Alzheimer’s disease might be argued to be a lifestyle condition, but it is not as much of a lifestyle condition as type 2 diabetes – it is not as reliably connected to lifestyle choices. Not everyone who lets themselves go, becoming fat and sedentary, winds up with a diagnosis of Alzheimer’s disease, despite it being clear from the data and what is known of the mechanisms involved that both of those environmental circumstances are contributing risk factors. So why do only some people with the risk factors suffer Alzheimer’s disease? Why do some people without the risk factors suffer from Alzheimer’s disease? Is there anything useful to be learned at this stage from comparing the biochemistry of various groups with and without the condition?
These are questions very focused on how exactly the condition progresses, which stands a little in opposition to the strategy of attacking all of the known root causes of disease – in other words striving to remove all of the accumulated protein aggregates thought to cause the condition. In the case of Alzheimer’s disease, that strategy hasn’t been doing so well to date; the amyloid clearance field is