Dementia Research Paper

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Although there is growing understanding of dementia, it remains a poorly understood condition that continues to be associated with negative attitudes and stigmas. Dementia is not a disease but a clinical syndrome, meaning a set of symptoms relating to the breakdown of intellectual (cognitive) functions. Operational diagnostic criteria for dementia stipulate (1) an impairment in memory; (2) an impairment in at least one other cognitive domain (e.g., language, visuospatial, knowledge and understanding, executive functions, control over social and emotional behaviors); (3) that the impairment represents a decline from the person’s previous levels of ability; and (4) that the impairments are severe enough to interfere with the person’s everyday life.

The main risk factor for the development of dementia is age. Prevalence rises from 1 in 1,000 for those aged 45 to 65; to 1 in 5 for those aged 80 to 90; to 1 in 3 among those over age 90. Until the late twentieth century, dementia in an elderly person (defined to be someone over 65 years of age) was commonly diagnosed as “senility” or “senile dementia.” These terms, however, are no longer recommended because they have been used with a lack of diagnostic rigor and there is a lack of scientific evidence to justify the diagnostic distinction between “presenile dementia” (dementia in someone under age 65) and “senile dementia” (identical symptoms in someone age 65 or more). Furthermore, the term senility carries negative connotations and implies that the dementia syndrome is an inevitability of old age. This implication is not supported by the evidence and leads to poor recognition of dementia syndrome. The symptoms of dementia in elderly people often get dismissed on the basis that these are just signs of old age, although dementia in middle-aged people is commonly misdiagnosed as a functional psychiatric disorder.

Most causes of dementia are slowly progressing neurodegenerative diseases with Alzheimer’s disease being the most common cause, accounting for 50 to 60 percent of all cases. Dementia is typically thought of as progressing from a mild stage, characterized by slips of the memory and confusion in complex situations, through a moderate stage, during which the degree of cognitive impairment intensifies to affect an increasing number of activities of daily living (e.g., use of language, ability to recognize friends and relatives, ability to make sense of the visual world, ability to use household objects or appliances effectively and safely, ability to dress and attend to personal hygiene). The severe stage of dementia is characterized by serious disability in which the person is likely to have limited language and understanding and to be totally dependent upon others for all their physical needs (eating, drinking, toileting).

However, typical schemes of dementia symptoms and progression need to be treated with extreme caution. The precise symptoms a person experiences will depend upon the particular cause of that person’s dementia and the parts of the brain that were damaged. Also, the symptoms of dementia must be understood as complex interplay between neurological damage and psychological and social variables, such as the person’s life history, personality, and quality of the care environment. These considerations are particularly important when assessing the non-cognitive symptoms of dementia, such as apathy, anxiety, wandering, or aggression. Such behaviors may reflect the individual’s personality or coping style, or they may be a valid response to an environment in which the person’s needs and personhood are being overlooked or neglected.

With over two hundred possible causes of dementia there is still a lot to be learned about how specific causes manifest. The stages of dementia outlined are strongly influenced by the specific characteristics of Alzheimer’s disease. Other forms of dementia are known to have different characteristics and growing knowledge of these differences is stimulating a move away from the generic criteria for dementia toward operational criteria for specific diagnoses (e.g., dementia of the Alzheimer type, vascular dementia). In particular, early memory loss is often cited as the key feature of dementia but this symptom has a specific link with Alzheimer’s disease and there are forms of dementia in which memory loss is not a central feature (e.g., frontotemporal and Lewy body dementia).

After Alzheimer’s disease, vascular dementia is the next most common form of primary dementia, accounting for 20 percent of all dementias. The blood supply to the brain can become fragile in old age and the term vascular dementia covers all forms of dementia that result from cerebrovascular pathologies. Lewy body disease, frontotemporal atrophy, alcohol abuse, and the AIDS complex are also significant causes of dementia. Some dementias are due to reversible causes (e.g., depression, hypothyroidism, vitamin B deficiency) and are called “secondary dementias.” It is important that the diagnostic procedure fully investigates secondary causes for dementia before diagnosing a primary (irreversible) cause.

Pharmacological treatments for primary dementias are limited. A number of anti-cholinesterases are available that aim to alleviate some of the cognitive and functional symptoms of dementia by boosting levels of the neurotransmitter acetylcholine. These drugs were designed to specifically target the Alzheimer’s disease process, although there is evidence that they may be beneficial in other forms of dementia, particularly vascular dementia and Lewy body dementia. Memantine is an alternative drug that aims to protect undamaged nerve cells from the toxic effects of high levels of the neurotransmitter glutamate, which is released in excessive amounts when cells are damaged. Both types of drug are aimed at damage limitation; neither can stop the underlying disease processes themselves. The evidence suggests anti-cholinesterases and memantine provide some benefit, but it is modest.

It is also important to support drug interventions with non-pharmacological interventions (e.g., reminiscence therapies, sensory therapies, support and discussion groups). These interventions will also not cure the problem but will protect well-being and ensure that the symptoms of dementia are not exacerbated through poor care, inappropriate expectations, and lack of support. The person with dementia’s well-being is critically dependent upon that of their care giver. When care givers are not properly supported there is a high risk that their own mental and physical health will be affected, leading to a poor outcome for both the care giver and patient.

In terms of prevention, control of vascular risk, particularly cholesterol levels and hypertension, is emerging as the main preventative strategy for both vascular dementia and Alzheimer’s disease. People can control their vascular risk either through diet or pharmaceuticals. An increased risk for dementia has also been associated with low education or intelligence, socioeconomic disadvantage, stress, and dietary factors (particularly the B vitamins) but untangling the direction of causation among this complex set of factors remains a significant challenge. For example, the well-established correlation between low intelligence and risk for dementia has been interpreted in terms of compensation, such that the effects of pathology are masked by higher ability, but some recent prospective studies, most notably the nun studies organized by David Snowden, suggest that low intelligence in early life may be directly involved in the pathogenesis of Alzheimer’s disease. Similarly, low intake of vitamin B12 and folate are associated with elevated levels of homocysteine, another vascular risk factor which has been associated with risk for Alzheimer’s disease. However, it is less clear whether increasing the dietary intake of vitamin B12 and folate has any protective effect.

Bibliography:

  1. Burns, Alistair, John O’Brien, and David Ames. 2005. 3rd ed. London: Hodder Arnold.
  2. Kitwood, Tom. 1997. Dementia Reconsidered. Buckingham, U.K.: Open University Press.
  3. Sabat, Steven R. 2001. The Experience of Alzheimer’s Disease: Life Through a Tangled Veil. Oxford: Blackwell.
  4. Snowden, David. 2001 Aging with Grace: The Nun Study and the Science of Old Age. London: Fourth Estate.

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