This essay will discuss the form of Alzheimer’s dementia Posterior Cortical Atrophy, from the aspects of the journey by Sir Terry Pratchett. In addition the essay will discuss symptoms of the disease, pathology, and anatomical structures and locations. Sir Terry Pratchett (Pratchett, 2013) has opened a discussion about dementia due to his diagnosis of Posterior Cortical Atrophy (PCA). PCA is a type of condition associated with Alzheimer’s disease (AD) that affects the parietal and occipital lobes damaging how the brain is able to process and understand visual information. This deterioration of visual processing can impact the person with PCA, in how the person can perform daily tasks such as reading, driving or even walking in certain …show more content…
The occipital lobe is in a posterior position and the function of the occipital lobe is vision including perception and colour and movement (Stannard Gromisch, 2012). Atrophy is described as a process of tissue wastage or cell death (Lippincott Williams & Wilkins, 2006). According to (Jones & Gaillard, 2005-2013) the pathology of PCA includes Neuritic plagues and neurofibrillary tangles which are found in the parieto-occipital and temporo-occipital areas, as well as occasionally in the primary visual cortex. It is thought that PCA is a version of AD, with very little difference in the pathology. “Neuritic plagues or senile plagues are extracellular and composed of a central core of beta-amyloid peptides aggregated together with fibrils of beta-amyloid, dystrophic neurites, reactive astrocytes, phagocytic cells, and other proteins and protein fragments derived from degenerating cells or liberated from neurons” (Weerakkody & Gaillard, 2005-2013). In addition PCA is identified by a significant concentration of plagues and neurofibrillary tangles (NFT) in the occipital lobe and the parietal lobe as well as the connection known as the occipitotemporal junction ( Tsunoda, et al., 2011). The author’s go on to explain that they hypothesise that PCA is connected to AD, dementia with Lewy bodies (DLB), corticobasal degeneration (CBD)
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
This report provides detailed information regarding the Alzheimer’s disease, and how it affects the individual as a person. It examines the facts and statistics of Alzheimer’s disease, as well as cover the survival rate. It covers the cognitive impacts that Alzheimer’s has on the individual, and also the emotional profiles of each of its victims. Gives a general concept of how Alzheimer’s disease has evolved over the past years, and it also shares the advances that it has made. It addresses the role of the public health and aging services, and how it affects the person. It goes into detail on how the brain is affected by this disease, and the impact it can cause for the individual. Overall, it stresses the importance of being aware of the Alzheimer’s diseases because it allows for there to be support, encouragement, and hope for the victims. Just having someone there can make all the difference to someone suffering.
Alzheimer’s disease is seen as deterioration in intellectual abilities as a result of degeneration within several regions of the
Certain qualities are consistently observed in the Alzheimer’s victim. These dysfunction’s, though, are not exclusive to Alzheimer’s disease. Consequently, declaring Alzheimer’s by these parameters is a matter of degree rather than an absolute. Characteristic dysfunction’s have been noted in Alzheimer’s victims, but the degree and severity of these varies from patient to patient. Thus, evaluation of the patient’s mental status must be made based on the sum, rather than a single characteristic. Memory is one of the first noticed deficiencies, beginning typically with the recent and short term memory, and progressing from there as the disease grows more severe. In addition, deterioration in language skills, attention span, praxis (performance of an action), and visuospatial skills are commonly seen. Also observed are changes in the actions and personality of the Alzheimer’s victim. These include changes in mood, motor activities, activities of daily living, socialization skills, psychotic disturbances, vegetative symptomology, and rise in anxiety levels. Again, the
Early 1900’s a man named Alois Alzheimer cared for a woman who had rapid severe declining dementia, after she died he was able to study her brain where he found atrophy of the grey matter along with plaques and neurofibrillary tangles, which when destroyed interrupts the messages sent from the neurotransmitters to the central and limbic regions of the brain resulting in early
A brain deteriorates, slowly being engulfed by a mysterious disease. The neurons being cut off and destroyed by two abnormal structures. First memory is affected gradually getting worse. Then one is unable to think properly, reason, and lacks of self control. Gaps are formed in the brain 's ventricles, due to the amount of dead tissue. In the end, it will lead to death. All of this may sound like something from a science fiction movie but infact its very real. These are all known possible symptoms of a common disease that affects about millions of Americans. It is known as Alzheimer 's disease (AD), and I plan on explaining it a bit more in this paper. First I will explain the disease and list some facts about it,then I will talk about some commonly asked questions about it.
