The first time I heard the term “inflammation” in the context of Alzheimer’s was when a cousin of mine mentioned it a couple months after I was diagnosed with Alzheimer’s. At first, the topic seemed exceedingly vague. Inflammation? Well, yes. The phenomenon is commonplace. At the end of the holidays, I experienced a freak accident. It was a day of mild weather, and Paula asked me to drag our Christmas tree further down our driveway. The unseasonable weather prompted me take off my gloves. A moment later I was reminded of World War II movies in the Pacific, when Japanese soldiers were purported to torture U.S. soldiers by jamming slender bamboo reeds beneath the fingernails. By the next day, during a meeting Paula and I was attending, I had to recuse myself for a time. No one on hand had any painkillers on hand. The next day I visited my doctor’s office, and one of the nurses was almost gleeful with the quantity of pus I produced.
A recent Time magazine article began with the curious question, “What does a snubbed toe or a splinter in a finger have to do with your risk of developing Alzheimer’s, suffering a heart attack or succumbing to colon cancer?” This rhetorical question is at the heart of cellular inflammation. Before the advent of antibiotics, anyone who developed a serious infection had a fair chance of dying, or sustain damage to their heart, as was the case of my paternal grandmother, who died in middle age.
“Most of the time inflammation is a lifesaver that enables our bodies to fend off various diseases. But the process is not failsafe. “Every once in a while,” the writers pointed out, “the whole feverish production doesn’t shut down on cue.” And sometimes the problem is a genetic disorder. In a grisly image, the writers remark, “chews up brain cells of Alzheimer’s victims.”
Do a search on “cellular inflammation,” as I did, and you are likely to be presented with a concise definition, provided, most likely, by Google: “Cellular inflammation is the type of inflammation that is below the perception of pain.” What it does is disrupt the hormonal signaling at the cellular levels that leads to increased fat levels,” which can lead to chronic diseases, including obesity.” But the most salient information I retrieved was supplied by Dr. James Ellison, of the Swank Memory Care Center.
“Our understanding of diseases often follows a predictable journey,” Ellison noted. “First, we begin to understand that a group of symptoms occur together”—a simple example is that a sore throat typically leads to a cough. But, “In the case of the more severe sore throat, its potential for leaving serious heart damage, was understood before its cause, strep infection, was made possible by diagnostics. Once a cure is in place”—Ellison is an optimist—“researchers may be able to design a specific treatment, but not always. We know the antibiotics are likely to defeat strep throat, but we still have no cure for the common viral sore throat.” This threshold must be frustrating to scientists.
But let’s assume that Ellison’s way is the most promising approach. Under the heading “Microscopic Guard Dogs,” he explores the possibility that large white blood cells, called macrophages, that “feed on pathogens.” In an extended metaphor, Ellison writes, “the body’s immune system, which functions as a security guard by identifying and attacking potential sources of harm, is armed with a variety of protective weapons. But “unlike an infection that can be defeated, the plaques remain as a persistent irritant. In the smoldering battle between microphages and plaques, inflammatory chemicals called cytokines and damaging chemicals…Healthy brain cells can be caught in the crossfire as well.”
Concluding, Ellison writes, “a current explanation of this failure focuses on the different effects that anti-inflammation treatment might have at different disease stages of Alzheimer’s.” This sounds reasonable, but perhaps a bit pat. The “cocktail” approach of medicine, which came into vogue when it became clear that Magic Johnson, after the former NBA superstar was diagnosed with HIV in 1991, defied expectations of his early demise. But when I am honest with myself, I feel that a real breakthrough remains quite down the road, perhaps another full generation.
Could cellular inflammation be the cause of my Alzheimer’s diagnosis? Nothing else, so far, checks out: no hint of Alzheimer’s in my family tree. No concussion serious enough to put me in danger of the much-feared “CTE,” short for chronic traumatic encephalopathy, which in recent years have disturbed many former football players. I will probably never know.
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