Abstract This review of Alzheimer's disease (AD) focuses on the various causes of the disease. It is a compilation of material gathered from various scientific journals. The review begins by giving an introduction of AD followed by a discussion of various factors believed to cause AD, such as: amyloid plaques, neurofibrillary tangles, apolipoprotein E, and genetic factors. The author concludes by stressing the need for more research into the causes of AD.
Introduction
Overview of Alzheimer's Disease
Pathological Causes of Alzheimer's Disease
Amyloid Plaques
Neurofibrillary Tangles
Genetic Factors in the Development of Alzheimer's Disease
Chromosome 19 and Apolipoprotein E
Other Genetic Factors
Presenilin
Conclusion
From the Paper "Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory loss and dementia. The precise mechanisms that cause AD are still unknown, however, certain factors that predispose individuals to Alzheimer's disease have been identified. Although no definitive cause has yet been discovered, this article reviews current research into various possible causes of AD, including the pathological causes, such as amyloid plaques and neurofibrillary tangles. Also the genetic factors that cause AD, such as apolipoprotein E (apoE) and presenilin gene."
Abstract Given the current ineffectiveness of drugs used to treat AD, what new treatment approaches may be feasible? The author looks at treatments that focuses on the development of amyloid plaques, and genetic therapy that may prove useful in treating the underlying causes of AD.
From the Paper "Despite the large number of prospective and currently utilized drugs used to treat AD, none have been shown to be clearly effective. Only one drug, Tacrine, has been FDA-approved specifically to treat AD. Therefore, while research on new drugs is important, the search for the cause of AD is even more vital. Only when the cause of AD is pinpointed can drugs which hope to impair, prevent or stop the progression of AD be expediently developed. "
Abstract This paper examines the research article "Cerebrospinal Fluid Beta-Amyloid(1-42) in Alzheimer Disease: Differences Between Early- and Late-Onset Alzheimer disease and Stability During the Course of Disease" by Teipel, Hampel, Pietrini, Alexander, Horwitz, Daley, Moller, Schapiro and Rapoport (1999) which investigates region-specific corpus callosum atrophy in relation to the pattern of cortical glucose metabolism in Alzheimer. It shows how the reviewed material examines the authors' primary research questions, their justification for the study, the general methods and main findings. The review ends with a statement of whether confidence can be placed in the findings.
From the Paper "Methods involved a two-group comparison of AD patients (N=12) and healthy controls (N=15). It is noted that controls were volunteers but no mention is made of how any of the subjects were recruited into the study. Further, AD patients were not authenticated as having the disease; rather it was noted that some patients were suspected of "possibly" having the condition while others were viewed as "probably" having AD. Tests of cognitive functioning were administered to the AD patients showing that they ranged in degree of dementia from mild to severe."
Abstract This paper examines Alzheimer?s; it's aetiology and symptoms, in order to question the orthodox and alternative treatments available. It discusses the considered main causes that include zinc, copper, iron and aluminium, as well as including a brief overview of the accepted commonest risk factors. It is concluded by considering and suggesting, that ginkgo biloba is the main contender as the alternative to orthodox medicine in treating and preventing, Alzheimer's disease.
Outline
Abstract
Introduction
Chapter 1
An Overview of Alzheimer's Disease ? Definition, Aetiology and Risk Factors
Associated Structural Abnormalities of AD
Beta Amyloid Plaques (BAPs)
Neurofibrillary Tangles
Risk Factors of AD
Chapter 2 ? The Biometals
The "Normal" role of Zinc
The Paradoxical Role of Zinc
Iron
Copper
Aluminium
Free Radicals and Oxidative Stress
The Cholesterol Theory
Chapter Three ? Ginkgo Biloba
Ginkgo Biloba as an Antioxidant and Preventative
Vitamin ?E? and Other Free Radical Scavengers
Chapter Four - The Role of Orthodox Treatments
Nerve Growth Factor (NGF), One of the Neurotrophic Factors
Selegiline
Oestrogen Replacement Therapy (ERT)
Metal Chelation Therapy
Non-Steroidal Anti-Inflammatory Drugs
Chapter Five ? Conclusion
From the Paper "Copper is another essential trace mineral in the human body; it is a constituent of many enzymes and takes part in the absorption of iron and in melanin formation. Lack of copper may result in anaemia and bone changes. Estimated safe and adequate dietary intake is 1.5-3.0 mg/day for adults, and 0.4-0.6 mg/day for infants (Tortora and Grabowski, 2000). Copper plays a crucial role, with cholesterol, in nutrition and normal brain function. Recent evidence indicates that copper and cholesterol may both be important factors in the aetiology of AD. Sparks et al (2003) explains how trace amounts of copper (0.12 ppm) added to water and given to cholesterol-fed rabbits induced BAP accumulation, including senile plaque-like structures in the hippocampus and temporal lobe."
This paper discusses Alzheimer's disease and dementias, neurological disorders involving problems with memory and thinking, which affect emotional, social and physical functioning.
Abstract This paper explains that Alzheimer's and other dementia characterized by gradual deterioration of memory and personality, is not part of the normal aging process and is marked by plaques of B-amyloid protein and tangles in the brain. The author points out that Alzheimer's is more likely to occur during the later years; but, when Alzheimer's disease begins in middle-age, it usually progresses quickly, reaching the last phase within 3-5 years. The paper relates that Alzheimer's disease progresses through a series of five developmental stages characterized progressively by absentmindedness, confusion, severe memory loss, need for full time care and, finally, complete withdrawal emotionally and physically leading to death.
