Alzheimer's Disease Essay

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

The beginning and symptoms of Alzheimer's are usually very slow and gradual. Alzheimer’s hardly ever occurs before the age of 65. It occurs (according to the AHAF) in the following seven stages: In stage 1 There are no impairment- Unimpaired individuals experience no memory problems and none are evident to a health care professional during a medical interview. Stage 2 Is a very mild decline- Individuals at this stage feel as if they have memory lapses, especially in forgetting familiar words or names or the location of keys, eyeglasses, or other everyday objects. But these problems are not evident during a

Alzheimer’s disease in many ways is not yet defined. It is a progressive disease afflicting between 5 and 15 percent of people over 65. Additionally, it is not restricted to the elderly, reportedly having

Due to the inability of the brain to replace nerve cells, some brain function is lost. The key question in Alzheimer’s disease is, what causes the neuron degeneration (Johnson, 1989)? The focus for finding the cause is on abnormal structures found in the brain of people with Alzheimer’s. Unfortunately, the abnormal structures the brain undergoes still has researchers uncertain as to how they are involved in Alzheimer’s and exactly how the disease occurs.

Alzheimer’s: Scientists know that during Alzheimer’s two abnormal proteins build in the brain. They form clumps called either ‘plaques’ or ‘tangles’. These plaques and tangles interfere with how brain cells work and communicate with each other. The plaques are usually first seen in the area of the brain that makes new memories. A lot of research is focused on finding ways to stop these proteins in their tracks and protect brain cells from harm.

Alzheimer’s disease is named after Dr. Alois Alzheimer who first discovered deviations from normal tissues of healthy individuals in the brain tissue of a lady in 1906. The woman, who showed symptoms of erratic behavior, loss of memory, and problems with communication, died of a then unfamiliar mental disorder. This led Dr. Alzheimer to investigate the cause of her unusual death. He assessed the brain of the woman and found that there were many anomalous masses (amyloid plaques) and intertwined bundles of fiber (neurofibrillary tangles). Scientists today have pinpointed the qualities of Alzheimer’s to be a) tangles in the brain (neurofibrillary tangles), b) plaque in the brain (amyloid plaques), and c) loss of connections among nerve cells.

Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal

A common observation in the brain of people who have died from Alzheimer’s is that plaques and tangles make from protein fragments are present. (A Century of Alzheimer’s Disease)

Alzheimer’s Disease is indicated by the break down of the nervous system, essentially the neurons within the brain (MacGill, 2009). The break down leads to nerve cell eradication, and the casualty of tissue throughout the brain (MacGill, 2009). As the disease progress, the brain begins to shrink fiercely, developing loss of its normal functioning (MacGill, 2009). Abnormal protein groups and structures of plaques and tangles characterize the disease (MacGill, 2009). Plagues and tangles are not able to be viewed or tested in the living brain, but are able to be observed in an autopsy of an infected deceased (MacGill, 2009).

Diagnosing Alzheimer’s may not always be easy for physicians since there are many diseases and disorders that closely relate to Alzheimer’s. Physicians and specialists can diagnose Alzheimer’s by asking the family questions about past health, conducting memory and problem solving tests, and performing a Computed Tomography (CT), a Positron Emission Tomography (PET Scan) or a Magnetic Resonance Imaging test (MRI). Conditions that are related to Alzheimer’s include dementia, psychosis, Parkinson’s, major depression, and insomnia. Since Alzheimer's is a progressive disease, there are many changes that occur in the brain. Abnormal deposits of proteins form plaques and tangles throughout the brain. Once the healthy neurons stop functioning, they lose connections with other neurons and eventually die. The damage mostly appears in the hippocampus, the part of the brain that is essential for forming memories. There is currently no cure for Alzheimer’s but medications can improve symptoms. Cognition-enhancing medications are used to improve mental function and balance

Until recently, two significant abnormalities were observed in the brain of patients affected by Alzheimer's Disease: twisted nerve cell fibers, known as tangles neurofibrilares, and a protein called beta amyloid (Qué es la enfermedad de Alzheimer?, n.d., para. 3).

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. “Its onset is generally insidious, with gradual deterioration of cognitive function, eventually resulting death.” (Falvo, D. 2009, pg. 226). Alzheimer’s is the most common form of dementia among people age 65 and older. “Nearly 70 percentages of all dementias are Alzheimer’s, and over 4.5 million Americans have Alzheimer’s.”(www.alz.org). This disease is not just a disease that happens to older people, but there is a small percentage that can also affect those in their 30s.

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Alzheimer’s is a type of dementia that causes complications with memory, thinking, and behavior. Long before any signs of memory loss, there a microscopic changes occurring in the brain, altering its functionality (Alzheimer 's Association Organization, 2016). The brain has billions of nerve cells that work together, and when one portion of the brains neurons are malfunctioning it leads to breakdowns in other parts of the brain. The two most noted abnormal structures that are suspected to damage and kill neurons in the brain in patients with Alzheimer’s are plaques and tangles. Plaques are deposits of a proteins fragment called beta-amyloid that build up in the spaces between nerve cells; and tangles are twisted fibers of another protein called tau that build up inside cells (Alzheimer 's Association Organization, 2016).

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.