Alzheimer’s Disease

Symptoms and treatment

Alzheimer’ s Disease (AD) is by far the most common type of dementia and is called after a German Psychiatrist, Alois Alzheimer, who in 1907 first described the changes caused by the condition.AD starts very gradually, sometimes insidiously, and progresses slowly but steadily.

The disability experienced can vary from one person to another and from day to day. Common difficulties experienced include, memory loss, impaired judgement, personality changes, difficulties with speech and conversation, difficulty with decision-making, wandering, repetitive questions, sleep disturbance and sometimes depression, suspiciousness, aggressive behaviour and incontinence.

This list is by no means exhaustive. The onset of AD generally occurs in later life (60 +) and its incidence increases with age. In some cases the disability associated with AD may be improved by drug treatments.

Such treatments work by boosting levels of a chemical called acetycholine, which is deficient in people with AD. It needs to be remembered that only about 50% of men and women with AD who are offered medication, respond positively. Not everyone with AD is suitable for such treatments.

Causes of AD

Unfortunately the cause of Alzheimer’s Disease is largely unknown. Increasing age and family history are known to be risk factors. The impact of genetics on AD is quite complex. A small number of families have a very strong genetic component to their AD.

There are a few kindreds with autosomal dominant transmission, which means that the person with a parent with AD has a 50% chance of getting it. However, these pedigrees are extremely rare and are characterised by early onset, usually before the age of 50.

A recent discovery has been that specific versions of the gene for a protein called Apolipoprotein E (alleles for ALP) that an individual carries, are related to the risk of developing sporadic (non-familial) AD. The gene for Apolipoprortien E is located on chromosone 19. However, not everyone with ApoE 4 will get a dementia so testing for Apo E 4 genotype is not predictive of AD.

Other non-genetic suggested risk factors for AD include head injury (with loss of consciousness), gender (women are more commonly affected than men), and lower level of education. In the dementia research literature, the association between educational level and AD is somewhat contested.

It has been noted that the lower risk of AD for people from a higher educational background may be an artefact, since there is a likelihood that those with more education have a higher baseline level of functioning and therefore do not meet criteria for AD as readily as others.

Older people with Down’s Syndrome are at risk of developing AD due to their having a triple copy of chromosome 21, the chromosome on which the amyloid precursor protein (APP) is found. In fact it is well established that all persons with Downs Syndrome aged over 40 will have the neuropathology for AD.

The importance of early diagnosis

The diagnosis of AD is primarily made on the basis of symptoms. Diagnosis usually means that the person meets the criteria for a diagnosis of probable AD and this diagnosis is usually only 80 to 90% accurate. More definitive diagnosis requires the examination of the brain tissue either by brain biopsy or after death to demonstrate the characteristic features under microscope. Brain biopsy is rarely recommended in view of the risks and discomforts associated with the procedure.

Unfortunately at the moment, there are no blood tests or brain scan that can definitely diagnose the condition. However it is most important to exclude other forms of dementia that may be treatable and even reversible. For this reason seeking an early diagnosis is very important and can help to empower the individual to take control of his or her legal and financial affairs and become actively involved in care plans.

An early diagnosis may also help to relieve much anxiety experienced by family members who may attribute the person’s memory problems or changed behaviour to other non-medical causes. In the past, many physicians shielded their patients from "bad news" such as the diagnosis of cancer, to reduce anxiety and medical decisions tended to be made by doctors sometimes in consultation with family members.

Now the accepted practice is to disclose all information to patients (provided they wish to know and are capable of understanding ) and to share all medical decision making with patients and their families.

Neuropathology of AD

The diagnostic characteristics features of AD are plaques and tangles found on post mortem in the brain. Plaques consist of a core of protein called amyloid. Amyloid is a medical term used to describe the protein deposited in the brain tissue and in blood vessels of people with AD. The specific amyloid protein in AD is called "beta amyloid" which is derived from a larger protein called Amyloid precursor protein (APP).

APP is normally produced by a number of different types of cells in the body. Its exact function remains unknown. By metabolic pathways which remain poorly understood, APP can in some people be broken down into Beta Amyloid which in turn deposits itself in the brain.

Beta amyloid is insoluble, resistant to degradation and does not form naturally. Dying brain cells can be found surrounding amyloid deposits in parts of the brain, which are important to memory and other cognitive functioning. Some believe that these amyloid deposits are the key factors leading to the development of AD.

Another characteristic of AD found under microscope are tangles. The term tangle describes the appearance of dense proteins found within neuronal cells. These tangles can appear as bundles of threadlike structures. One particular protein component of tangles is called Tau. Tau protein found within tangles in AD differs from Tau protein found in normal brains and has been chemically modified.

There is now an on-going debate among scientists over, which is more important in relation to the aetiology of AD, plaques or tangles. Some researchers argue that tangles correlate more clearly with the clinical features of AD while others maintain that an increased production of amyloid protein, represents a critical early step, and that tangles mark the death of neurones from exposure to amyloid protein or other toxic compounds.

Dementia: A person-centred approach

While undoubtedly, understanding the neuropathology of the brain and the genetic and metobolic pathways leading to the development of AD is very important, for a long time researchers (and it could be argued the public at large) have concentrated almost exclusively on visualising AD, in terms of atrophied brains, riddled with plaques and tangles.

This over-medicalisation of AD has it is argued, served to further dehumanise and disadvantage the individual experiencing the symptoms of dementia by squeezing him or her out (Stokes, 2000).

An energetic dementia movement led primarily by British and American clinical psychologists and sociologists, has over the last decade, helped to shed light on the important contribution non-medical factors play in relation to the subjective experience of dementia. Recent research now suggests that social, psychological and environmental factors play a key role in the way in which AD is diagnosed, experienced, and managed (Chester & Bendon, 1998; Phair & Good, 1998).

Person-centred care or care that places the individual with dementia at the centre stage and sees that person in the context of his or her past and present social world of roles, relationships, likes, dislikes and hobbies has been shown to improve quality of life. It has been demonstrated that people with dementia have an acute sensitivity to their local environment and may feel anxious, frightened and at times vulnerable.

A poorly adapted environment, may aggravate confusion and may contribute to excess disability. Examples of poorly adapted environments include day centres or nursing homes where there is excessive noise, poorly controlled temperature levels, harsh or limited natural light and inadequate sign-posting and cueing. The positive manipulation of the environment is one way in which cognitive deficits associated with AD can be reduced.

DSIDC subscribes to a holistic model of dementia that draws on research and clinical contributions made by both medicine, psychiatry and the social and behavioural sciences to better understand AD.

Underpinning all of its professional activities is an emphasis on promoting a positive approach to the care of people with AD. Each of the Centre’s professional activities has developed from a practical knowledge-based perspective and the fundamental belief is that people with AD have a right to be treated with dignity and respect and that many of the so called problems associated with AD can be minimised or resolved through creative management.