Alzheimer’s disease is growing with our ageing population, but with no real preventative cure available, we’re all looking to science fiction.
For the first time in its history, America’s ageing population is predicted to soon outnumber children, and with life expectancy forecast to surpass 80 years in most areas across the globe by 2050, this means that by then, more than two billion people will be aged over 60 years. It’s alarming to realise the current social welfare and healthcare systems around the world are probably not robust enough to accommodate the massive volume of age-related health issues that could potentially ensue.
One such health issue is dementia. According to Dementia Australia, there are almost 426,000 people living with dementia, and around 300,000 people involved in their care. Interestingly, there are, in fact, around 100 different types of dementia, largely because “dementia” itself refers to a collection of symptoms which are caused by disorders affecting the brain, and not one specific disease per se.
Of course, the most common form of dementia around the world is Alzheimer’s disease.
Alzheimer’s disease is a decline in cognition, which impacts behaviour and thought, as well as the capacity to perform routine tasks, to the point where the person’s normal working or social life is disrupted. While the majority of those with Alzheimer’s are aged 65 years or older, it’s important to understand that dementia is not actually a normal part of ageing, and not all older people get dementia. People aged in their 40s and 50s can also suffer from this decline in brain function. In fact, the term “younger onset dementia” refers to any form of dementia diagnosis in people aged less than 65 years, and figures indicate there are around 26,000 Australians living with younger onset dementia, with some being diagnosed in as early as their 30s.
Every 66 seconds in the States, a new case of Alzheimer’s disease is diagnosed. In 2018, the total cost of care for all of these people is anticipated totally around $1 trillion.
Dementia is actually a highly complex condition. In order to receive appropriate treatment and medication (if applicable), an early diagnosis is important. However, there are a number of conditions that can elicit similar symptoms (such as infections, depression, deficiencies in vitamins or hormones, over-medication, medication clashes or brain tumours), which can, of course, make an accurate diagnosis tricky to come by. What’s more, these early signs can be extremely subtle and may vary enormously from individual to individual. Interestingly, dementia can be hereditary, but only in around 1% of cases.
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Typically, symptoms include an inability to remember recent events, becoming withdrawn or apathetic, experiencing an inability to undertake routine tasks, personality changes and confusion. But because these signs may not be obvious or are irregularly apparent, it’s not unusual for people to fail to recognise that something is seriously wrong. Often, they’re brushed off or assumed to be just a normal part of the ageing process – which, as we mentioned earlier, they most certainly is not.
Alzheimer’s disease was named after Alois Alzheimer, who was a German psychiatrist working around the turn of the 20th century. Alzheimer was the first person to identify the existence of more than one type of dementia. He’d treated numerous dementia patients, but in 1906, one of his patients died from advanced dementia, and at age 55 this was the youngest person he’d seen lose their lives to the disease.
An autopsy on the woman – a few years later – revealed to Alzheimer that her brain had shrivelled and contained clumps of hard plaques and knotted fibres, which was distinctly different to all the other postmortem brains he’d examined from patients with dementia. Over the years, more physicians began to recognise the disease and it soon became known as “Alzheimer’s”, after Alois.
Over time, through postmortem analyses, it became apparent that Alzheimer’s patients had unusual build ups of proteins in their brain, called “amyloids”. In healthy people, these proteins are a normal part of everyday function, but in those with Alzheimer’s, instead of breaking down, they form plaques that eventually destroy neurons.
At the same time, there are proteins called “tau”, which form connections between neurons. These become dense with extra phosphorus atoms to the point where they eventually become knotted, resulting in the destruction of the neurons they’re attached to. Of course, this also damages the connection between other neurons. And even worse, the tau then begins to spread throughout the brain, beginning in the hippocampus, and expanding until it eventually takes over the entire brain.
With the dying neurons and malformed proteins, the brain can still retain normal function for a while, but eventually, the hippocampus will decrease in size, causing cognitive decline, anxiety and confusion. And eventually, a physical decline will follow, which is ultimately fatal.
Even if there was some type of treatment that stopped the disease from progressing prior to symptoms showing up, you’d still need a reliable method of identifying these people with the early build up of amyloid.
Sadly, at this point in time, for most forms of dementia, no prevention or cure exists. Some medications have been found to reduce symptoms such as anxiety, depression, sleep interference, agitation, aggression and delusions or hallucinations (psychosis), but oddly, despite its global prevalence and extensive cost, there have been no advancements in treatment options for 15 years.
There seem to be three main reasons behind this scientific stagnation.
