Alzheimer’s disease is a progressive, degenerative brain disease and the most common form of dementia, a group of brain disorders that affect a person’s memory, thinking and ability to interact socially. Alzheimer’s disease affects about 1 in 15 people over 65 years, and almost 1 in 4 people over 85 years.
At present, we don’t know what causes Alzheimer’s disease. We do know that people with this illness have abnormal material that builds up in their brain. These protein ‘tangles’ and ‘plaques’ disrupt communication between brain cells and lead to eventual cell death and brain shrinkage. There is currently no cure for Alzheimer’s disease. Available treatments only target symptoms, not the underlying biological cause of the disease.
We are conducting research into the role of inflammation in Alzheimer's disease in order to find potential targets for therapeutic intervention. We are also studying how Alzheimer’s disease affects the brain and body early in the disease, with the aim of developing a diagnostic test. Through our research on healthy ageing, we are working with Indigenous communities to increase our knowledge about ageing and dementia in Australian Aboriginal people living in urban areas.
While each person experiences a slightly different set of symptoms, the first noticeable symptoms of Alzheimer’s disease in most people is typically memory loss and difficulty in finding words in both speech and writing. Because such lapses are common and a normal part of ageing, the onset of the illness may not be recognised immediately.
As the disease progresses, people around the affected person may begin to notice signs of the disease. The person with Alzheimer’s disease may begin to find it difficult to plan and organise, for example keeping track of monthly finances, and have less knowledge or memory of recent events. They may become withdrawn.
Later in the disease larger deficits in thinking and thought processes may appear, for example difficulties with basic mental arithmetic or inability to remember important personal details, such as their address. The affected person may become confused about where they are or what day it is.
In the severe stages of the disease, the affected person’s personality and behaviour may change. They may experience delusions and hallucinations, have disrupted sleep patterns and need help with dressing and toileting.
We don’t know what causes Alzheimer’s disease. Risk factors include age, having a first degree relative with the disease, having had a head injury in the past, and having low levels of physical activity, hypertension, diabetes, high cholesterol or atrial fibrillation.
There are two types of Alzheimer’s disease: early-onset and late-onset. Early-onset Alzheimer’s disease is rare, affecting only about 5% of people with the disease. People with the early-onset form usually develop the disease between the ages of 30 and 60. Late-onset Alzheimer’s disease makes up the bulk of cases, and affects people after the age of 60.
Although we are still teasing the details out, we know that genetic factors play some role in the disease as people with an affected first degree relative are at a higher risk of developing the disease. The only genetic risk factor that we know of so far for developing late-onset Alzheimer’s disease is a particular form of the ApoE protein gene (called the ApoE e4 allele).
Early-onset Alzheimer’s disease also has genetic links. A particular type, called familial Alzheimer’s disease, is caused by one of three known genetic mutations. Children of affected people have a 50% chance of inheriting their parent’s genetic mutation; those that do will almost certainly develop the disease. The mutations we know of so far are in the genes for amyloid precursor protein (APP), presenilin 1 (PS1) or presenilin 2 (PS2). These mutations cause abnormal proteins to form in the brain, which leads to an increased amount of a protein called beta amyloid.
All people with Alzheimer’s disease – both early and late-onset – have been found to have an abnormal build-up of this protein in their brains, which clusters between the brain cells in what we call plaques. Another protein called tau forms what we call tangles inside the brain cells.
While researchers have shown that the amount of these proteins in the brain corresponds with the severity of symptoms in Alzheimer’s disease, we don’t yet understand the role of beta amyloid and tau in the disease process.
We do not yet have a cure for Alzheimer’s disease. However, there are several drug treatments that can help alleviate the symptoms of the disease.
Acetylcholine Esterase Inhibitors (also known as cholinesterase inhibitors) prevent the breakdown of acetylcholine, a neurotransmitter that is important for memory and attention. NMDA receptor antagonists prevent the over-activity of a neurotransmitter called glutamate, which is also involved in learning and memory.
Right now, researchers are working to understand the biological basis of the disease so we can develop new treatments that target the cause, not just the symptoms.
Inflammation, a biological response to harmful stimuli, is associated with the loss of neurons in Alzheimer's disease. Our studies, lead by Prof Glenda Halliday, suggest that a protein called MCP-1 is an important mediator of this response. We are studying the role of MCP-1 in the progression of Alzheimer's disease. The aim of our research is to determine whether this protein is a potential target for therapeutic intervention. Read more about this project: Inflammation and cell death mechanisms in Alzheimer’s disease.
The Schofield Group, lead by Prof Peter Schofield, is part of the DIAN (Dominantly Inherited Alzheimer Network) study, a six-year, international project set up to study how Alzheimer’s disease affects the body and the brain before there are any obvious outward symptoms. The DIAN project recruits people with familial (early onset) Alzheimer’s disease. The aim of the project is to develop a test for Alzheimer’s disease that would allow us to detect the disease early. Read more about this project: Genetics of early onset Alzheimer's disease.
We are also exploring healthy ageing and cognition in urban Aboriginal communities. The aim of the Koori Growing Old Well Study, lead by Prof Tony Broe, is to increase our knowledge about healthy ageing and dementia in Australian Aboriginal people living in cities, smaller towns and country areas. High rates of dementia (around four times the non-Indigenous rate) have been found in people aged 45 years and older living in remote Kimberley Aboriginal communities but little is known about dementia in urban Aboriginal communities. Read more about this project: The Koori Growing Old Well Study.
Alzheimer’s disease is neurodegenerative cognitive disorder with an inflammatory component. Interestingly, the endocannabinoid system plays a role in neuroprotection, has anti-inflammatory potential and modulates cognition. Recent animal research suggests that manipulations to the endocannabinoid system might have beneficial effects on the pathophysiology of Alzheimer's disease and related cognitive impairments. Dr Tim Karl is testing the neuro-behavioural response of genetic mouse models to non-psychoactive cannabinoids.
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