Discuss the biology of Alzheimers disease

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Discuss the biology of Alzheimer’s disease

Alzheimer’s disease (AD), a form of dementia is a progressive neurodegenerative brain disorder, which involves memory and cognitive deficits as well as deterioration of intellectual functioning including language, visual spatial skills, judgment and intellectual abilities. Although the etiologies of Alzheimer’s are largely unknown, researchers believe that biological factors and genetic factors contribute to AD. Firstly, there are pathological characteristics associated with the disease, including brain atrophy, neuronal cell loss in the hippocampus (Mayeux, R, 2006). Secondly, extracellular amyloid plaques and neurofibrillary tangles are believe to contribute to the development of AD. Finally, it is widely believed that genetic factors contribute significantly to AD. While at present there are no cures for AD, some second-generation drugs have the ability to slow the progression of the disease (Irons-George, 1995). However, much of the etiology of Alzheimer’s still remains inconclusive.

In 1907, Alois Alzheimer first discovered the neuropathological changes that are found in the brains of Alzheimer affected patients. According to Khachaturin & Radebaugh (1996), Alzheimer found clusters of proteins in the brain and also noticed brain atrophy, the shrinkage of the brain caused by neuronal death  (Paladino, 1997, p.276). These observations are now known as the pathological characteristics of AD. Cooper (2003, p.101) asserts there are three main neuropathological characteristics that are associated with Alzheimer: neuronal cell loss in the hippocampus and cerebral cortex, formation of twisted nerve cell fibres, known as intracellular neurofibrillary tangles and a sticky protein known as beta amyloid forming amyloid plaques, which surrounds the debris during nerve cells in the brains (Small D H & Barrow C J, 2007). The significant loss of cells and volume in the regions of the brain occurs in the hippocampus, affecting the short-term memory of the brain and the cerebral cortex affecting the languages skills and ability to make judgments (Longe, 2006, p141).

Cooper (2003) suggests that it is the formation of the amyloid plaques and neurofibrillary tangles that are responsible for neuronal loss. An autopsy has shown that persons with AD have regions of the brain affected with neurofibrillary tangles and amyloid plaques (Longe J L, 2006). Neurofibrillary tangles are twisted nerve cell protein fibres composed of highly insoluble paired helical filaments of the cytoskeletal protein, tau (Katzman & Bick, 2000). In the nerve cells, there are normally tau proteins that bind together and contribute to the stability of neurons (Maslow, K, 2008). However, the defective tau, tangled and twisted fails to perform these actions, thus the neurons are no longer stabilised. Reynolds and Crowe (2003) believe that the tangles, by disrupting energy metabolism, affect the movement of nutrients and communication between nerve cells that affect the cell’s microtubule structure. Amyloid plaques are found in the spaces between the nerve cells of the brain, known as synapses, and consist of insoluble deposits of beta-amyloid (Aβ) and accumulations of degenerative nerve endings (Reynolds & Crowe, 2003). Studies indicate that high levels of Aβ cause reduced levels of the chemical messenger in the brain known as neurotransmitters, disturb sodium, potassium and calcium levels and causes oxidation and inflammatory process (Shi, Q & Gibson, G E, 2007). The interference of the neurotransmitters in the brain leading to the death of neurons is responsible for the problems related to AD (Terry, 1999). However, the problems associated with the structures of amyloid plaques and neurofibrillary tangles remain unknown.

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Many researchers believe that genetic factors contribute significantly to the development of AD. Longe suggests that a gene on chromosome 19, apolipoproteinE (ApoE) involved in the transportation of lipids into neurons may have a significant genetic link to AD. According to A.D.A.M (2006), results show that:

Table 1. The percentage of developing AD depends on the number of ApoE4 present in an individual

 

Nevertheless, less than 5% of Alzheimer’s disease worldwide is caused by genetic mutations (Bertram L, 2007). Although the knowledge of etiology still remains incomplete, Bertram argues that inheritance of specific genes plays a critical role ...

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