The first is, as mentioned earlier, the complex nature of this condition. Alzheimer’s disease, for example, is often asymptomatic until the disease has progressed to the point where irreversible damage has occurred. Obviously, earlier detection and thus treatment would be a great solution, but this leads to the second reason for the lack of progression in treatment development, which is that there are currently no succinct tests to confirm if someone is in the early stages. Present procedures tend to be expensive or invasive and as a result are usually reserved for when the symptoms strongly suggest Alzheimer’s or another form of dementia is present.
Most of the knowledge we have about the treatment of dementia stems from epidemiological studies, where individuals who have been treated are compared with a control group of individuals who have not. Unfortunately, it’s often quite difficult to find willing subjects to participate in clinical trials because they usually require a group of people who could develop Alzheimer’s, and the efficacy of the therapy is determined by how many from each group develop the condition. The challenge here is that healthy people are not likely to find participation in these trials appealing, and like we mentioned earlier, there are currently no early indicators of whether someone is at risk of the disease. This pretty much leaves researchers with no option of studying Alzheimer’s patients for the duration they require to adequately test memory-loss prevention drugs.
Earlier this year, the FDA in the US modified its assessment processes for clinical trials for Alzheimer’s drugs. The draft report indicated the FDA would consider a decline in biomarkers for Alzheimer’s disease (e.g., smaller levels of buildup in tau or amyloid) as sufficient evidence that a particular treatment is effective. While these guidelines are still in draft form, they appear to have the support of many researchers in the field.
Studies indicate that reducing risk can be achieved with exercise and has also been linked to diets rich in omega 3 fatty acids and vitamin E, while a diet high in processed foods may increase the risk.
In the past century, research into Alzheimer’s disease has achieved some significant accomplishments, but the condition is so complex that nowadays, there seems to be more questions emerging than there are answers.
Obviously, the ultimate way to treat Alzheimer’s disease would be to avoid the brain-cell destruction before it begins. However, given that signs and symptoms only occur once the damage is done, this preventative course of action is not currently possible. And even if there was some type of treatment that stopped the disease from progressing prior to symptoms showing up, you’d still need a reliable method of identifying these people with the early build up of amyloid.
For so long, the only definitive confirmation of Alzheimer’s was a brain autopsy. Today’s technology that captures brain images to check for tumours, or to examine the size of the hippocampus and surrounding areas in the brain, are still too inconclusive to be considered reliable.
Scientists are currently exploring the use of blood tests to detect the presence of early amyloid plaques in the brain, but this line of study is still in its infancy stage.
In the meantime, the best use of research funds appears to be the continued exploration into the effectiveness of diet, exercise and social interaction on the prevention of Alzheimer’s. In 2017, the National Academies of Sciences published their “inconclusive but encouraging” report outlining the preventative impact from modifications to lifestyle. For example, longitudinal studies have found that dementia may be prevented with social interaction, while small studies in humans and mice have indicated that reducing risk for developing Alzheimer’s can be achieved with exercise. A reduced likelihood of developing Alzheimer’s has also been linked to diets rich in omega 3 fatty acids and vitamin E, while a diet high in processed foods may increase the risk.
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Government funding for research into Alzheimer’s has increased over time, but the truth remains that drug companies are still the go-to source for clinical trial funding. This is because although they may need to outlay billions of dollars to deliver a clinical trial, they can usually rely on future sales to well and truly reimburse them for their investment. In the case of Alzheimer’s however, it’s unlikely they’ll be waving their chequebooks at researchers any time soon, considering they can’t patent physical activity or tuna-rich diets.
Here in Australia, various research projects into dementia have been completed or are underway, with new findings and initiatives continuously being generated. For example, an Australian research team has shed light on a neuro-protective mechanism in Alzheimer’s disease, challenging previously held ideas and unlocking new treatment possibilities.
In addition, another team of Australian researchers, also funded by the Dementia Australia Research Foundation, recently discovered a potentially feasible treatment for Alzheimer’s disease and fronto-temporal dementia, as well as a way of enhancing the delivery of this treatment.
Furthermore, a new program aimed at reducing the public stigma associated with dementia is being developed by Dr Sarang Kim, an ANU researcher and the 2016 recipient of the Alzheimer’s Australia Hazel Hawke Research Grant in Dementia Care.
So there is good news. After all, getting more exercise and improving the diet are treatment options that are both easy and accessible to everyone. The question is, of course, whether it’s enough.
Unfortunately, for right now, it’s going to have to be.