Alzheimer\'s Disease Is the Seventh

Alzheimer's disease is the seventh leading cause of all deaths in the United States and the fifth leading cause of death in Americans who are 65 years of age or older. The reason that the number of people afflicted with Alzheimer's is growing so fast is simple: the baby boom generation is quickly becoming the older generation. This paper presents factual data about this dreaded disease, and unfortunately it reflects that fact that the literature available in scholarly and in popular publications does not seem optimistic about a formula for prevention or for a cure. As of 2008, about 5.2 million Americans had Alzheimer's; of those, 5 million were 65 years of age or older. In fact one in eight persons 65 or over -- that is 13% -- currently are afflicted with Alzheimer's. The data available indicates that every 71 seconds someone in the U.S. develops Alzheimer's; in forty years that number will change to every 33 seconds. The overall number of people with Alzheimer's is expected to reach 7.7 million by 2030. But millions upon millions of dollars of federal and private money are being poured into research, so there is a reason to hope for a positive outcome. Meanwhile, this paper reflects the failed research projects of the past, the potential remedies still unproven for the future, and it also reviews the price that caregivers pay in terms of their emotional, physical, and their psychological health.

Basic Information on Alzheimer's

Alzheimer's disease is a brain disease that seriously interferes with a person's memory, a person's thinking and hence the behavior of the person is greatly impacted as well. The Alzheimer's Association (AA) explains that the symptoms generally arrive "slowly" but they get "worse over time, becoming severe enough to interfere with daily tasks." Alzheimer's is the most common form of "dementia," which is a general term for the loss of memory and the loss of the ability to reason and think with clear intellectual faculties. Fifty to seventy percent of cases of dementia are categorized as Alzheimer's, according to the AA. This paper will delve into the literature on Alzheimer's, including the discouraging lack of preventative or curative solutions, the realities for those who have Alzheimer's as well as those who will be (or already are) caregivers, and the data on how many people can expect to be afflicted with the disease in the near future. The exact chemical dynamics that take place in the brain will also be reviewed.

Body of Paper

Is Alzheimer's just a normal part of growing old? Absolutely not, the AA reports, albeit the "greatest risk factor is increasing age." The majority of people with Alzheimer's are indeed over 65 but five percent of those afflicted with the disease have what is called "early-onset" -- that effects mainly people in their 40s and 50s (AA). And it is pertinent to mention that just because a person is getting up in age and is becoming somewhat forgetful, doesn't mean that Alzheimer's is setting in. There are a variety of causes to explain memory loss, but rather than guess at the reason for the memory loss the professionals strongly suggest a visit to the doctor to determine the exact cause of the forgetfulness. The Alzheimer's Association has a "helpline" that is available night and day [HIDDEN] ); AA will refer callers to doctors in their area who have professional experience evaluating memory problems.

The progressive nature of Alzheimer's takes a toll on sufferers, AA reports. At first the symptoms are there, and they are for the most part mild in the early stages. But over the years the individual with Alzheimer's begins to lose the ability to carry on a simple conversation, or respond appropriately to what is going on in the environment around them. The person who has the disease can live roughly eight or so years after their symptoms have become obvious, AA explains, but some people live up to twenty years after being diagnosed with Alzheimer's.

Is there a cure? No, there is no cure known to healthcare professionals at this time, but there is a great deal of research ongoing. In fact though there are treatments that "temporarily slow the worsening of symptoms" and that "improve the quality of life for those with Alzheimer's," and improves the quality of lives their families and other caregivers experience, AA continues. Ninety percent of what is known to scientists about Alzheimer's has been learned over the past 15 years, and worldwide there are multiple research teams working on finding a cure, or at least a deeper understanding of why people fall prey to this debilitating disease.

Are there any remedies for prevention of Alzheimer's? A scholarly journal article in CNS Drugs (Sano, et al., 2008, p. 887) points to the disappointments that have been reported in several clinical trials over the past twenty years. To wit, while observational studies and animal models have offered "promising findings" and have "generated excitement," the truth is that observational studies aren't recognized as valid or helpful, Sano explains (p. 887). What is required are placebo-controlled clinical trials, Sano writes, and there have been clinical trials involving: a) symptomatic treatments; b) cholinesterase inhibitors; c) antioxidants; d) NSAIDs; e) hormone replacement; f) nutritional supplements; and g) "non-pharmacological interventions" (Sano, 2008, p. 887).

Sano and colleagues agree that while success in the area of "true prevention" of Alzheimer's right now could be thought of as "fiction" it is nonetheless "fiction with a hopeful theme" (p. 888). While most of the money spent on research emphasizes a cure, Sano believes that there are "many advantages" to zeroing in on prevention, "including the fact that it would expand the period of high quality-of-life in aging populations (p. 888). Indeed, if some form of prevention could be made available, the delay of the onset of Alzheimer's by "as little as 1 year" could "reduce prevalence by 25% over the next 50 years" (Sano, 2008, p. 888).

