Are they completely removed so they can never be remembered again?
All of these possibilities are the product of brain activity that is progressively lost as Alzheimer’s disease onsets and progresses to full-fledged dementia. Since the brain is an organ, it is made up of cells. A large number of these cells are specialized nerve cells or neurons. Neurons, through their interactions with other neurons and other cells in the brain, serve to process incoming information and to store this information as the basis of our memories. Thus, in one way or another, our memories are stored within cells in our brains. Because neurons are the primary unit of brain function, Alzheimer’s disease can be considered a disease of brain cells.
Cells of the Alzheimer’s Brain
As we will see in Chapter 5, the brain is actually made up of many types of cells but it is the neurons that are of primary interest in Alzheimer’s disease because it is these cells that show the first clear evidence of the disease. The brain neurons are the central place where the changes of the Alzheimer’s brain begin and end. As a result, they are the site where scientists hope to find the cure for Alzheimer’s disease. Searching the brain for the cause of Alzheimer’s is much like an episode of the television show CSI; it is a true Crime Scene Investigation. Rather than investigating a dying person, we are essentially looking at the slow death of the brain—the site of all reason, learning and memory. So, like a crime scene, we want to see what is different from the normal brain as compared to the Alzheimer’s brain. Then we want to understand how those differences arose: what caused a good brain to go bad. Finally, when we understand what caused the disease, we want to learn how to prevent it. But science and crime scene investigation are like life: sometimes the culprit is elusive and evades detection or capture. In that case, we have to compromise. Since we can’t prevent the death of the brain, we want to at least be able to slow its degeneration or, even better, stop it in its tracks. This approach will have to do until the cause or biochemical culprits responsible for Alzheimer’s disease are finally found and scientists can begin to prevent the disease, slow it or, hopefully, develop a cure.
So that’s what we’re going to do in the book. We’re going to see what we know about the underlying events of Alzheimer’s disease as it relates to brain cells. What causes these brain cells to lose their ability to function properly? What causes them to die? How can we slow this sequence of events? And, ultimately, how can we determine how the disease starts? Before we get out our microscopes and our biochemical tools to understand these changes, let’s look at a short history of Alzheimer’s disease to understand how this disease was first identified and how that discovery set the stage for how things sit today.
A Very Short History of Alzheimer’s Disease
Unofficially, Alzheimer’s disease has been around as long as human beings have existed as thinking entities. It didn’t become an official disease until it was properly diagnosed by Alois Alzheimer. Dr. Alzheimer described the behavioral characteristics of Alzheimer’s disease over 100 years ago, which in itself was a major medical advancement. His work, however, went much further. He also delved into the underlying changes in the brain that were associated with the disease. To this day, his prescience defined the three primary neurological attributes of Alzheimer’s disease: the appearance of senile plaque and tangles coupled with the death of brain cells (Figure 1.2). These are still the primary criteria that are used today for defining the disease. As such, while plaques and tangles are introduced later in this chapter and will be covered throughout this volume, they are presented in much greater detail in Chapters 6 and 7.
Figure 1.2. Alois Alzheimer discovered the primary hallmarks of Alzheimer’s disease: plaques and tangles.
The Personal Side of Alzheimer’s Disease
What is Alzheimer’s disease? This might sound like a simple question to answer but it is not. This is because this disease is different things to different people. To a clinician or biomedical researcher, it is the buildup of bad stuff in the brain, the loss of specific nerve cells or changes in cognitive behavior. To a doctor, it’s the emotional challenge of having to diagnose a person with the disease and telling them they can no longer do the things they want to do. To a caregiver, it’s a 24-hour-a-day challenge without a positive outcome. To a family member, it’s the loss of the person they knew and loved. To the Alzheimer’s sufferer, it begins with the loss of their memory and dignity and ends with the loss of their whole world. To anyone who has seen the face of Alzheimer’s, all of these points of view are important because they all play a part in helping us understand this devastating disease. So let’s start with the currently held view of how the disease starts and progresses. Then, as we work our way through this book, we will develop this knowledge into the full picture of Alzheimer’s disease as it is understood today.
Figure 1.3. The basic stages in the progression of Alzheimer’s disease.
Alzheimer’s disease involves a progressive loss of mental ability that begins with mild cognitive impairment (i.e., decreased ability to think, reason, remember), or MCI, that can progress, in the worst case, to true dementia (Figure 1.3). One of the problems in research has been that different biomedical researchers and clinicians have formulated a diversity of stages and sub-stages for the disease. While these are well intentioned and of value for the researcher, they make it more difficult to discuss the disease in lay terms. So in this book, except when absolutely needed, the disease will be discussed in terms of mild cognitive impairment occurring as a prelude to dementia.
As we age our ability to remember things declines gradually. In Alzheimer’s disease, this decline is often more rapid and more devastating. Rather than symptoms like forgetting a name or the inability to immediately remember it, the disease is reflected in more severe memory impairment. Initially the memory loss is mild but worse than a normal individual of the same age and health. As it progresses, the person who is afflicted may not even realize where they are, even when in their own home or neighborhood. They may not recognize family members and friends. By the time the disease has affected a person’s ability to function socially or to continue in their job, they are in the clinical stage of dementia.
Alzheimer’s disease is a cruel affliction that progressively robs a person’s sense of self and awareness. Following a pathway to cognitive oblivion, it turns loved ones and friends into strangers and, at its worst, enemies. The very world in which the Alzheimer’s sufferer lives becomes foreign if not frightening, as altered brain cells slowly erase that person’s past and their grip on reality. Then those brain cells die, signaling the final stages of this horrific disease.
The problem with Alzheimer’s disease is that it is not like typical medical disorders like heart disease, diabetes or even cancer. Those diseases have specific symptoms that, for the most part, are clearly definable. In most cases, medical intervention and well-defined approaches for a cure are available. The course of these diseases is also fairly predictable. This is not the case with Alzheimer’s. There are multiple pathologies associated with the disease. The disease is person specific and doesn’t follow a predictable pathway. There are no available cures and even attempts to slow the disease are not well developed.
The Reality of Alzheimer’s Disease
No matter how you slice it, Alzheimer’s is a devastating disease that wreaks havoc on the lives of individuals and their families. We notice that, as we age, it can be difficult to remember a work or a name. As a senior, I was shocked when I was playing Mario Kart on my Nintendo with my grandson. I thought I was doing quite well motoring along, dropping
