We already know from studies of other complex diseases like cancer, that rarely is one gene in isolation responsible for the disease. In fact, there are relatively few diseases, with Huntington’s disease and cystic fibrosis being two exceptions, where a mutation in a single gene causes the specific disease. Instead, a disruption may occur at one part, or at many places throughout the elaborate network of genes, proteins and signalling pathways between the key elements, both within and outside of our cells. If the network cannot maintain its balance, a tipping point is reached that likely triggers the cascade of events that leads to the onset of disease.
Alzheimer’s is in fact a disease of brain tissue, so it is critically important to not just consider genetics, but to study the many other layers of the disease from the genetic to the molecular and tissue levels, and right up to the whole person affected by the disease.
While we have a good idea of some of the interaction networks involved in Alzheimer’s disease, I believe it is crucial that we study Alzheimer’s more holistically; treating it as the complex system it is in reality. Taking into consideration not only the affect the disease has on our neurons (brain cells), but also on other cells that make up brain tissue, and how they all interact together. Through taking an integrative systems approach – a paradigm shift from the conventional ways we have been investigating Alzheimer’s to date – we will have the opportunity to be able to identify multiple targets for combination therapies to help enable personalised treatment and prevention strategies.
It’s clear that if we can make use of the complete arsenal of techniques and knowledge from across different scientific disciplines, we could move onto a faster track to gain new insights and potential breakthroughs. Only through this understanding will we be in the position to slow the progression and eventually prevent the onset of Alzheimer’s disease.