Understanding the Process and Experience of Dementia (Unit 101) (DEM 301)
Dementia – ‘generally accepted by clinical psychologist and psychiatrists is outlined in DSM-III-R (APA, 1987) and DSM-IV (APA, 1994). In summary, it states that for diagnosis of dementia, there should be demonstrable evidence of impairment in short-term and long-term memory. Impairment in short-term memory (inability to learn new information) may be indicated by an inability to remember three objects after five minutes. Long-term memory impairment (inability to remember information that was known in the past) maybe indicated by an inability to remember past personal information (for example, what happened yesterday, birth place, occupation) or facts or common knowledge (for example, past Prime Ministers, well known dates).’ (Thompson, 2006)
(a) Alzheimer’s Disease
‘Alzheimer's disease is the most common form of dementia affecting around 417,000 people in the UK. Alzheimer's disease was first described by a German neurologist Dr Alois Alzheimer. Alzheimer's disease is a physical disease of the brain. During the course of the disease plaques and tangles develop in the brain leading to the death of brain cells.’ (www.alzheimers.org.uk, 2011) Alzheimer’s disease affects the brain by nerve cell death and tissue loss. As time increases with this disease it causes the brain to shrink, affecting almost all its functions. In the early stages of Alzheimer’s, before symptoms can be detected plaques and tangles begin to form causing difficulty in learning, memory, thinking and planning. In the moderate stages (stages of Alzheimer’s being diagnosed) the plaques ad tangles spread further around the brain causing difficulty in speaking and understanding speech and a sense of where you body is in relation to objects. In advanced Alzheimer’s the cortex is severely damaged. In the advanced stages of Alzheimer’s disease the cortex shrivels up, damaging areas involved in remembering, planning and thinking. There is severe shrinkage in the hippocampus (an area of the cortex that plays a key role in the formation of new memories). Also the Ventricles, which are fluid-filled spaces, grow larger. Looking closely at the brain tissue of an Alzheimer’s patient, it can be seen that the brain has fewer nerve cells and synapse than a healthy brain. There is a build up of Plaques (abnormal clusters of protein fragments) between nerve cells. Plaques form when protein pieces called beta-amyloid are clumped together. Beta-amyloid is formed from a larger protein found in the fatty membrane surrounding nerve cells. The texture of the protein beta-amyloid is sticky, which helps the build up of the protein into plaques. Large groups of pieces, rather than plaques, cause more damage, as the small clumps block cell-to-cell signalling at synapses. They also active immune system cells that trigger devour disabled cells and inflammation. There is also Tangles located in dead and dying nerve cells, which are made up of twisted strands of another protein. Tangles destroy important cell transport systems made of protein. In healthy areas the transport systems are organised straight parallel cells, the protein ‘tua’ helps keep the stands parallel. The strands get formed when tau collapses and tangles are formed, they then fall apart and disintegrate. Scientists are unsure what the cause of Alzheimer’s death and tissue loss in the brain is but they suspect the Plaques and Tangles to be the cause. There are many symptoms an individual suffering with Alzheimer’s mite experience. Memory loss that disrupts daily life is seen as the most common symptom. An Alzheimer’s patient may forget recently learnt information. Challenges in planning or solving problems are a symptom of Alzheimer’s. They find it hard to work with a work plan and have difficulties dealing with numbers, for example, difficulty paying a monthly bill. Alzheimer’s patents...