The problem with launching preventative research is that "…trials to assess this type of intervention must enroll large numbers of subjects…with long periods of observation and monitoring," Sano explains (p. 889). This boils down to a great expense, and it is clear that most of the money going into research is being funneled into cure, not prevention. But that hasn't stopped some scholars, including Sano, from researching for possibilities. For example, there is evidence that there is a link between cholesterol and Alzheimer's, Sano asserts (p. 890). There is also a reported connection between the reduction of hypertension and a reduced risk of "cognitive impairment and dementia," Sano reports, as she reviews the possible approaches to finding a preventative solution (p. 893).

And while it appears that cardiovascular risk "worsens the clinical presentation of Alzheimer's disease" it is not clear if it effects the "pathology of Alzheimer's disease," Sano continues on page 893.

Sano and colleagues may be a bit idealistic by working towards a prevention for Alzheimer's, especially following the report of an expert panel that gathered in April, 2010, under the auspices of the National Institutes of Health (Traynor, 2010, p. 960-61). The panel looked at existing research into drugs, dietary supplements, exercise, diet, "social and cognitive engagement" along with other factors that are believed to be potentially useful in preventing Alzheimer's. But the report's findings were "negative" (in terms of any potential breakthrough for prevention) and the reasons for the negative results are several, Traynor explains. There is a lack of "well-conducted, randomized clinical trials" and there is a lack of "standardized methods for diagnosing Alzheimer's disease and cognitive decline," Traynor concludes (p. 961).

What are the earliest symptoms? What testing can be done to verify that the person in question indeed has Alzheimer's? The Alzheimer's Association reports that the most common symptom that people experience is "…difficulty remembering newly learned information." That is, the part of the brain that affects learning begins to fail and that leads to the following: "disorientation; mood and behavior changes; deepening confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more serious memory loss and behavior changes; and difficulty speaking, swallowing and walking" (AA).

How does Alzheimer's affect the brain? The AA materials (www.alz.org) explain that the brain has approximately 100 "nerve cells" that are also called "neurons," and every nerve cell links (microscopically) with "many other" cells to create networks of communication. Every cell group has a specific task to perform in the brain; some cell groups assist leaning, thinking and remembers while other cell groups provide sight, hearing and smell, AA explains. The cell groups behave a bit like "tiny factories" because they do things that factories do.

For example, the cell groups receive supplies, they generate energy and they actually build equipment within the brain. Also, cell groups get rid of waste and coordinate with each other thanks to available oxygen they use for fuel. (It is common knowledge that when a person's oxygen supply to the brain is cut off, the person dies, so oxygen is a vital component of the cell groups.) Researcher believe that when Alzheimer's begins to attack, it hits the "factory" of cell groups that otherwise are functioning perfectly. There are breakdowns in the communications that the cell groups hitherto provided, and although scientists don't know precisely where the attack is first launched by Alzheimer's, but they do understand that "as the damage spreads, cells lose their ability to do their jobs and, eventually die, causing irreversible changes in the brain" (www.alz.org).

Prime "suspects" in that attack on the cell groups are "plaques and tangles," AA explains. Plaques are deposits of a certain protein called "betaamyloid" (pronounced "BAY-tuh AM-uh-loyd"); the protein fragments build up in the spaces between the nerve cells. Tangles are "twisted fibers" from a different protein called "tau" (that rhymes with "wow") that build up inside the nerve cells. It is known that all humans develop tangles and plaques to some degree, but those who are afflicted with Alzheimer's tend to get many more. And, AA continues, the plaques and tangles that attack Alzheimer's patients tend to appear in "predictable patters," notably starting in the area of the brain that deals with memory. Eventually, the plaques and tangles move on to other parts of the brain, researchers have found (www.alz.org).

Although researchers aren't exactly certain as to what precise role the plaques and tangles play in the Alzheimer's condition, they believe that the plaques and tangles simply block the cell groups' (nerve cells) ability to communicate normally. The communication processes, in other words, are disrupted, and the disruption -- along with the death -- of nerve cells is a pivotal part of the personality changes and other problems faced by Alzheimer's patients (www.alz.org).

Alzheimer's genetics fact sheet: The Alzheimer's Project (a component of the U.S. Department of Health and Human Services and the National Institutes of Health) published a fact sheet that is somewhat esoteric and technical, but overall quite straightforward. The "early onset" of Alzheimer's (early-onset AD is also called "familial AD" or FAD) can be inherited, the authors explain (p. 2). For example, FAD is linked to gene mutations on chromosomes 21, 14, and 1; what happens is a gene mutation causes "abnormal proteins" to form on the chromosome.

