Saturday, June 23, 2018


My plan this week was to write about the corrosive effect of anxiety among people with dementia. That is still my aim, but not quite the way I expected. As a prologue, I must confess that I lost most of my first draft of this blogpost. I thought I was immune to this kind of mistake. I always back up my drafts, off-site. Where the vulnerability was exposed was in the name of the file. The two files were almost identical: only one or two key strokes were different. I was left with a rump end. From time to time, I aim to hit a lyrical vein, or even a stream-of-consciousness flow—if the piece had survived. My writing was flowing. I felt this would be one of my better blogposts. But the next day I had almost no recollection of what I had written the day before. That speaks volumes about this insidious disease.
The file should have been in the trash-can icon, from which I could easily have retrieved it to my desktop. I was pleased with my first draft. And when I realized I was having trouble finding it, I didn’t panic. I assumed that there was a way to bring forth my missing file. But the other file, the shorter one, was overwritten. One file held the entire draft. The other one held a fragment, about one-third of my full draft. Unknowingly, I had wiped out a large portion of my blogpost. And as any writer can tell you, rewriting what you’ve lost can be profoundly challenging—especially if you have dementia. I could remember almost nothing from the brunt of my lost first draft.
This, of course, was profoundly frustrating. I knew that I was writing well, but I was unable to transfer the information to my long-term memory. Anxiety runs on one side of my family, so it’s no surprise that I would have anxiety problems once I developed Alzheimer’s. But it wasn’t until I developed Alzheimer’s did my anxiety became a problem for me.
What he did struggle with was anxiety. It’s one reason why he didn’t do as well as he might have in his dual careers, in teaching and commercial fishing. How is this connected with dementia?  Because anxiety on its own can be terribly corrosive. To introduce a metaphor from the drug culture, fentanyl, used to speed up the high from opiates, is like adding anxiety to people who already have Alzheimer’s disease. The less stress you have on your shoulders, the better.

Friday, June 8, 2018

Why we sleep

This book by Matthew Walker is a revelation. Most people rarely think deeply about sleep, unless they are running a sleep deficit, or worse. Occasionally, in my twenties, I would have a severe bout of insomnia. The worst was in Berlin, about six months after the Wall came down. I felt like a husk of myself. As dawn was rising, saliva was pooling in my mouth. But since that lonely dawn more than a quarter-century ago, I’ve only rarely had pronounced sleep problems. These days, Paula is the one who isn’t sleeping very well, thanks in part to my penchant for tossing and turning in my sleep.
Aptly, Walker devoted a section of his book to Alzheimer’s disease. Most people recall learning about REM [rapid eye movements] in high school biology classes. But I had not heard of, or long forgotten, NREM [non-dreaming] sleep. As Walker noted, people have less of the deep NREM sleep as they age. But those with Alzheimer’s suffer this symptom much more acutely: “Sleep disturbance precedes the onset of Alzheimer’s disease by several years, suggesting that it may be an early warning sign of the condition, or even a contributor to it.”
Walker continued, “What struck me was the location in the brain where amyloid accumulates early in the course of Alzheimer’s disease, and most severely in the late stages of the disease. That area is in the middle part of the frontal lobe...the same brain region essential for the electrical generation of deep NREM sleep in healthy young individuals.”
Walker collaborated for several years with Dr. William Jagust at the University of California, Berkeley. The research teams developed a hypothesis: “The more amyloid deposits there were in the middle regions of the frontal lobe, the more impaired the deep-sleep quality was.” Walker stated that their research added “a key piece in the jigsaw puzzle of Alzheimer’s disease,” namely  “a new pathway through which amyloid plaques may contribute to memory decline later in life.” He goes on to explain: “Despite Alzheimer’s being typified by memory loss, the hippocampus—that key memory reservoir in the brain—is mysteriously unaffected by amyloid protein,” which is usually regarded as the most prominent feature in Alzheimer’s disease, with its canary-in-the-coal-mine feature.
Walker believed sleep disruption could be “the missing intermediary factor—one that was transacting the influence of amyloid in one part of the brain on memory, which depended on a different region of the brain.”
In a clinical study to test this theory, elderly patients with varying amounts of amyloid plaque were asked to learn a new set of facts. “We discovered a chain-reaction effect,” Walker wrote. “Those individuals with the highest levels of amyloid deposits in the frontal regions of the brain had the most severe loss of deep sleep and ... [thus] failed to successfully consolidate those new memories. Overnight forgetting, rather than remembering, had taken place. The disruption of deep NREM sleep was therefore a hidden middleman brokering the bad deal between amyloid and memory impairment in Alzheimer’s disease.” The distinction, according to Walker, was that this was not just “normal aging”; it was “a departure from what otherwise is the signature of sleep decline as we get older.”
While Walker was doing his research, he became acquainted with Maiken Nedergaard. The Dutch researcher “found a kind of sewage network called the glymphatic system within the brain. Its name is derived from the body’s equivalent lymphatic system.” (Named from the Greek root word for “glue.”) There was a second major breakthrough, according to Walker: “Think of the buildings of a large metropolitan city physically shrinking at night, allowing municipal cleaning crews easy access to pick up garbage . . . , followed by a good pressure-jet treatment of every nook and cranny. When we wake each morning, our brains can once again function efficiently thanks to this deep cleaning.”
Walker asked rhetorically, “So what does this have to do with Alzheimer’s disease? One piece of toxic debris evacuated by the glymphatic system during sleep is amyloid protein—the poisonous element associated with Alzheimer’s.” Walker went on to suggest, coyly, that “wakefulness is low-level brain damage.” And, in a more serious vein, Walker observed, “Can we begin supplementing the declining deep sleep of vulnerable members of our society during midlife?” That is a laudable goal. But I have two comments. The first is that, within a week to 10 days after leaving my job, I was sleeping well after many years of difficulty sleeping. And that wasn’t just a flash in the pan. It’s been three years since my diagnosis, and I usually go to bed around 11:30 and wake up around 7:30. But something tells me that sooner or later, I will not be sleeping soundly. More than six years since my first symptoms, I am cherishing my sleep.