Getting the covid vaccine

I am in the vulnerable population for covid-19, first because of my age, but also because of my "underlying condition" of Alzheimer's disease.  Why is Alzheimer's disease of concern?  Because covid infections have been reported to have neurological consequences, and, by some reports, to spark an unusually strong inflammatory response.  You will recall from Beating the Dementia Monster that neuroinflammation, primarily inflammation in the brain, is an important part of the Alzheimer's disease process.  In fact, some believe that the accumulation of amyloid plaques is not actually part of the disease process, but rather results from inflammation interfering with the process for removal of beta amyloid and other trash in the brain.  So it's possible that a covid infection might undo all that I've fought for in the past 5 years.  People I've know who developed covid infections reported headaches, suggesting neuroinflammation.  So getting the vaccine seems to make a lot of sense for me.

But ... on the other hand ... vaccines in general, and perhaps the covid vaccines in particular, also produce an inflammatory response.  This is called post-vaccine inflammatory syndrome.  Perhaps taking the vaccine could also cause destructive neuroinflammation.  So I did not immediately dive into getting the vaccine.

Can post-vaccine inflammatory syndrome aggravate Alzheimer's disease?  Maybe, but the picture is complicated.  We reported in July 2020 on research presented at the biggest Alzheimer's Association conference correlating flu shots with a reduced incidence of Alzheimer's disease.  Now correlation is not causation, and no one proposed a causal relationship.  Instead, the best explanation to date (of which I'm aware) is that people who get their flu shots every year tend to be people with more healthful lifestyles -- people who get exercise, eat right, take care of their sleep, etc.  So it may be that lifestyle is a strong enough positive force to overcome any mischief caused by an inflammatory response to the flu vaccine.

So I kept my eyes open for news on covid vaccines and inflammation, noting that some people reported headaches after getting the vaccine.  I consulted with my neurologist, who told me that she was unaware of any reported correlation of the vaccine with neuroinflammation of a sort that could aggravate Alzheimer's disease.  

I also consulted with a friend in a management position at a retirement/assisted living facility regarding her observations, since pretty much the whole population of her facility had been vaccinated.  She had not observed any issues, but she also consulted with a nurse in her company who would have some insight.  The nurse also had not seen anything concerning.

So I decided to go ahead with vaccination, and I got my first Pfizer shot today.  I return for my second shot in mid-April.  It's only been a couple of hours, but so far no sore arm and no headache.

93% on the FAA professional drone pilot exam

I very occasionally sell stock photography and stock video footage.  (That's no way to get rich.)  Recently, it seemed that more and more of the stock video that's selling was taken by drones.  So I wondered if I might want to try my hand at that.  But, on investigation, I found that it's illegal to take aerial drone photography and videography for business purposes unless you have an FAA license as a "remote pilot" -- a drone pilot.  Well, I don't own a drone -- I've never even touched a drone -- but I thought I might see what's involved in actually getting a license.

Initially, I was going to get a license and then move ahead with getting a drone.  But as I contemplated the cost vs. how much I'd likely use the drone, I became less sure that I would follow through.  However, I thought it would be a great test of the effectiveness of the Dementia Toolkit strategies we discussed in Beating the Dementia Monster to simply pay $160, take the test, and see how I do.  And, who knows, maybe I will get a drone some day.  I told my neurologist that I was going to do this, and she was quite enthusiastic about the exercise.

So, three weeks and six jillion hours of YouTube exam prep videos later, I sat for the exam.  That was today, and I scored 93%.  The test center was in Walla Walla, which is a little more than an hour away.  Amy went with me and waited outside while I took the test.  It didn't help that I had terrible insomnia, both the night before and the night before that.  It did help that Amy's nephew, Eddie, is studying to be an airline pilot at Central Washington University, and he was able to coach me during exam prep on questions I had on air space and elevations.

In watching the exam prep videos, I saw a number of people on YouTube discussing their experiences and test scores.  The highest score I saw anyone report was 93%.  (The proctor for today's test said that she'd seen two 100% over her time there.)  You can pay one, two, or three hundred dollars for on-line exam prep courses, but I decided to do it by only learning from free resources I found on line and those provided by the FAA.  I doubt that I would have scored higher if I'd taken a course.

So was the purpose of the test to see if you know how to fly a drone?  Hardly.  The test consisted of 60 questions on reading the FAA's "sectional charts," understanding Class A, B, C, D, and E air space, decoding the FAA's cryptic weather reports, understanding aircraft traffic patterns around airports, understanding what pilots and towers are saying to each other on the radio, understanding such aeronautical concepts as "stall," knowing a whole raft of FAA regulations (some of which seem irrelevant to drones), understanding the role of human factors in accidents, etc.  (As it happens, much of my career before retirement involved applying human performance concepts in investigating and preventing accidents.) 

I feel pretty good about this.  When I recall the problems I had remembering my zip code and my phone number back in 2015-16, how I couldn't drive, how I couldn't even cross the street safely, I have to say that I've come a long way! 

