Neuropathology and Etiology of Alzheimer’s disease

Scientists have not as yet fully come to full grips with the real causes of Alzheimers illness, however, wholeness clear aspect of the schooling of this disease arise from a very complex chain of activities taking place in the brain over a long period of lifetime. It has been argued that genetic, environmental and even lifestyle factors have contributed to major causes of this disease. Risk and protective factors may admit genetic, medical, biological, environmental, dietary, social and cultural aspects (Draper, 2004).In genetic aspect, APOE E2 is rare and creates protection against Alzheimers disease and in case it does occur in much later years than in people with APOE E3 and APOE E4. APOE E3 forms the or so common Allele and is assumed to perform a neutral role in Alzheimers disease. This means it neither stimulates nor increases reactions that would lead to the development of Alzheimers. The APOE E4 occurs in the most common and occurs in approximately 40% in those who suff er from late onset Alzheimers disease. It is therefore common that people with APOE E4 are more likely to suffer from Alzheimers disease (Kuhn & Verity, 2007).It is infact known as the risk factor gene in that it increases ones level of risk of developing Alzheimers disease. Early onset Alzheimers disease, affecting fewer people is as a result of chromosome different gene mutations on specific chromosomes (Martinison&Musaswes, 1993). These include chromosome 21, 14 and chromosome 1 and all these produces abnormal proteins. Permanent changes in chromosome 21 lead to the creation of APP (Abnormal Amyloid Precursor Protein) while the same process in chromosome 14 leads to the formation of abnormal presenilin and mutation in chromosome 1 lead to creation of abnormal presenilin.Inheritance of even one of these genes from both or one parent is most likely to develop first onset Alzheimers disease. This kind of inheritance pattern is referred to as abnormal dominant inheritance. Another possible risk towards the development of Alzheimers disease is SOR1 (Roudier et al, 1991). This gene is exclusively responsible for the transportation of APP (Abnormal Amyloid Precursor Protein) within the cells and was discovered to be connected to Alzheimers disease. While it is present in low levels, beta farinaceous levels increase and may have a negative effect on neurons (Ramanathan, 1997).The difference in genetic make up from one person to another(prenominal) either delays or completely prevents the onset of Alzheimers disease, also known as Familial Alzheimers disease. It is mainly inherited from parents and is caused by mutations in 3 genes. (APOE E2, APOE E3, APOE E4). There is a 50-50 chance of an offspring developing early onset Alzheimers diseases if one of the parents had it, averagely at the age of 30-60. As many as 5. 3 million Americans are living with Alzheimers disease.It is know to destroy brain cells and hence cause problems with behavior, thinking and memo ry severely enough to affect work, womb-to-tomb hobbies or social infract It has been graded the sixth-leading cause of death in the United States (Mace & Rabins, 2007). There is no known cure to Alzheimers disease yet but an attempt to control it is going on. Scientists and researchers have come up with brain implants aimed to controlling it. These implants contain proteins called Nerve Growth Factors (NGF) which directly delivered to brain mettle cells, which in turn stimulates their growth and thus quashs the chances of their degeneration.Nerve Growth Factor (NGF) is responsible for controlling cell regeneration in the entire body but it is denied opening into the brain, this makes brain cells lack ability to self-regenerate (Taylor, 2006). Alzheimers disease has no cure however and irreversible. It is as a result of progressive brain damage characterized by the building up of amyloid plagues and neurofibrillary tangles, lack of connection in the brain cells and the eventual death of these verve cells. Symptomatic treatment in combination with even out support and proper service can lessen the pain of living with this disease.Change in different forms of lifestyle choices can also reduce the prevalence of this disease. It is a complex disease to understand because it affects individuals differently in the order in which symptoms come to surface, their order of appearance, the duration it lasts before end point and variation in the duration of stage. Increased vigor worldwide to find a lasting break through in proper treatment of this disease is underway (Coste, 2004). These include efforts to delay its onset, reduce late of its development and eliminate it from the body.Research also suggests that different forms of lifestyle such as nutrition, social activities mentally involving activities are factors likely to reduce Alzheimers disease. Progression of series of Alzheimers disease consists of five stages expanded to seven stages by the use of a Modif ied Global Deterioration shell (GDS). This scale assists doctors to measure the exact level of progression of the disease in a patient and administer right medication. Stages of Alzheimers disease include the early stage where the individual has mild impairenent arising from this disease (Pearce, 2007).Symptoms in this stage include rapid changes in mood and behavior, forgetfulness, and lack of proper communication. This group still contains most of their capabilities and thus needs very minimal life support. Further handicap in this stage one leads to the middle stage. Mild cognitive impairment (MCI) is a condition in which a person has memory problems greater than those expected for his or her age. However, people with MCI do not have the personality changes or cognitive problems that characterize (Callone, 2007).Memory loss, difficulty in identifying people and objects are symptoms of middle stage although there may be little awareness. The late stage eventually does not allow verbal communication or one to take care of himself. This level require external support although their lives. The fourth stage, at end of life, is when one comes close to death and comfort is the main focus.Global Deterioration Scale (GDS) or Reisberg scale provides care givers with a better accurate measure of the level of deterioration stage. References Draper B., (2004) Dealing with Dementia A Guide to Alzheimers Disease and separate Dementias. ISBN-10 1865088536, ISBN-13 978-1865088532, Allen & Unwin. Roudier, M. , Marcie, P. , Podrabinek, N., Lamour, Y. , Payan, C. , Fermanian, J. and Boller, F. , (1991) Cognitive Functions in Alzheimers Disease Interaction of Cognitive Domains. Developmental Neuropsychology. Volume 7. Issue 2. Kuhn, D. & Verity, J., (2007) The dodge of Dementia Care. ISBN-10 140189951X, ISBN-13 978-1401899516, Delmar Cengage Learning. Martinson, I. M. and Muwaswes, M. , (1993) Care giving Demands of Patients with Alzheimers Disease.Journal Title Journal of Community Health Nursing. Volume 10. Issue 4. 1993. Page Number 225. Ramanathan, V. , (1997)Alzheimer Discourse Some Sociolinguistic Dimensions. ISBN 9780805823554, Lawrence Erlbaum Associates. Mahwah, NJ. Taylor, R.. , (2006) Alzheimers from the inside out. ISBN-10 1932529233, ISBN-13 978-1932529234, Health Professions undertake. Coste, K. J. , (2004) Learning to Speak Alzheimers A Groundbreaking Approach for Everyone Dealing with the Disease. ISBN-10 1864710632, ISBN-13 978-0618485178, Mariner Books. Pearce, N., (2007) Inside Alzheimers How to Hear and Honor Connections with a Person who has Dementia.ISBN-10 0978829905, ISBN-13 978-0978829902, Forrason Press Callone, P. , (2007) A Caregivers Guide to Alzheimers Disease 300 Tips for Making Life Easier. ISBN-10 1932603166, ISBN-13 978-1932603163, Demos Medical Publishing. Mace, L. N. & Rabins, V. P. , (2007)The 36-Hour Day A Family Guide to Caring for People with Alzheimer Disease, Other Dementias, and Memory Loss in Later Life, 4 th Edition, ISBN-10 0801885094,ISBN-13 978-0801885099, Johns Hopkins University Press