The Shriver Report

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

When it comes to Alzheimer’s, I know firsthand how it affects individuals and their families. My great grandfather had Alzheimer’s for many years before his passing late last year, at age 92. Alzheimer’s is a disease that many individuals suffer with each year, but yet with all the advancements in modern medicine we still have no cure for it. There are different ways to conquer this disease, understanding the causes, knowing effects, and researching possible treatments.

A great number of patients with Alzheimer’s disease have less amount of Acetylcholine in the cerebral cortex. Acetylcholine function is for the cognitive activity of the brain. A big amount of neuritic plaques in the cerebral cortex found in brain of a Alzheimer’s patient. Beta amyloid is a type of protein that engage the center of the plaques that destroy the neurons that provide Acetylocholine (Ach) that are necessary element for learning and memory process. The brain of a person with Alzheimer’s shows marked with atrophy, widened sulci and shrinkage of the gyri. Majority of the most cases, every part of the cerebral cortex is involved, but the occipital pole is save from strain. The cortical ribbon may be reduced and ventricular dilatation visible, especially in the temporal horn, due to atrophy of the amygdala and

In addition, decreased cerebral blood flow, environmental toxins and a decrease in acetylcholine have all been labeled potential culprits. Various theories for the cause of Alzheimer’s have been put forth but as yet none have been shown true.

The symptoms of Alzheimer’s are extremely detrimental to the individual whom it affects, as the disease attacks the brain cells and their connections. As the illness progresses, many

By the numbers, Alzheimer’s disease looks even worse than it may be. The cost of Alzheimer’s overwhelms the caregiver and everyone involved with the patient. The price businesses pay for Alzheimer’s it detrimental to their industry, show by “A 2002 study showed that United States businesses lost $36.5 billion that year because employees missed work or quit and had to be replaced so that they could care for someone with Alzheimer’s disease” (Adams 24). The caregivers play vital roles in the lives of the sufferer, but the business take an even heavier loss. Heath care is necessary for someone with Alzheimer’s disease, however it can get expensive “The costs of

In the United States there are approximately 5.4 million people living with Alzheimer’s. Every sixty-nine seconds a person is diagnosed. This is an ongoing issue, and unless something is done, sixteen million people will be affected by 2050 (Latest).

A major devastating and debilitating disease, Alzheimer 's is a public health issue that affects not only the United States but also countries all around the world. In 2010, there were 35.6 million people living with Alzheimer’s. Researchers and medical personnel expect this number to triple by the year 2050. The disease is costing America an exorbitant amount of money and has become a burden on families, caregivers, medical personnel, the healthcare system, and the nation’s economy. If attention is not focused on this major problem, “nursing homes will be overloaded, caregivers will be burned out, healthcare system will be overwhelmed, and federal and state budgets will be overtaxed” (Alzheimer’s Association, 2011).

Health care needs become more challenging every day; in fact, it is one of the biggest problems the American economy faces today. However, within the next 20 years the population of adults ages sixty-five and older is expected to increase and “age is the key factor for development in later life” (Dilworth-Anderson, Pierre & Hilliard, 2012, p. 27). Recent studies have shown there are approximately 5.3 million Americans that have Alzheimer’s disease and it is expected to increase over

Cholinesterase inhibitors are used to breakdown the acetylcholine, which is a neurotransmitter that is connected to memory, by blocking the enzyme acetylcholinesterase. The donepezil, rivastigmine, and the galantamine are three commonly prescribed cholinesterase inhibitors. The known side effects are nausea, vomiting, diarrhea, upset stomach, and dizziness (Wattmo, Londos, & Minthon, 2014). To block the NDMA receptors, the memantine is prescribed to improve cognition and regulate the glutamate that acts as a neurotransmitter in the brain around the learning and memory area. Excessive glutamate could cause damaged, killed nerves. Common side effects of memantine consist of dizziness, confusion, and headaches (Koch, Szecsey, & Haen, 2004). Additional medication can be prescribed to patients with symptoms such as depression, psychosis, disturbed sleep, and apathy. Howes (2014) supported the commonly used drug treatments as he compared AD to the issues of the cardiovascular disease. The reduced blood flow to the brain, the reduction of oxygen, clogged arteries and vessels could damage the brain cells, making the Alzheimer’s disease worse. The treatment of AD reduces some of the effects of the cardiovascular (Howes,

Alzheimer’s disease is a form of dementia that can be directly related to a person’s age. The main physical manifestation of Alzheimer’s disease detects nerve cell deterioration which is demonstrated as an amplified loss of lucidity and a

There has only been one way to confirm if a person suffering from dementia truly had Alzheimer’s disease, an autopsy after death. Alzheimer’s disease has been found to leave a distinct effect on the human brain. The disease has been found to cause significant brain shrinkage. Neurological plaques and tangles have been the distinct lasting effect from the disease. Large deposits of the protein beta-amyloid have been associated with the neurological plaques, and abnormal tangles that lead to a failed transport system have been found all those suffering from the disease (Alzheimer’s Association, n.d.).

The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.

In 1906 a physician, named Alois Alzheimer, cared for a fifty-one year old patient with severe dementia. Upon her death, he was able to examine her brain at autopsy. Dr. Alzheimer was able to take advantage of recent innovations in microscopy and histological techniques that allowed him to study in detail the cellular components in nervous tissue. He found that the brain of his patient had severe cortical atrophy and described the neurofibrillary bundles and plaques that are now the hallmark for definitive diagnosis of what he at that time called “presenile dementia”. An account of his first patient was published in 1907. It is a little ironic that reevaluation this case has lead some to believe that this first patient did not suffer from the Alzheimer’s disease at all. Instead they believe she suffered from a different, rare disease called metachromatic leukodystrophy (Izenberg, 2000).

Research on pathologies of Alzheimer’s disease has been ongoing, however, the exact pathology of the disease is difficult to pinpoint as the known pathologies are very convoluted, and it is unknown which is the initial pathology. Current therapeutics include targeting the acetylcholinesterase pathway, decreasing levels and degrading amyloid beta plaques and tau tangles, and decreasing neuroinflammation.