‘When it came to choosing my PhD, I was tossing up between Alzheimer’s, Post Traumatic Stress Disorder and Schizophrenia. At that time there was an opportunity to be part of a research group in Melbourne called the Australian Imaging, Biomarkers and Lifestyle (AIBL) Study. This team was making massive advances in understanding Alzheimer’s disease. Given the large dataset and an incredible number of collaborators, I managed to complete my PhD within the short timeframe of March 2011 to December 2012.
I have always been involved in memory research and both my Honours and Master theses had a bit of an Alzheimer’s disease flavour. I have a personal relationship with the disease as my grandmother suffered from its cruelty until she passed away in 2009. In Australia, it is the third leading cause of death after heart disease and cancer. It is also the only leading cause of death for which there is no cure. Statistically, dementia, of which Alzheimer’s is the most common form, affects 20 per cent to 30 per cent of the population over 65 and nearly 50 per cent over 85. In fact, by the year 2050 the number of people living with Alzheimer’s disease in Australia and in the world will have tripled. We’re looking at a huge epidemic and with no cure.
These population statistics are staggering, even if we just consider the economic burden. By 2050 it will cost the Australian economy $83 billion. We can’t even begin to estimate how much the psychological and social burdens will cost.
“Just like the plaques in our teeth, everyone has some level of these amyloid plaques. But for people who are genetically predisposed, their brains may not be as effective at clearing them. It’s like having a faulty toothbrush with missing bristles.”
In my PhD, I attempted to understand and characterise the very early stage of the disease. I examined healthy older adults who didn’t show any form of impairment but, after following them for a number of years, showed a very real and unremitting decline.
This decline is associated with the presence of abnormal levels of beta-amyloid plaques in the brain, which are now considered to be the catalyst for the disease. The biochemistry surrounding the formation of these plaques is as yet unclear.
We know that they are sticky substances that can build up around our brain cells and cause them to die. Just like the plaques in our teeth, everyone has some level of these amyloid plaques. But for people who are genetically predisposed, their brains may not be as effective at clearing them. It’s like having a faulty toothbrush with missing bristles.
A build-up of these plaques in the brain may lead to neuronal death and memory decline.
During my PhD, I had access to cutting edge neuro-imaging through which I was able to determine the amount of these plaques in people’s brains.
Approximately 30 per cent of the healthy older adults we tested had abnormal levels of beta-amyloid plaques.
“I am now investigating a type of protein in the brain that is secreted during exercise. This research is providing some preliminary results that may suggest that this protein could provide some form of protection against the toxic effects of these beta-amyloid plaques.”
This focus on early detection has come about as the therapies and drugs being used in clinical trials have failed to halt or slow the disease. Expert opinion is that healthy older adults with abnormal levels of beta-amyloid plaques, but who do not yet display any signs of memory impairment, may in fact be in the very early stages of the disease. These people may benefit from participating in clinical trials aimed at treating the disease early.
Detect it early and treat it early. A major breakthrough would be if we could delay the onset of the disease by even four to five years. Of course, that doesn’t disqualify the hope that in the future there might be a cure.
The public want a straightforward answer and it’s very frustrating when we can’t provide them with one, but that’s just the nature of this complex disease.
Studies show that the relationship between brain pathology and the development of the disease is also influenced by environmental factors like lifestyle, exercise, diet, genetics, years of education and social and occupational activities.
I am now investigating a type of protein in the brain that is secreted during exercise. This research is providing some preliminary results that may suggest that this protein could provide some form of protection against the toxic effects of these beta-amyloid plaques.
The hypothesis is that increases in this protein may ensure the health of these brain cells and perhaps buffer against the toxic effects of the plaques.
A cure for Alzheimer’s disease is not something that would be nice to have, it’s something we need to have … we need to figure out a solution to this problem very soon. ’
Yen Ying Lim is completing a post-doctoral research fellowship at Brown University. Her PhD was titled: “Memory decline and Aβ amyloid as markers of neurodegeneration in preclinical Alzheimer’s disease.”* My PhD is an irregular series in which The Citizen speaks with recent Melbourne University PhD graduates.
