to Harborview in Seattle for my annual cognitive testing—almost four hours worth. I was anxious because I had slept very poorly the night before, and I had foolishly scheduled the testing for the afternoon. I’m a morning person, and when I’ve missed sleep it might not hit me until the afternoon. But, we went ahead with the tests, and I was surprised at how well I felt about how I’d done.

Not being a patient person, I wanted to know the results immediately. But they needed to be analyzed and assessed before the doctors could share them with me. So I needed to wait; we would need to return more than a week later to hear the results.

Before the test began, I had a discussion with the new neuropsychologist who will be following my case. We discussed the status of the SNIFF (insulin) study, and the fact that I had been getting quarterly psychometric testing from them. I wondered about how “the practice effect” might influence my results. She said that was a consideration, and she had made some changes to the test suite to differentiate these tests from what I had taken before.

Yesterday (June 23) we made the trip back over the mountains to meet with my neurologist and review the results. They were even better than I had anticipated.

It was true that the neuropsychologist had shaken up the test suite, and so I can’t make the sort of year-over-year, test-by-test comparisons that I’ve made before. Nevertheless, there were 42 individual assessments, and I could easily get an overall sense for how things were compared to 2015 through 2017. In 23 tests I scored high average, superior, or very superior. As I write this, I’m still in Seattle, and I don’t have my old tests available. But I don’t recall ever having received a “very superior” before. There was only one low average, and none of the below average scores that I had sometimes scored in the past.

In her summary assessment, the neuropsychologist identified five areas in which I had improved (single-trial learning and delayed recall from a word list, both semantic and phonemic verbal fluency, basic attention, and visual tracking/psychomotor speed), adding that some of them may have been inflated due to the practice effect. But from a broad cognitive standpoint, she wrote, “Mr. Brown is doing very well across all domains.”

My neurologist was quite enthusiastic about the results, and agreed that the improvements were likely a consequence of the lifestyle changes I’ve made. She mentioned that at least one other professional in her office had gotten a copy of Beating the Dementia Monster.

During the visit, we reviewed images from my most recent MRI (February) and compared it to the MRIs of 2012, 2015, and 2017. Some of these were done using the research machine for the SNIFF study. What we specifically looked for was a way of understanding the assessments of hippocampus volume. (The 2015 radiologist report had me in the 36 percentile of people my age, but the SNIFF study reports had me at less than the 1 percentile.) She didn’t try to assign numeric values from the images, but it was evident that there was little or no deterioration from the time I made the lifestyle changes I describe in Beating the Dementia Monster (December 2015). Nevertheless, there were notable changes (atrophy) between the 2012 images and the 2018 images.

So how do these results affect my future course? The neurologist said that we should not do cognitive testing next year. I will have a closeout suite for the SNIFF study in August, but I should take a break from cognitive testing after that until the summer of 2020. She said I should return next summer for an annual visit to see how things are going. We’ll be alert for anything unusual or unexpected, especially when the SNIFF study ends, and I’m taken off the insulin.

I won’t lie. Some mornings it’s really hard to get on that treadmill and keep it going for 45 minutes. But it’s really worth it.

Another one bites the dust

This week's ALZForum carries the story of another Alzheimer's disease drug trial that was terminated early.  The drug is Lanabecestat, which is a "BACE inhibitor."  The concept behind BACE inhibitors is that they can inhibit the generation of an enzyme that is specified in the BACE1 gene.  The enzyme cuts the "amyloid precursor protein (APP)," and a fragment from the cutting process is beta amyloid.  In AD, the amyloids accumulate on the neurons in the brain and interfere with their function.

What is the purpose of APP? No one knows.  Why does the BACE1 enzyme cut APP molecules?  No one knows.  But suppression of the BACE1 enzyme suggests logically that it could help control AD.

Several BACE inhibitors have been tried, but drug trials have been terminated prematurely because of bad side effects (e.g., liver damage), or they just weren't working.

This is just one more discouragement in a long string of discouragements in AD research.  When I was first diagnosed in 2015, the buzz I was hearing in the science media was that we would have an effective AD drug to market by 2019.  How things have changed.

At this point in time all we have for treating AD is what I explain in Beating the Dementia Monster:

• Get daily aerobic exercise (45 minutes a day, 6 days/week)
• Eat a Mediterranean or similar low-carbohydrate diet that favors leafy green vegetables, fish and poultry, and blueberries and strawberries
• Maintain social activity
• Get good, regular sleep
• Reduce stress (e.g., do Yoga)

The Alzheimer's Progression

We discussed earlier that the term Alzheimer's disease is now applied to the entire progression of the disease, not just the Alzheimer's dementia stage.  This has caused confusion among some people I've spoken with because we have always thought of Alzheimer's disease as simply dementia.  But the disease may actually begin a decade or more before the first symptoms appear (we don't really know).  The first symptoms produce the condition we call MCI. 

Each case is different, but a person with AD will often be considered to be in the MCI stage for about five years.  This, of course, assumes there is no intervention.  We contend that lifestyle interventions, such as exercise and diet, will delay the progression to Alzheimer's dementia by as much as 10 years.  That's a long time.

(There are other diseases and issues that can produce MCI.  MCI identifies a broad category diseases and disorders; AD is just one.)

I have prepared this graphic to help explain the progress of AD.

 

Ghost Blood Vessels -- Correction

In my post of June 30, I said the Ghost Blood Vessels video said that the calf is the biggest muscle in the body, but my brother wrote me and challenged that.   So I went back and watched the video again to see what they actually said.  What they actually said was that we think of the heart as the most important mover of blood, but the calves also play an important role in blood circulation.   They didn’t say anything about how big the calf muscle is.  Ooops.

Remember from your middle school biology that, while the heart pushes blood through the circulatory system, flow is very much assisted by the flexing of muscles.  Blood vessels are designed such that blood can only move in one direction, so that each muscle can serve as a sort of booster pump.  Flexing muscles squeeze the blood vessels and force the movement of blood, but it can only move one way--the direction the heart is working to push it.  This is why we stretch when our body wants to increase blood flow.