Neuropathology and Etiology of Alzheimer’s disease
Scientists have not yet fully come to full grips with the real causes of Alzheimer’s disease, however, one clear aspect of the development 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 include genetic, medical, biological, environmental, dietary, social and cultural aspects (Draper, 2004).
In genetic aspect, APOE E2 is rare and creates protection against Alzheimer’s disease and in case it does occur in much later years than in people with APOE E3 and APOE E4.
APOE E3 forms the most common Allele and is assumed to perform a neutral role in Alzheimer’s disease. This means it neither stimulates nor increases reactions that would lead to the development of Alzheimer’s. The APOE E4 occurs in the most common and occurs in approximately 40% in those who suffer from late onset Alzheimer’s disease. It is therefore common that people with APOE E4 are more likely to suffer from Alzheimer’s disease (Kuhn & Verity, 2007).
It is infact known as the risk factor gene in that it increases one’s level of risk of developing Alzheimer’s disease. Early – onset Alzheimer’s disease, affecting few 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 early onset Alzheimer’s disease. This kind of inheritance pattern is referred to as “abnormal dominant inheritance”. Another possible risk towards the development of Alzheimer’s disease is SOR1 (Roudier et al, 1991). This gene is solely responsible for the transportation of APP (Abnormal Amyloid Precursor Protein) within the cells and was discovered to be connected to Alzheimer’s disease. While it is present in low levels, beta amyloid levels increase and may have a negative effect on neurons (Ramanathan, 1997).
The difference in genetic make up from one person to another either delays or completely prevents the onset of Alzheimer’s disease, also known as Familial Alzheimer’s disease. It is mainly inherited from parents and is caused by mutations in three genes. (APOE E2, APOE E3, APOE E4). There is a 50-50 chance of an offspring developing early onset Alzheimer’s 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 Alzheimer’s disease.
It is know to destroy brain cells and hence cause problems with behavior, thinking and memory severely enough to affect work, lifelong 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 Alzheimer’s 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 nerve cells, which in turn stimulates their growth and thus reduces the chances of their degeneration.
Nerve Growth Factor (NGF) is responsible for controlling cell regeneration in the entire body but it is denied entry into the brain, this makes brain cells lack ability to self-regenerate (Taylor, 2006). Alzheimer’s’ 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 right 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 Alzheimer’s disease. Progression of series of Alzheimer’s disease consists of five stages expanded to seven stages by the use of a Modified Global Deterioration scale (GDS). This scale assists doctors to measure the exact level of progression of the disease in a patient and administer right medication. Stages of Alzheimer’s 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 deterioration 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 Alzheimer’s Disease and Other 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 Alzheimer’s Disease: Interaction of Cognitive Domains. Developmental Neuropsychology. Volume: 7. Issue: 2. Kuhn, D. & Verity, J., (2007): The Art 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 Alzheimer’s 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): Alzheimer’s from the inside out. ISBN-10: 1932529233, ISBN-13: 978-1932529234, Health Professions Press. Coste, K. J. , (2004): Learning to Speak Alzheimer’s: A Groundbreaking Approach for Everyone Dealing with the Disease. ISBN-10: 1864710632, ISBN-13: 978-0618485178, Mariner Books. Pearce, N., (2007): Inside Alzheimer’s: 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 Caregiver’s Guide to Alzheimer’s 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, 4th Edition, ISBN-10: 0801885094,ISBN-13: 978-0801885099, John’s Hopkins University Press