From the Paper "People with Alzheimer's disease are unable to care for themselves and to communicate their needs. They become very confused when it comes to the most simple activities and often alienate their family members because they accuse them of stealing the possessions that they have misplaced due to their inability to remember where they put them last. Eating becomes a problem because the person may eat multiple meals or forgot to eat entirely. Therefore, their meals need to be supervised. The personality that dominated during earlier life is likely to become more dominant at this time. Therefore, they are capable of having angry outbursts and/or becoming very dependent and clingy to others. Depression is also common in this population. Researchers are still struggling to find out the causes of Alzheimer's disease and there is always the hope that a cure is not far away. There has been some evidence for genetic factors involved in Alzheimer's disease; however, this does not apply to all cases."
Abstract This paper discusses the condition of Alzheimer's disease. The paper opens with a review of the disease symptoms. Next the paper provides genetic background about the disease. The paper concludes with an investigation of the pharmacological approach to treating Alzheimer's disease.
Abstract This paper describes Alzheimer's disease, its symptoms, risk factors and treatment options. The paper examines the efficacy of the various medications currently used to treat Alzheimer's disease and evaluates the new therapies being developed. The paper also discusses how to provide long-term care for Alzheimer's patients.
From the Paper Alzheimer's disease is a progressive brain disease causing severe mental deterioration. It is found most often in the elderly..."
Tags:amyloid plaques, neurofibrillary tangles, dementia, memory loss
Abstract This paper explains that Kuru disease is found among natives in the eastern highlands of New Guinea who eat the brains of deceased relatives to honor them. The author points out that it is similarity to other spongiform encephalopathies, now known as prion diseases. The paper looks at the biochemical features of the disease and reviews prion diseases in general.
From the Paper "Kuru disease is one of a family of diseases known as prion diseases because they are caused by an abnormal form of the prion PrP protein found in membranes. The family includes Creutzfeldt-Jacob disease."
Abstract This papr explains that the current drugs being used only treat the symptoms of Alzheimer's disease. The author points out that the new generation of drugs being tested hold promise for being able to slow or halt the onset of Alzheimer's disease in individuals with mild dementia. The paper describes these drugs.
From the Paper "There are more than ... million Americans who currently suffer from the disorder known as Alzheimer's disease. The current generation of Alzheimer drugs were designed chiefly to treat symptoms of the disease but have little to no impact on slowing or stopping its progression. However, a new generation of drugs aimed at slowing and stopping the progression of the disease are in late phases of testing. The following drugs are in late phases of FDA testing to treat Alzheimer's disease and related disorders: ..."
Abstract This paper takes an in-depth look at Alzheimer's disease, a degenerative brain disorder that was first identified in 1906 by Alois Alzheimer. This disease represents the single most prevalent form of brain disorders and is also the leading cause of dementia, affecting approximately 4.5 million people in the Untied States. The paper provides a brief overview of the disease, the symptoms, the diagnostic procedures and the treatment methods in order for us to gain a better understanding of this degenerative brain disorder.
Outline:
Introduction
Alzheimer's Disease
Early and Late onset Alzheimer's Disease
Symptoms of the Disease
Memory Loss and Language Disorder
Depression
Dyspraxia and Agnosia
Diagnosis
Tests for Cognitive Impairment
Positron Emission Topography
Major Causes of Alzheimer's Disease
Amyloid Plaques
NeuroFibrillary Tangles
Metal ions
Treatment Methods
Restoring Cholinergic Transmission
Anti-inflammatory Drugs
Conclusion
From the Paper "Considerable reduction in cholinergic transmission is one of the primary causes for the loss of memory and other associated symptoms of Alzheimer's disease and other kinds of dementia. Hence pharmacological treatment for AD mainly revolves around rectifying this circulatory deficit within the brain. Compounds designed to enhance cholinergic transmission constitute an important part of the treatment plan. Acetylcholine the neurotransmitter of the brain is considerably broken down in-patients suffering from AD and other dementias. The underlying mechanism of the neurotransmitter can be simplified as follows. An electrical impulse generated passes along the nerve and when it reaches the end it triggers the release of chemical messengers known as neurotransmitters, which in turn diffuse along the synaptic cleft and react with the specific receptor sites on the organ. Activation at the receptor junction initiates a series of chemical reactions resulting in a specific biological response. "
Abstract This paper discusses Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive memory loss and dementia that affects millions of people worldwide each year. Although no definitive cause has yet been discovered, this paper reviews current research into various possible causes and risk factors for AD, including pathological causes and lifestyle factors that have been shown to contribute to the development of Alzheimer's disease and the implications of these factors for health promotion, disease prevention, and treatment.
Outline:
Pathological Causes of Alzheimer's Disease: Amyloid Plaques and Neurofibrillary Tangles
Genetic Factors in the Development of Alzheimer's Disease
Health Promotion, Disease Prevention, and Treatment
Conclusion
From the Paper "Briefly, the formation of amyloid plaques and neurofibrillary tangles are thought to contribute to the degradation of the neurons (nerve cells) in the brain and the subsequent symptoms of Alzheimer's disease. In AD, plaques develop in areas of the brain used for memory.8 Amyloid is a general term for protein fragments that the body produces normally. Beta-amyloid is a fragment of a protein that breaks off from another protein in the body. In a healthy brain, these protein fragments would be broken down. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques.8
"Neurofibrillary tangles consist of a series of insoluble twisted fibers found inside the brain's cells. These tangles are made of a protein called tau, which forms part of a structure in the brain called a microtubule. The microtubule helps transport nutrients and other important material from one part of the nerve cell to another. In Alzheimer's disease, however, the tau protein is abnormal and these microtubule structures collapse."
