A Tour around Alzheimer's Disease

(Date of publication 23 May 2005)

"It bothers me that I asked my daughter if she would take the clothes home with her to put them in her dryer. After she left I realised that I have my own dryer that I have been using for the past three years."

"I confess to being unable to remember some conversations at all. Some, I can vaguely remember bits of."

"I went shopping yesterday and left the keys in the car and the engine on. I've had to have my poor car broken into so many times that the door is practically wrecked."

These excerpts from a first person account of the early stages of Alzheimer's Disease (AD) bring home the intense personal anguish caused by the condition. But this is not the only cost; the economic impact in the United States is currently estimated to be over $100 billion per year, with an average lifetime cost per patient of $174,000, often far more than the resources of the sufferer and his or her family.

In the United Kingdom, dementia currently affects over 700,000 people, of whom more than 18,000 are less than 65 years of age. Alzheimer's Disease is the most common cause, responsible for 55% of cases. There are two basic types: familial and sporadic. Familial AD is rare, affecting less than 10% of sufferers, and always early-onset, developing before the age of 65. The cause is genetic mutations on chromosomes 1, 14 and 21, which are inherited as an autosomal dominant characteristic. Sporadic AD is generally late-onset, has no known cause and shows no obvious inheritance pattern. However, researchers have identified an increased risk associated with a particular form, or allele, of the apolipoprotein E gene found on chromosome 19.

Both forms of AD involve a progressive, irreversible deterioration of brain cells resulting in the loss of cognitive function: primarily memory, judgment and reasoning, co-ordination of movement and pattern recognition. Once the disease has become advanced, all memory and mental functioning may be lost. In the early stages, new or recent memories are difficult to recall, but eventually, older or more distant recollections are gradually lost. Next, other symptoms may appear, including difficulty expressing thoughts as spoken words (aphasia), difficulty carrying out simple, directed acts (apraxia), and difficulty interpreting familiar faces or other well-known objects (agnosia).

The parts of the brain that are predominantly affected are the cerebral cortex and the hippocampus. The most significant findings in victims' brain tissue are neuritic plaques, neurofibrillary tangles and greatly reduced levels of acetylcholine, which is required for cognitive functioning. Excessive numbers of neuritic plaques, composed of a protein called beta amyloid surrounded by fragments of deteriorating neurons, are present in the cerebral cortex. In this photomicrograph, normal axons are stained black and the plaque itself contains heavily stained, swollen and distorted axons and dendrites. Neurofibrillary tangles are the twisted remnants of an intracellular protein called tau, which is required to maintain proper cell structure and function – an example is situated near the top centre of this photomicrograph.

There is a fairly basic RealPlayer video about the formation of neuritic plaques and neurofibrillary tangles at the Alzheimer's Disease Education and Referral Center site, which can be viewed via either broadband or a 56k dial-up connection. It lasts about two minutes. To see the gross changes which take place in the brain, including abnormal shrinkage, widening of the intraparietal sulci and atrophy of the hippocampus and amygdala, Harvard Medical School has a tour of magnetic resonance images at different levels through the head of an Alzheimer's patient.

No treatment can stop AD, but there are drugs which may delay its progression in the early and middle stages of the disease, allowing patients to maintain certain daily functions a little longer. Most of these agents (Aricept, Exelon, Reminyl, and Cognex) work by slowing down the breakdown of acetylcholine, and appear to be beneficial only when symptoms are mild or moderate. Namenda, which helps to regulate glutamate activity, is prescribed for patients with moderate to severe Alzheimer's. For more information about these drugs, click here.

Much research activity is focused on Alzheimer's Disease and it has recently thrown up some interesting results. Patients with mild cognitive impairment who take Aricept may delay the progression of their condition to AD, suggesting that earlier intervention may be beneficial. A diet high in docosahexenoic acid, one of the omega-3 fatty acids found in cold water fish, dramatically slows the progression of Alzheimer's disease in mice, by reducing the build-up of amyloid plaques. A high concentration of silica in drinking water may help to prevent AD, but diabetes mellitus has been linked to a 65% increase in risk. Also, preliminary results of a pilot study show that mental function improved in six out of seven patients who were treated with an immunoglobulin fraction containing antibodies to beta amyloid.

Finally, the nature of the care that the AD patient receives is vitally important. Carers must help the victim to retain a sense of identity and self worth, and take into account his or her abilities, interests and preferences. Sufferers must feel respected and valued for who they are now, as well as for who they were in the past. A very good description of such 'person-centred' care is provided by the Alzheimer's Society.

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