Term Paper: Alzheimer's Disease While Most People Know

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Alzheimer's Disease

While most people know someone who has a family member with Alzheimer's Disease (AD), most people still have little idea about what causes it. Indeed, because there is no definitive method of even diagnosing AD until after the patient dies and the condition of the brain can be assessed post-mortem, even the medical profession has had a difficult time deciphering the origins of this disease. Even now, as the information presented here will demonstrate, there are myriad theories concerning the cause of AD, but here, as in diagnosis, no single definitive answer.

German physician, Alois Alzheimer, is credited with the first description of the disorder; he told a medical group, in 1906, about a patient whose problems with memory loss, beginning when the patient was 51 years old, progressed to include disorientation, then depression and hallucinations, and finally sever dementia and death (Hecht, 1985). Upon Examining the dead patient's brain, Alzheimer found "severe trophy (shrinkage) and an unusual clumping and distortion of fibers in the nerve cells of the cerebral cortex, or outer layer of the brain" (Hecht, 1985, p. 23+). It has been noted, by a respected medical journal, that definitive diagnostic sign for AD is the presence of plaques and tangles in brain (Genetics and Pathobiology, 2004, p. 950+). This is still a hallmark of AD, noted by virtually all of the research dealing with anatomy of AD and quoted here.

It should be noted that, while many fear the onset of AD when they experience memory loss, only when it becomes severe and there is also loss of other cognitive functions such as reasoning, concentration and judgment, is it likely the patient is suffering from a variety of dementia, including AD (Hecht, 1985). In addition, in the years after Alzheimer's work, it was noted that the same changes found by Alzheimer appeared in older patients with what was then called senile dementia, and in some younger patients having dementia. By the time Hecht (1985) wrote, however, it had been generally agreed that AD is AD no matter what age it begins.

Genetics and Pathobiology (2004) predicts that dementia will triple in the United States over the next 50 years, and that the best-known form of dementia, AD, is likely to be responsible for much of that increase. Blank (1998) noted that brain-based injury and disease costs the United States more than $500 billion in health care costs, lost productivity in the workplace and care giving expenses even then. Odle (2003) confirmed these figures. Thus, it is imperative to find causes in order to find cures.

Suspected causes of AD

Genetics and Pathobiology (2004) reported that a worthy are for exploring possible causes of AD was the genes, as well as other risk factors linking neural and vascular pathways; this link, they publication suggested, makes people susceptible to neuronal damage and cognitive impairment, at least in response to cerebrovascular diseases such as stroke.

Blank (1998) also noted that genes are important in such studies, and that genes had already been implicated in Huntington's disease, one that caused progressive deterioration of mental faculties as well as muscular control. Duchenne and myotonic muscular dystrophy, he noted, causing healthy muscles to atrophy, is also linked to genes as are Tay-Sachs, Gauchers and Niemann-Pick diseases, and AD.

Droller (2005) noted that AD and Parkinson disease (PD) are, however, of purely genetic origin in only a minority of cases; in most cases, he noted, for either to appear there must have been repeated interactions among genetic and environmental factors known to be at least partially at cause. Droller cited research that demonstrated that in a minority of cases of PD and AD, especially early-onset cases, genes were the primary cause. IN most cases, however, not only is the interplay between environment and genetics needed, often multiple genetic factors must be present. Droller hypothesized "exposure of the developing brain to still undefined toxic environmental agents during windows of vulnerability in early life -- in utero and in early postnatal life -- may be an important contributor to causation (Droller, 2005, unpaged database).

Rutter and Silberg (2002) examined the role of environment in relation to the genes so far identified as having some contribution to make to Ad. They noted that so far, only one allele, the Apo-E-4 allele, had been the subject of very much study concerning heighten risk of AAD. Mayeux et al. (1995) had found no increase in risk for AD associated with head injury if Apo-E-4 was not present, a two-fold increase if Apo-E-4 was present, but a ten-fold increase in the likelihood of AD if both Apo-E-4 and head injury were present.

