Pathophysiology of Alzheimers Disease - Research Paper Example

? Running Head: PATHOPHYSIOLOGY OF ALZHEIMER’S DISEASE Pathophysiology of Alzheimer’s Disease of Introduction Definition Dementia Dementia is one of the most severe progressive irreversible impairment in the intellect that progresses with age and illustrates a serious concern in public health (Yamasaki, et al, 2012). Anderson (2011) noted that economically, dementia is identified as the major public health problem in the United States (US). Wayne, et al (2009) stated that in adulthood, the mass and speed of a healthy brain may decline; and yet, despite of this natural phenomenon, the vital connections is still continuously being formed by this “miraculous machine” throughout life. Along the way, certain conditions such as inflammatory process, diseases, or neuronal injury may eventually lead to neuronal death, and consequently, loss vital connections that may ultimately result to dementia (Wayne, et al, 2009). According to its anatomical relationship in the cerebral lesion, dementia has been classified as cortical and subcortical in origin. Alzheimers, which is classified under cortical dementia, is the most common form of dementia that affects around 4.5 million people in the US, and manifest normally as aphasia, agnosia, apraxia, and executive functioning disturbances (Yaari and Bloom, 2007, Yamasaki, et al, 2012). Alzheimer’s Disease Alzheimer’s disease (AD), which accounts to about two – thirds of diagnosed cases of dementia, is characterized by a progressive neurodegenerative dementia in the elderly and progressive cognitive decline that results in gradual and irreversible memory and cognitive loss (Yaari and Bloom, 2007, Wayne, et al, 2009, and Yamasaki, et al, 2012). AD is an incurable disease that is believed to be an acquired impairment in cognition and behaviour that hinders markedly with the social and occupational performance of an individual (Anderson, 2011). AD is difficult to diagnose because patients may initially have a normal IQ functioning. At the onset, patients may have memory, language, and visuospatial deficits, which would later progress to depression, obsessive, suspiciousness, anger outburst, and violent acts (Anderson, 2011). The aforementioned characteristics of AD bring detrimental effects on the patients as well as duties and responsibilities on the family and caretakers of the patients (Anderson, 2011). History of Alzheimer’s Disease The first reported case of Alzheimer was made in 1901 by Dr. Alois Alzheimer, a German psychiatrist, who observed a patient who suffered from short term memory loss at the Frankfurt Asylum. The patient eventually died in 1906 and, and Dr. Alzheimer sent her brain together with the medical records to Munich. Together with Dr. Kraeplin, Dr. Alzheimer noted amyloid plaques and neurofibrillary tangles on his histological findings by staining section of the brain of the patient (Yaari and Bloom, 2007 and Anderson, 2011). The pathology and clinical symptoms of Alzheimer’s disease (previously known as presenile dementia) was presented by Dr. Alzheimer in his speech in 1906, and subsequently published his findings in the year 1907.   Pathophysiology of Alzheimer’s Disease Anderson (2011) stated that alzheimer’s disease normally affects the three processes that maintain a healthy neuron. These are communication, metabolism, and repair. Any disruption of these processes may cause certain nerve cells in the brain to be ineffective, losing its connections with others neurons, and ultimately lead to cell death. As a result, memory starts to fail causing changes in the personality of a person, and difficulty in achieving day to day activities (Anderson, 2011). Alzheimer’s disease (AD) has a complex pathophysiology since it involves pathophysiologic processes and neurotransmitter systems (Morrison and Lyketsos, 2005, and Siegal, 2005). The three (3) well – known and central factor in the neurodegenerative process as well as the universally accepted hallmark of AD described by Dr. Alzheimer in his 2007 speech, and is now the anatomic pathology of AD consists of: (1) neurofibrillary tangles, (2) senile plaques or beta – amyloid plaques, and (3) atrophy in the cerebrocortical area or neuronal cell death (Morrison and Lyketsos, 2005, Siegal, 2005, and Anderson, 2011). Changes in the Cerebrocortical Area of the Brain On macro level, the pathology of AD is characterized as the progressive loss of the tissues in the brain. As AD progresses over time, neurons notably in the hippocampal area of the cortex will die in a particular pattern, and manifests as loss of short – term memory recall (Morrison and Lyketsos, 2005, and Siegal, 2005). Morrison and Lyketsos (2005) noted that memory loss is identified as one of the earliest signs of AD. Patients with Alzheimer presents with a brain characterized with marked atrophy associated with a widened sulci and gyri that have shrunk (Yaari and Bloom, 2007). Generally, cerebral cortex is involved in the pathology of AD and relatively sparing the occipital pole. As AD progresses from mild to moderate memory loss, the atrophy is distinguished to have enlarged to other areas of the cerebral cortex (Morrison and Lyketsos, 2005, and Siegal, 2005). During this stage, the patient is observed to have experienced a more pronounced loss of memory, and is now associated to have a decline in their ability to process thoughts that are complex as well as changes in personalities and