About Alzheimer’s disease
Alzheimer’s disease (AD) is the most common form of dimentia, a disease characterised by severe memory loss, mood changes and communication problems. AD is a progressive disease which gets worse overtime. Patients suffering with rapidly degenerative AD eventually require full-time care as they become unable to complete day-to-day tasks, such as cleaning and cooking.
AD was first reported by German neuropathologist Alois Alzheimer in 1906 when he identified abnormal clumps of proteins called amyloid deposits in the brain of a woman who had suffered with strange behavioural symptoms, including severe memory loss . This later became the basis for the amyloid plaque hypothesis of AD, however how these plaques cause AD remains unknown (1).
With the latest statistics revealing that over 820,000 people are currently living with AD in the UK and one person being diagnosed every 3.2 minutes, the requirement for effective early diagnostics tests and curable treatment is becoming increasingly urgent (2). One in three people aged over 65 will die with a form of dementia. Dementia costs the UK approximately £23 billion per year. Caring for each person with dementia has an economic impact of £27,647 per year, which is 4.6 times greater than the figure for cancer.
To date, despite intense research efforts, there is no identified single cause of Alzheimer’s disease. However, several factors have been demonstrated to play a part in increasing the risk of AD. The first is age. Statistics revel that 1 in 14 over 65 year olds and 1 in 6 over 80-year-old suffer with AD. The second factor is genetic inheritance. Although the majority of cases are sporadic, 0.1% of cases are familial forms of AD, meaning that risk genes may be passed on through families. Other studies have linked the risk of AD with other factors, including head injury, tobacco smoking and lack of exercise (3).
Although Alzheimer’s disease remains an incurable disease, management is available, but remains only able to treat certain symptoms in the aim of improving the quality of life of AD sufferers. There are three branches of management available, including drugs, care giving and psychological treatment. A total of 5 drugs have been approved for treatment towards AD. Four of the approved drugs are acetylcholinesterase inhibitors, these include Tacrine, Rivastigmine, Galantamine and Donzepil. These drugs are recommended based on the hypothesis that AD patients brains reveal a loss of nerve cells that send messengers through the hormone acetylcholine. These drugs break down acetylcholine to improve symptom severity. The fifth drug is an glutamate blocker called Memantine. This drug is prescribed based on the theory that AD brains release excessive amounts of the messenger, glutamate. Memantine blocks these effects. Efficacy, however, is patient-specific (4).
At present, the diagnosis for Alzheimer’s remains a combination of different tests, including patient and family history, clinical observations, such as neurological and neuropsychological features, memory tests, and the absence of other conditions. Brain imaging is becoming an increasingly useful examination for Alzheimer’s.
Positron emission tomography (PET) is a neuroimaging tool which is used in combination with memory tests as part of the diagnostic methods for AD. PET imaging is used based on the hypothesis that areas of high brain activity are associated with high radioactivity. As it has been demonstrated that glucose levels are greatly decreased in AD brains, a measurement of glucose is able to distinguish AD from other types of dimentia (5).
News: Alzheimer’s test approved
On the 6th April, the FDA approved Amyvid (a Florbetapir F18 Injection) a new drug for PET 3D imaging of the brain for adults being evaluated for AD. In this method the compound florbetapir binds to amyloid plaques and is detected by PET imaging (6,7).
Currently, a reagent called Pittsburgh Compound B is used to image amyloid plaques in people suspected to have Alzheimer’s disease. However, as this compound is labelled with carbon-11, which has a half-life of just 20 minutes. Therefore, its use is limited. Another more useful chemical florbetapir is labelled with fluorine-18, which has a half-life of nearly two hours. Thus, long enough would be long enough to be used in the brain and be imaged without losing too much dye. Not only will imaging with florbetapir be able to reveal the development of amyloid plaques in AD brains, but it will also be able to demonstrate the relationship between amyloid plaques and AD, in order to work towards a cure.
There is, however, controversy surrounding the approval of this drug and it’s use in a diagnostic test. As reported in a Blog by Nature, although scientists were initially hopeful for the potential of Amyvid in the AD diagnosis; autopsies of AD brains have demonstrated that one-fifth of suspected AD patients did not have amyloid plaques. Therefore, the diagnosis was wrong. It is important to acknowledge that amyloid plaques alone are not solely indicative of AD. Additionally, other forms of dimentia also present with amyloid plaques in the brain. As the underlying mechanisms of the amyloid hypothesis and its involvement in AD have not been fully elucidated, further research is required (8).
Therefore, although the approval of this test could be a step toward determining the pathology of AD and producing a diagnosis test, we are a long way from a fully elusive testing procedure. With this in mind, possible patients need to decide whether they wish to undergo a test, that may produce a false-positive result that may change their lives forever.