No disease terrifies me like dementia. Losing one’s physical capacity is scary, but I can’t imagine how awful it would be to lose one’s mental agility, often with a dose of depression thrown in. Being overweight and never having learned a language or to play an instrument make me more vulnerable than most, even if the differences from these factors are not huge.
On a social level it is frightening as well. The social and economic cost of an aging population in which a lot of other diseases have been removed, but dementia is largely untouched, will be enormous – right when we will be short of money as a result of the failure to tackle problems like climate change.
I’m hardly Robinson Crusoe on this one, so serious money is being poured into dementia research, particularly Alzheimer’s as the most common form. When it comes to actual treatments there has been very little to show for this so far, but it does feel to me like we are starting to get somewhere in understanding the causes.
I’ve written before about the debate between the traditionalists who see Alzheimer’s as caused by the beta amaloid plaques that are its defining feature (BAPtists) and those who think insoluble tau protein inside brain cells is the real cause (tauists) including a subfaction that think the problem is the shortage of soluble tau left behind when too much precipitates.
This week I did an interview with the Garvan Institute’s Bryce Vissel, who points the finger at a third component – inflammation. A student he supervised has shown that in mice inflammation and a loss of brain cells precedes the development of plaques by a significant amount of time. While this might be taken as a straight blow to the BAPtists, Vissel thinks the situation is more complex. He thinks there may be a cycle where plaques, inflammation and tau each produce the other. Which one comes first may vary depending on the individual.
One implication here would seem to be that we should put more resources into finding ways to fight inflammation and possibly tau. However, Vissel says there may be good news for the BAPtists as well. Several clinical trials of drugs designed to fight the plaques have produced disappointing results, leading to much despair. But Vissel says that we may just be applying the drugs too late. Moreover, if his theory is right, they might be effective against a subset of Alzheimer’s patients – those where the plaques are the original source of the problem. If this is a small or even medium sized section of the sample in the trials the benefits might not be large enough to reach statistical significance. Yet there might still be millions of people around the world who might benefit from these drugs, if we can just work out which Altheimer’s patients have which initial trigger.
While this is pretty much a straight science piece, I will mention that 21 years ago I worked on Vissel’s campaign when he was the Australian Democrats candidate for the state seat of Melbourne. He was one of the first candidates I voted for at a parliamentary level. It was not, it has to be said, a very successful campaign – a prelude to a career in political activism with far more defeats than victories. There were a lot of factors to this, including the fact that while Vissel might have made a good MP, he wasn’t really cut out for being a candidate, at least without a strong campaign team. Nevertheless, I always felt great confidence in his outlook, policies and worldview. It’s no surprise at all that he is making the world a better place through a different mechanism. When one looks at the people who get elected, as well as those who try and fail, very few would achieve as much.