Save the Date! September 13 -- 15

Last year I served on the planning committees for two regional Alzheimer's disease conferences -- one for creating dementia-friendly communities (by Harborview Medical Center in Seattle), and the other for educating both Alzheimer's disease professionals and caregivers (by the Alzheimer's Association).  In fact, I spoke twice at the conference on dementia friendly communities.  Both conferences are annual events, and I am again on the planning committees for both.

Both conferences will again be entirely virtual events, so people are free to join in from just about anywhere.  However, the conference on dementia-friendly communities is focused on the state of Washington.  Even so, I have found it useful to see what other states are doing to help inform us here about the ideas of others.

Regarding the conference on dementia-friendly communities, we are opening registration July 30, but we are hoping you will save the dates now: September 13-15, 2021.  Please feel free to share this information, including the following graphic with those you think would benefit. 

Why do we sleep?

Back in July 2019, I recommended a video by Dr. Matthew Walker about sleep.  He is director of the Center for Human Sleep Science at Berkley, and is regarded as one of the leading authorities on sleep in the world.  In 2018 he published the book Why We Sleep, which articulates much of what science understands about sleep.  Which isn't as much as we want to know, and much of what we do know has only been discovered in the past few years.

So I bought the book, and am now reading it.  I'm reading it now, because insomnia has risen to a crisis point, and I was wondering what insights it might bring.  At this point, I have a few takeaways. 

In case we didn't get it already, Dr. Walker emphasizes throughout the book the importance of sleep.  He also says that older people need just as much sleep as younger people, focused on the traditional 8 hours.

But older people have a lot more trouble sleeping.  This is not because they need less sleep, it's because even normal aging causes atrophy of the brain.  One particular part (located in the frontal area) that is particularly important to sleep is a casualty of atrophy.  But in Alzheimer's disease, this part of the brain is damaged earlier and more thoroughly than in normal aging.  So people with Alzheimer's disease suffer profound damage to their sleep.  If you speak with people working in memory care facilities you know that many of their residents will be up all night, at least without a sleep aid.  We should also recall that poor sleep aggravates Alzheimer's disease, resulting in a vicious cycle. 

The most commonly prescribed sleep aid for the elderly is trazadone.  Trazadone is not a hypnotic like Ambien, but is a low dose of an anti-depressant.  

The chemical that actually causes sleep is called adenosine.  It builds up in the brain while you are awake, but is degraded and removed from the brain while you are sleeping.  The steady build-up during wakefulness creates "sleep pressure" which is only relieved by sleep.  Sleep pressure is behind the sense of sleepiness you feel toward bed time.  (Caffeine blocks the adenosine receptors in the brain.) 

But it's more complicated than that.  Beside this cycle driven by buildup and exhaustion of adenosine, there is your circadian rhythm.  This is another cycle of alertness, one that may vary between people who are "morning people" (like me) and those who are not.  The hope is that the two cycles -- adenosine and circadian rhythm -- will align, because both promote sleep and alertness.  When the don't align (as in jet lag), you will have problems.

Another chemical associated with sleep is melatonin.  Some people treat melatonin supplements as a sleep aid, but it is not.  Both Dr. Walker and my sleep doctor say that when it seems to work, it is only acting as a placebo.  But that doesn't mean that it's not important to sleep.  And Dr. Walker cautions not to underestimate its power as a placebo.  (I have used melatonin off and on for a long time, but have never experienced a change in my sleep from either starting it or stopping it.)

The generation of melatonin is promoted by fading sunlight.  It then acts as a signaling mechanism to the body to say that it is now night.  This may, or may not, promote adenosine's action to cause sleep.    This is one reason why the adenosine cycle and circadian rhythm must be kept in sync for good sleep.

Dr. Walker likens melatonin to the race official firing the starting gun at the Olympic 100 meter race.  It declares the start of the race, but it's up to the runners to actually run the race.  

Dr. Walker also noted that it takes the body a day to adjust to one hour of jet lag.  So after traveling from the west coast to the east coast, it takes three days to adjust and align your rhythms.  But here, melatonin supplements have something to offer.  He says that a jet lagged person should take a melatonin supplement at about 7 or 8 p.m. to shock the body into realization that the sun has actually gone down.  This helps speed the adjustment.  In Dr. Walker's case, London, England is home, but he works and lives in California.  So he makes that trip regularly and must deal with 8 hours of jet lag each time -- and each way.  So he knows whereof he speaks.

For the moment, I am using trazadone to help me sleep.  It aggravates my balance and dizziness problems (when standing or walking), but I am at least feeling much more rested throughout the day.    

        

Alzheimer's Association Facts and Figures Report is now out

Each March I wait eagerly for the Alzheimer's Association to publish their Facts and Figures Report -- and it's now out.  Here are the links:

Full report

National Fact Sheet

I want to see it as soon as it's available, because it gives us the latest reports on research, treatments, and models of how the disease actually works.  This year however, covid-19 has put something of a lid on research, and there wasn't much to talk about there.  However, the report did focus on something important: Race, Ethnicity and Alzheimer’s in America.

Why is this important?  Minorities, especially African Americans, Hispanics, and Native Americans, have a higher incidence of Alzheimer's disease and other dementias than the rest of the population, but the focus of research and care options has largely been on people of European ancestry.