A mutation on chromosome 21 creates abnormal amyloid precursor protein (APP) to form; a mutation on chromosome 14 causes "abnormal presenilin 1 to be made," and a mutation on chromosome 1 leads to "abnormal presenilin 2" (The Alzheimer Project). The bottom line is this: if a child inherits even one of those above-mentioned mutated genes from a parent, that child will "almost always develop early-onset AD (FAD)" (p. 2).

It should be mentioned again that only five percent of all people who are afflicted with Alzheimer's get it between the ages of 30 to 60 (called FAD). The great majority of course suffer from "late-onset AD" and unfortunately while a specific gene mutation has been identified for FAD, no such gene has been identified for late-onset Alzheimer's, The Alzheimer Project (TAP) reports on page 2). That said, there is a "predisposing genetic risk factor" that has been identified that "does appear to increase a person's risk of developing the disease" (TAP, p. 2). That risk is related to the apolipoprotein E (APOE) gene that is found on chromosome 19.

What does APOE do to contribute to late-onset Alzheimer's? The TAP material explains that APOE contains "the instructions" that are required to create a protein "that helps carry cholesterol in the bloodstream" -- and it comes in several forms. The form that is most likely to be found in people with late-onset Alzheimer's is APOE #4. Indeed, "dozens" of empirical studies confirm that APOE #4 increases one's risk of getting Alzheimer's -- but as yet no one knows why that is true (TAP). About 40% of all people who get late-onset Alzheimer's have APOE #4 in their bodies -- and 30 to 40% of the American population have APOE #4. And the obvious next question -- is there a test to determine who has APOE #4? Yes there is but even though researchers can identify APOE #4 in a person, APOE #4 is just a "risk factor" and is not a guaranteed precursor to getting Alzheimer's.

Latest research fails to help Alzheimer's patients: An article in The Washington Post (Tanner, 2010, p. 1) reports that a once-hopeful idea -- using Omega-3 pills -- has turned out not to be helpful. Scientists hoped that Omega-3 would boost memory in those with Alzheimer's, but it didn't turn out that way. "We had high hopes that we'd see some efficacy," said Dr. Joseph Quinn, a researcher at Oregon Health and Science University, the author of the $10 million study.

The bottom line in this study is that 300 men and women (average age 76) with "mild to moderate" Alzheimer's were randomly assigned to take either DHA pills (containing Omega-3 fatty acid) or fake pills. The research went on for 18 months, Tanner explains. The discouraging end result of the research project was that the DHA pills "…provided no benefits in slowing Alzheimer's symptoms" (Tanner). And so Quinn commented that "There is no basis for recommending DHA supplementation for patients with Alzheimer disease."

The program director of Alzheimer's studies at the Institute on Aging, Laurie Ryan, used the word "discouraging" to describe the failure of Omega-3 to slow down the onrushing Alzheimer's disease (Tanner). But she added that her institute is spending "millions of dollars on research into other possible treatments" and those include biomarkers, drugs, and lifestyle changes that may lead to "…more targeted drug treatment" (Tanner).

Smoking (heavy smoking) raises the risk of Alzheimer's: A study published by Kaiser Permanente involving 21,123 men and women over a 23-year period showed that 5,367 of those 21,123 became afflicted with dementia later in life. And of the 5,367, exactly 2,367 were cigarette smokers -- and 261 of those were "heavy smokers" (up to or more than 2 packs a day). And so the data produced from this study shows that smoking 2 packs a day increases the risk of getting Alzheimer's "by more than 157%" according to the U.S.A. Today article.

Why would smoking increase the chances of getting Alzheimer's? Researchers believe that people who smoke have "…increased inflammation, and we know inflammation also plays a role in Alzheimer's," according to Rachel Whitmer, a research scientist with Kaiser Permanente. The chief medical and scientific officer for the Alzheimer's Association, William Thies, was quoted saying that a large enough sample was used in this research "…to look at different ethnic groups, and it shows smoking's effect on dementia does not differ based on race" (USA Today, 2010, p. 1).

The Timeline -- Including Major Milestones -- for Understanding Alzheimer's

1906: To answer the question as to how Alzheimer's got its name, in 1906 Dr. Alois Alzheimer, a German physician who was a pioneer in "linking symptoms to microscopic brain changes" (www.alz.org) began working on strategies to unravel the clues vis-a-vis memory loss. Dr. Alzheimer was providing a physician's care for "the haunting case of Auguste D., a patient who had profound memory loss" and who had "unfounded suspicions about her family" along with other "worsening psychological changes" in her body. After Auguste D. died, Dr. Alzheimer performed an autopsy and saw "dramatic shrinkage and abnormal deposits in and around nerve cells" (www.alz.org).