Throughout history there have been reports of decreased memory and mental deterioration that accompanied old age. Alzheimer’s disease (AD) was named after Dr. Alois Alzheimer who described the symptoms in a woman in Germany in the 1907 but it was not until the 1970’s that AD was considered to be a major disorder and AD continues to be a major health concern worldwide (Reger, 2002).
Dementia is a condition resulting from obtained brain disease and distinguished by progressive decay in memory and other cognitive fields such as judgment, abstract thinking, language, and executive functioning. This disease is usually caused by degeneration in the cerebral cortex, the part of the brain responsible for thoughts, memories, actions, and personality. Death of brain cells in this area leads to the impairments that distinguish dementia. Though the cognitive outline of single diagnosed with dementia vary somewhat by etiology, the degree of deterioration stands for a decrease from previous levels of cognitive functioning and is enough to impede with social and occupational functioning. This downfall is beyond what might be expected from normal aging in a person. It can cause impairment with everyday activities such as dressing, feeding, and bathing.
Dementia is a disease which causes mental debility and affects one’s way of intelligent, attentiveness, recollection and problem-solving (NHS, 2013). As a result of dysfunction of brain cells in some parts of the brain it affects the thinking process then dementia occurs and it usually comes with age (Ibid). It is estimated that 560
There are categories of brain dementia, which are cortical and subcortical. Subcortical dementia is marked by motor disruption. An example of subcortical dementia would be parkinson’s disease. On the other hand, Alzheimer’s is an example of cortical dementia, which as previously established is marked by memory loss. Although Alzheimer’s is classified as cortical dementia, it eventually destroys cells in all four lobes of the brain thus resulting in motor disruption as well. The ventricles, the fluid filled spaces in the brain begin to enlarge as the disease develops. The symptoms of memory loss and impaired cognitive functioning in Alzheimer’s disease can be attributed to damage in the hippocampus and cerebral cortex. The earliest detection
“I want to tell you how much I miss my mother. Bits of her are still there. I miss her most when I’m sitting across from her,” (Crowley, Candy. October 21st, 2014). This quote refers specifically to Alzheimer’s, which is defined as progressive mental deterioration that can occur in middle or old age, due to generalized degeneration of the brain. It is the most common cause of premature senility. However, Alzheimer’s is merely only a form of many debilitating diseases under the umbrella of Dementia, defined as a chronic or persistent disorder of the mental processes caused by brain disease or injury and marked by memory disorders, personality changes, and impaired reasoning. Some examples of these disorders include: Vascular dementia, Frontotemporal dementia (Pick 's disease), Creutzfeldt-Jakob disease, and of course as was previously for mentioned, Alzheimer 's disease. Each form of dementia will be discussed in depth including their symptoms, treatments, and their histories.
The brain is composed of billions of neurons, which interact and connect with each other, which allow us to perform our everyday activities. Plaques and tangles are the two structures that are suspected for the damage of nerve cells. Plagues are deposits that build up between neurons and tangles build up inside the neurons. Most people develop these abnormal obstructions as they age, but those with Alzheimer’s have a tendency to develop much more.
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).
Alzheimer’s is a progressive and deteriorating condition that affects the brain`s nerve cells, resulting in the declining of mental functions. Posterior Cortical Atrophy is referred to as the loss of brain cells within the outer layer of the brain, mainly affecting the area in the back of the head, where visual information is processed.