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...

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…