1910: Dr. Emil Kraepelin, a German psychiatrist who was a colleague of Dr. Alzheimer, gave the disease a name -- "Alzheimer's Disease" -- in the 8th edition of his book called Psychiatrie.

1931: The electronic microscope was invented by two Germans, Max Knoll and Ernst Ruska; this allowed researcher to delve into brain cells "in more detail"; the electronic microscope was not used often in research environments though until after WWII.

1968: The very first "validated measurement" scale for assessing "cognitive and functional decline in older adults" was developed; this advancement paved the way for scientists to "correlate the level of measured impairment with estimates of the number of brain lesions" along with the amount of tissue that had been damaged in the afflicted individual.

1974: The National Institute on Aging (NIA) was established by the U.S. Congress; this has become America's principle agency on the federal level that supports research into Alzheimer's disease. The NIA is grouped with the National Institutes of Health (NIH).

1976: Alzheimer's is recognized as the most common cause of dementia; neurologist Robert Katzman made that identification in his editorial published in Archives of Neurology.

1980: The Alzheimer's Association, a nonprofit, independent organization was established; Jerome H. Stone was the founding president.

1984: The beta-amyloid protein was identified as "the chief component" of Alzheimer brain plagues, and was named a "prime suspect" in triggering nerve cell damage.

1987: The first clinical trial for the drug tacrine was launched; volunteers were recruited to be part of the research.

1993: The first Alzheimer drug was approved by the Food and Drug Administration (FDA); it was tacrine (Conex), and was specifically targeted towards symptoms that disrupt a person's thinking and memory.

2004: Compound B (PIB) was considered "a major breakthrough" in monitoring early detection of Alzheimer's; PIB gets into the brain through the bloodstream and "attaches itself to beta-amyloid deposits, where it can be detected by positron emission tomography (PET)."

2005: Alzheimer's & Dementia: The Journal of the Alzheimer's Association is launched.

2010: The Alzheimer's Association announces the establishment of a database that includes information on 4,000 patients that have participated in 11 pharmaceutical industry-sponsored clinical trials. Those trials were focused on treatments that are ongoing or were conducted in the past yet still require monitoring for their effectiveness.

Recent Relevant Information on Alzheimer's Disease

Meantime, according to a scholarly article in the journal Alzheimer's & Dementia, as of 2008 Alzheimer's is the seventh leading cause of "all deaths in the United States" and the "fifth leading cause of death" in Americans who are 65 years of age or older (A&D, 2008, p. 110). Women are more likely than men to be afflicted with Alzheimer's -- and other forms of dementias -- because they live longer and their longer life span "…increases the time during which they could develop Alzheimer's or other dementias" (A&D, p. 113). The reason that the number of people afflicted with Alzheimer's is growing rapidly is simple: the baby boom generation is fast aging and becoming the older generation.

As of 2008, about 5.2 million Americans "of all ages" had Alzheimer's; of those, 5 million were 65 years of age or older, A&D continues (p. 113). In fact A&D estimates that one in eight persons 65 or over -- that is 13% -- has Alzheimer's. The data shows that "every 71 seconds" someone in the U.S. develops Alzheimer's; in forty years that number will change to every 33 seconds, according to A&D (p. 113). The overall number of people with Alzheimer's is expected to reach 7.7 million by 2030, which, if it turns out to be accurate, would be "a greater than 50% increase from the 5+ million age 65 and older who are presently afflicted (A&D, p. 116).

Unless science discovered a prevention (or a cure) for Alzheimer's, by 2050, A&D explains, up to 16 million Americans could be Alzheimer's patients.

Education has an impact on whether or not a person will develop Alzheimer's, according to A&D (p. 114). Those with fewer years of education are "more likely" to get Alzheimer's than those with more years of education. Likewise, having fewer years of education translates into higher chances of getting dementia, the A&D research shows. In one study it was determined that individuals with less than 12 years of formal schooling "…had a 15% greater risk of developing dementia than people with 12 to 15 years of education" (p. 114). That same study indicated that people with less than a dozen years of education have a 35% "greater risk" of developing dementia that those with more than 15 years of education.

Why would a person's education have anything to do with getting Alzheimer's or dementia? The Alzheimer's & Dementia journal explains that more years of education might give a person a "cognitive reserve" that in some way protects a person from Alzheimer's and dementias. Like a reserve amount of battery power, a brain that has been used to learn for more years may allow the well-educated person "…to compensate for a longer time before the symptoms of Alzheimer's and dementia are observable," according to A&D (p. 114).

Other research takes the position that additional years of education might be "…a surrogate marker for factors that affect access to education in childhood." Those markers could be socioeconomic situations and "where one lived as a child," A&D explains (p. 1140.