Alzheimer's Disease in the Elderly

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

Alzheimer’s disease is a common problem in today’s society and within the older population this disease makes up the largest form of dementia. Although it is a problem in mainly older people, this disease can still occur in the younger population also. People in their 30s-50s can be diagnosed with this disease, even though it is not as common as people in their 60s-90s. The number of people with Alzheimer’s in the U.S. is close to five million and is expected to double within the next 30 years. With our modern medicine and advancements one would think a cure would be available, however, getting to the cause of the disease is a major factor. The cause of Alzheimer’s disease is one that is very debatable and questionable and most likely is a result of multiple factors rather than one. The main issue with finding the cause is because this disease affects the brain and can

Alzheimer 's disease (AD) is a progressive degenerative disease of the brain from which there is no recovery. There are three brain abnormalities that are the hallmarks of the Alzheimer’s disease is initially caused by plaques buildup in the brain’s neurons as illustrated in figure 1. The support structure that allows the flow of the nutrients through the neurons gets damaged and ultimately there is loss of connection among the neurons and they die off (National Institute of Health, 2015). This causes the brain tissue to shrinks, which is called atrophies. All this ultimately lead the victim of this disease to face difficulties in governing emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.

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).

Some other researchers are trying to determine the possible roles of cholesterol metabolism, oxidative stress (chemical reactions that can damage proteins, DNA, and lipids inside cells), estrogen, vitamin E, and microglia in the development of AD. Scientists also are investigating the role of aging – related proteins (Florida Health Care Association 2005).

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).

Alzheimer’s disease (AD) is a progressive and fatal form of dementia, frequently seen in the elderly altering their cognition, thought process and behavior. AD is reported in about half of patients that have a dementia diagnosis; one study states that about 10.3% of the population over 65 years is affected by dementia with an increase to almost 50% over the age of 8 (Beattie, 2002). Alzheimer’s disease is not a normal part of the aging process in humans, but rather found in a group of diseases that affect the brain leading to a decline in mental and physical control. AD when diagnosed has a very slow and gradual course, initially affecting the individual’s short term memory (Beattie, 2002). Alzheimer’s disease is the 6th leading cause of death, affecting more than five million people in the United States and is also one of the most common forms of dementia. Dementia can be defined as a disorder of progressive cognitive impairment severe enough to affect daily functions of an individual’s life (Fillit, et al., 2002).

The onset of symptoms is usually between 40 and 90 years of age, although onset before 65 years of age is considered to be the early onset form of the disease and onset at 40 is very rare (Reger, 2002). Characteristics of AD are extracellular deposits of senile plaques made of complexes of the protein amyloid β and neurofibrillary tangles

It is a disease that we haven’t cured yet but instead have only come up and still coming up with treatment strategies to alleviate its symptoms. AD was first described in 1906 by a German psychiatrist by the name of Alois Alzheimer whilst he was performing a histophathologic study of his patient’s brain, a patient who had been suffering from dementia. His patient’s brain’s autopsy brought to light the presence of two types of lesions, which are senile plaques and neurofibrillary tangles. He saw a visible difference in the brain tissue for it was severely damaged by these lesions. Since then, our knowledge of AD’s cellular and molecular alterations has increased and we have come up with various hypotheses for AD that may soon help in developing effective preventative and therapeutic strategies. One of the most prevailing hypotheses that have already leaded to a number of therapeutic approaches is the amyloid cascade hypothesis. Hence, the following essay will explore the pathology of the amyloid cascade hypothesis and the evidence for and against it. It will also touch upon current progress in clinical trials that test the

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.

The production and accumulation of amyloid-beta (Aβ) peptides, in neuritic plaques, as well as, the increase of an abnormal hyperphosphorylated form of tau protein in neurofibrillary plaques or tangles, inside the neuronal cells, are the two main alterations believed to be the hallmarks of AD. (1) AD can be referred as a synaptic disease because the flow of information decreases due to depletion in the number of synapses and, with the development of AD, the death of a lot of neurons. This results in impairments at cognitive and emotional processing.(2, 3) The production and accumulation of Aβ, associated with the aggregations of Tau protein, are likely the precursors to the interference in the communication between neurons, promoting the blockage of nutrients and other essential molecules to the

Nevertheless, both types of AD are recognised pathologically by the build-up of intracellular neurofibrillary tangles, extracellular amyloid plaques, and massive neuronal and synaptic loss (Carmo & Cuello, 2013). Neurofibrillary tangles are aggregates of hyper-phosphorylated tau protein and plaques are mostly insoluble deposits of β-amyloid, resulting from the cutting of the amyloid precursor protein (APP) (Farooqui & Farooqui, 2011). The discovery of mutations in the APP gene which cause familial AD lead to the articulation of the amyloid cascade hypothesis (ACH) (Hardy & Asllop, 1991). A large amount of evidence supports this view; however a number of findings are contrary to its proposal. As a result, Armstrong (2011) proposed a revision of the hypothesis, postulating that the main trigger for the development of the disease is the ageing of the brain and related wear and tear such as head trauma and stress; collectively referred to as the “allostatic load” (Carroll, 2002). Furthermore, a greater emphasis has now been placed on the role of small, soluble amyloid oligomers which seem to be the cause of early cell dysfunction in AD, rather than the large, insoluble amyloid fibrils. (Ferreira, Vieira & De Felice, 2007).

According to Kerr, (2007) AD is largely related to the degeneration of brain weight because plaques and neuro- fibre tangles form, causing inflammation, disrupting neuronal transmission and killing brain tissues. AD is a progressive disease which harms the temporal and parietal brain lobes. This causes memory loss, deterioration of visual spatial skill, complexity in communication, judgement and recognition which in long term, results in death of brain cells (Alzheimer’s Association, 2011).

Alzheimer’s disease affects 1 out of every 8 people in the United States. It is a long and debilitating disease that affects every aspect of a person’s life from the way they preform daily tasks, to the physical and mental abilities that are diminishing. Along with the lifestyle changes that Alzheimer’s disease presents, it also affects one’s psychological perspective as well their view on what they can offer their family and society. There are some ways to maintain a level of independence with a disease of this magnitude but there are also factors in lifestyle choices that can make it worse. Alzheimer cannot be cured, it cannot be slowed, but there are ways to keep the effected person at a certain level of comfort, independence and safety

There are different variations of AD, a rapid onset and late onset, both having the same ending result of the destruction of neurons in the brain. AD appears as inflammation in the brain that can affect memory, speech and motor skills. Unfortunately, the only way of diagnosing AD is through post-modem evaluation. Dementia and AD are tracked by certain memory tests scores and then ranked to determine the disease scale; however, this does not act as a diagnosing factor. From an anatomy standpoint, a blood brain barrier surrounds and protects our brain, which in some theories, is very close to the