moods (Morrison and Lyketsos, 2005, and Siegal, 2005). During the severe stage of AD, atrophy in the cortex is now becoming prominent in the areas controlling the speech, reasoning, sensory processing, and conscious thought. Morrisson and Lyketsos (2005) and Siegal (2005) noted that there is an increase in the size of the lateral and third ventricles when an apparent atrophy is observed in the larger areas of cortex and hippocampus. Yaari and Bloom (2007) also noted that as a result of the atrophy of amygdala and hippocampus, there is also thinning of the cortical ribbon with apparent dilatation of the ventricles. During this stage, symptoms of AD increases in severity and would now manifest as impairment in long – term memory, seizure, incontinence, loss of weight, non recognition of loved ones, inability to sit up, and moaning/grunting (Morrison and Lyketsos, 2005, and Siegal, 2005). Amyloid Hypothesis and Development of Plaques Yaari and Bloom (2007) reported that in addition to large cortical neuron shrinkage, a significant neuronal loss has been observed microscopically. Hence, the critical pathological substrate seen in Alzheimer is believed to be associated with shrinkage of drendritic arbour of large neuron and the loss of synapses. As noted previously, the presence of neuritic plaques and neurofibrillary tangles is believed to be the neuropathological hallmarks of alzheimer’s disease (Yaari and Bloom, 2007, Morrison and Lyketsos, 2005). According to Yaari and Bloom (2007), Morrison and Lyketsos (2005), and Siegal (2005), the spherical neuritic plaque that consists of amyloid surrounds the degenerating nerve endings. In the brain of patients with alzheimers are types of amyloid – related plaques known as diffuse plaque and burnt – out plaques. The abnormal processing of precursor protein molecule of amyloids results in the most toxic fragment, which is identified as A?1 peptide, is believed to form insoluble clumps in the brain. The aforementioned cascade of event has been postulated in the dysfunction and death of the neurons. However, Yaari and Bloom (2007) believed that A? accumulation is not responsible exclusively in alterations of the neurons that underlie its symptoms even though it is believed to be critical in the pathogenesis of Alzheimer. Neurofibrillary Tangles According to Morrison and Lyketsos (2005) and Siegal (2005), when seen under histologic staining, the neurofibrillary tangles are seen as dying or dead neurons. On the other hand, Yaari and Bloom (2007) noted that neurofibrillary tangles found inside the neuron is believed to be one of causes of histopathological changes in Alzheimer. It is composed of helical filaments of hyperphosphorylated micro – tubule that is paired and is associated with tau protein. It is believed that disruption of normal cytoskeletal architecture is caused with intracellular deposition with subsequent death of cells in the neuron. Yaari and Bloom (2007) believed that neuritic plaques and neurofibrillary tangles is concentrated in vulnerable neural systems and are not distributed evenly across the brain of the person with alzheimer’s disease. Likewise, neuropil threads, granulovacuolar degeneration and amyloid angiopathy are believed to play an important role in the pathological alterations seen in patients with alzheimer. Among the aforementioned factors, a distinct lesion in the blood vessels consisting of amyloid deposition in the small to medium size arterial wall and leptomeningeal arteries, known as amyloid angiopathy, is believed to have caused hemorrhage compromising the vessels involved (Yaari and Bloom, 2007). Conclusion Learning the pathophysiological processes of alzheimer’s disease plays a significant role in the concept of advanced nursing practice. The complex and disorderly progression of patients with alzheimer’s disease is challenging to the caregivers. Learning the processes of AD and its clinical progression helps the caregiver anticipate the specific demands of the patient and provides the best care, attention, and approach the patient deserves. References Anderson, H. (2011, June). Alzheimer Disease. Retrieved November 10, 2011, from http://emedicine.medscape.com/article/1134817-overview Morrison, A.,& Lyketsos, C. (2005, October). The Pathophysiology of Alzheimer’s Disease and Directions in Treatment. Advanced Studies in Nursing, 3(8), 256 – 270. Retrieved from http://www.jhasin.com/files/articlefiles/pdf/asin_3_8_p256_270.pdf On Aging, N. (2009). What is Dementia?. Psych Central. Retrieved on November 11, 2011, from http://psychcentral.com/lib/2006/what-is-dementia/ Siegal, J. (2005, August). Our Current Understanding of the Pathophysiology of Alzheimer’s Disease. Adv Stud Pharm., 2 (4), 126 – 135. Retrieved from http://utasip.com/files/articlefiles/pdf/ASIP_Issue_2_4p126_135.pdf Wayne, M., White, M., and Smith, M. (2009, May). Understanding Dementia. Retrieved November 10, 2011, from http://helpguide.org/elder/alzheimers_dementias_types.htm Yaari, R. & Bloom J. (2007, March). Alzheimer’s Disease. Semin Neurol, 27(1), 32-41. Retrieved from http://www.medscape.com/viewarticle/553256 Yamasaki, T., Muranaka., H., Kaseda, Y., Mimori, Y., and Tobimatsu, S.(2011, May). Understanding the Pathophysiology of Alzheimer's Disease and Mild Cognitive Impairment: A Mini Review on fMRI and ERP Studies. Neurology Research International, 2012(2012). doi:10.1155/2012/719056. Retrieved from http://www.hindawi.com/journals/nri/2012/719056/ Read More