The report spends time on two issues: health disparities and health care disparities.  A health disparity is "a higher burden of illness, injury, disability or mortality experienced by one group relative to another."  A health care disparity is a "difference between groups in health insurance coverage, access to and use of care, and quality of care."  Combined, they are "differences that are not explained by variations in health needs, patient preferences or treatment recommendations and are closely linked with social, economic and/or environmental disadvantage."

What I found interesting in the report was the variance in perceptions about how people of color fare in the health care system and perceptions regarding what the system does to aid people with dementia.  Many care givers were concerned about people being used as research guinea pigs, and others were concerned they would receive the placebo in a drug trial.  The latter is especially understandable, since a drug trial will eat up the precious few years someone might have for getting better with a successful drug.

The eye -- window into the brain?

My ophthalmologist once told me that the eye has more nerve connections to the brain than any other part of the body.  He had a number for how many connections there are, but I don't remember what it was.  I read elsewhere that some neuroscientists consider the eye to simply be an extension of the brain.  Consistent with that view, it turns out that beta amyloid can be found in the retina.  Of course, we understand the generation of beta amyloid and its destructive effect on brain cells to be a central feature of Alzheimer's disease.  So, if the eye is part of the brain, whatever is going on in the brain proper would also be going on in the eye.

My friend Mike in Virginia sent me this article last week about research into biomarkers for Alzheimer's disease and Parkinson's disease "focusing" on what can be found on the retina of the eye.  The hope is that such biomarkers can provide an early diagnosis of pre-clinical disease -- before the first symptoms appear.  This can help with research, because it is believed that emerging treatments will work better the earlier in the course of the disease they are applied. 

As far back as 2018, we have discussed the value of inexpensive and easily observed biomarkers in the diagnosis of Alzheimer's disease.  Currently, doctors and researchers may use expensive MRIs and PET scans, but there is hope that blood tests will soon provide cheaper and earlier diagnosis.  So the idea is that, in the future, pretty much the same equipment your optometrist uses to check for glaucoma can be used to help diagnose Alzheimer's disease.

The article focused on the work of the leaders of two different research teams:

• Maya Koronyo-Hamaoui at Cedars-Sinai in LA who leads a team that has been developing a technique for finding amyloid plaques in the retina using a machine similar to that used in an ophthalmologist's exam.  The cost is said to be about $285 per scan.
• Ruogu Fang, an electrical engineer specializing in AI working at the University of Florida, leads a team learning to use an iPhone image to examine blood vessels in the retina. 
  

In the case of Koronyo-Hamaoui's device, the subject drinks a liquid containing curcumin, the substance that gives the spice turmeric (and hence, curry) it's flavor.  (This will resonate with those of us who love Indian food.)  The curcumin has an affinity for beta amyloid, and it can be detected by shining blue light on it.  So blue light can be used to identify amyloid plaques developing in the retina.

Fang's iPhone technique looks for changes in blood vessels associated with Parkinson's disease, but not Alzheimer's.

Early detection of Alzheimer's disease continues to be an important area of research.  The downside is what it will mean for those seeking long term care insurance.  I remember that when I applied for long term care insurance (before I had cognitive issues), they examined me very closely for memory problems.  

 

I'll speculate.  A person with a positive test for beta amyloid, but prior to cognitive symptoms, will be unable to get insurance at a reasonable price.  The insurance companies will likely insist on the tests unless curbed by legislation.  A person who tests negative my not see a justification for the cost of insurance.  This could be destructive to the industry.

 

It may not be a wise decision to skip insurance, especially since the price might go lower with Alzheimer's patients ruled out.  There are many other causes of dementia and other debilitating diseases that afflict the elderly.  

The biomarker blood tests have not rolled out as quickly as I had hoped.  We'll see what unfolds in the coming months.

Herpes continues to interest research

A few weeks ago we wrote about an assessment of thinking on the role of the herpes simplex virus in Alzheimer's disease.  (We have actually been writing about this for some time.)  We noted that the connection is controversial, and it sparks emotional discussion among researchers.  Well, there's some new fuel for the fire coming from Sweden.  

The February 14 issue of the journal Alzheimer's & Dementia (the Journal of the Alzheimer's Association) carried the results of a study of about 265,000 subjects, age 50 and above, who were either diagnosed with either of two herpes simplex infections and/or were otherwise prescribed certain antiviral drugs targeting herpes simplex.  In older adults, herpes simplex is commonly associated with ailments such as cold sores and shingles infection.  The researchers were looking for a link between antiviral treatment and the incidence of Alzheimer's disease, hoping to show that these treatments would have a protective effect.  Of course, the assumption going in was that herpes does have agency in the development of Alzheimer's disease, although not everyone fully embraces this.

Data about the subjects were derived from two Swedish nationwide databases: the National Patient Register and the Swedish Prescribed Drug Register.  Data collected was from 2005 to 2017.  Subjects who had received antiviral treatment had generally received acyclovir or valacyclovir.

The results? "Our findings together with previous reports suggest that antiviral treatment might reduce long‐term risk of dementia. In contrast, untreated herpes infection increases the subsequent dementia risk."  Of course, they called for further study.