In fact, in 2002, an Australasian business publication reported that researchers at the University of Pennsylvania's School of Medicine had found evidence that AD could be linked with mild repetitive concussions. The concussions increased the formation of plaque-like deposits of amuloid beta proteins. What was interesting about this study was that recurrent trauma was thought to cause dementia pugilistica, or Punch Drunk syndrome in boxes, but nothing until the University of Pennsylvania Medical School studies on transgenic mice had linked similar events to the origin of AD (Australasian Business, 2002).

Another environmental factor being assessed included period of undernutrition during critical development periods. David Barker, a British researcher, hypothesized that this led to persistent changes in hormone levels as well as altering tissue sensitivity to the hormones, a progressions that permanently altered metabolism and body structure, and in turn created a predisposition to AD: however, it is only a hypothesis (Droller, 2005).

While trauma was linked to AD, at last, estrogen also was emerging as a factor to consider in AD formation. In older women who are apo-E-4 positive, estrogen use provided no protection from AD, while AD was more evident among those who were Apo-E-4-positive (Rutter and Silberg, 2002). As a result of this sort of research, Chandra and Pandav (1998) reported that cholesterol might play a role in AD. Apo-E-4 is a form of apolipoprotein E. that is involved with lipoprotein disorders -- what the layman commonly refers to as cholesterol (Magnesium Research, 1996), further substantiating the link between these disorders laymen think of as vascular problems and what appears to be cerebral as well.

According the Alzheimer's Association (2003) everyone has apolipoprotein in the blood and brain. It comes in three varieties, ApoE2, ApoE3 and ApoE4. About one-fourth of al people have inherited a copy of the ApoE4 gene, increasing their risk up to four times, with those who have inherited a double dose -- one from each parent -- experiencing a ten times greater risk (Alzheimer's Association, 2003).

In terms of enzymes already in all human bodies, one has also arisen as a possible precursor of AD. More precisely, the lack of choline acetyltransferase (CAT) in AD patients has been found to be much greater than the lack in patients who aged normally (Hecht, 1985).

Is AD contagious?

Hecht (1985) noted that there were already studies underway regarding genetics and AD, but also noted that there was some concern that the causative agent might be a virus. Researchers based this possibility on the fact that scrapie, a neurological disorder of sheep, can be transmitted to animals bin injecting diseased brain tissue into their brains. In addition, plaques like those found in AD patients have been found in scrapie-infected sheep, as well as in those whose dementia was caused by Creutzfeldt-Jakob disease (a disease similar to Mad Cow disease) and kuru, which is thought to be contracted when humans in certain tribes consume the brains of their slain enemies.

Work based on this research led to the theory that prions, protein participles first isolated form scrapie-afflicted sheep, might be at case (Hecht, 1985).

Proteins, not necessarily those consumed but rather those made in the body, have also formed a basis for AD research.

Pathologist George C. Glenner, in 1983, examined the molecular structure of [beta]-amuloid, a structure that constitutes the tip of the plaques present in AD, and discovered that the concentration of these amyloids is particularly high, appearing like strips of sticky substance spilled on a floor and gumming up the works (Odle, 2003). Since Glenner's work, new research indicates that [beta]-amyloid is toxic to neurons, and could therefore easily lead to cell destruction.

The Alzheimer's Association (2003) reports that about fifteen families globally have a genetic fault on chromosome 21 in a gene called the amyloid precursor protein (APP), affecting production of amyloid, which has been linked to Alzheimer's. Unfortunately, an even larger number of families carries a fault that causes early onset familiar AD; that fault is on chromosome 21. A Web site called Healing With Nutrition found the same results.

Is it caused by something we eat?

Injecting animals with aluminum also led to speculation about that metal as a cause of AD, sending many consumers out to buy cookware that was not made of aluminum. In fact, researchers did fine excess aluminum deposits in the neurofibrillary tangles in… [END OF PREVIEW]

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