Footballers 'no more likely' to get Alzheimer's disease
“Footballers and boxers are more likely to develop Alzheimer’s,” is the entirely spurious claim from the Mail Online.
The study it reports on did not involve footballers, or boxers, or indeed, any living humans.
It looked at how abnormal clumps of proteins found in the brains of people who have died from Alzheimer’s disease can spread between cells. This was an attempt to find out more about the possible causes of Alzheimer’s, which while common, remains poorly understood.
What is known is that in people affected by Alzheimer’s there is a loss of brain cells and a build-up of abnormal ‘clumps’ and ‘tangles’ of proteins. The clumps are made up of amyloid proteins and the tangles of Tau proteins.
Both can be present because of ageing, but it is not known what causes there to be so many in people with Alzheimer’s disease.
The Tau protein forms chains with other Tau proteins. This disrupts the transport of nutrients and it is thought that this leads to cell death.
This study explored how cells absorb Tau proteins and join the proteins together to make the chains that resemble neurofibrillary tangles. They found that this process caused nearby cells to do the same.
The researchers speculate that a traumatic brain injury could provide the opportunity for the Tau proteins to spread, causing new tangles.
However, this speculation is not proof that footballers are more likely to develop Alzheimer’s. If anything, footballers may have a reduced risk as regular physical exercise may help protect against developing the condition.
Where did the story come from?
The study was carried out by researchers from Cambridge University, the Cambridge Institute for Medical Research and centres for Neurodegenerative diseases in Germany and Toronto. It was funded by grants from the Wellcome Trust and Medical Research Council (MRC), Alzheimer’s Research UK, the Engineering and Physical Sciences Research Council (EPSRC) and the European Research Council.
The study was published in the peer-reviewed medical journal, The Journal of Biological Chemistry.
The Mail Online reporting was widely speculative, resting on two key unproven assumptions.
The first assumption being that traumatic brain injuries can trigger the onset of Alzheimer’s. The second assumption being that playing football would expose individuals to regular traumatic brain injuries.
While an association between professional boxing and head injuries seems a given, a similar association with football is less clear-cut; especially as modern footballs are now a lot lighter than those used in the past.
A 2013 study did look at whether football players had an increased risk of brain damage. The results were inconclusive.
Any potential risk of brain injury has to be balanced against the wide range of health benefits from playing football regularly.
What kind of research was this?
This was a laboratory study of Tau proteins and neuron-like cells, looking at how they behave differently and join up to form neurofibrillary tangles. This is an important study as neurofibrillary tangles are found in the brains of people with Alzheimer’s disease and may be a cause of the neuron cell death. As this was a laboratory study, it cannot directly show what would happen in the human brain but it does further the understanding of this complex process.
What did the research involve?
The researchers took human Tau proteins and changed parts of the molecular structure to make slightly different protein molecules that they would be able to later identify with scans. They measured:
- how these proteins clumped together in different solutions
- what happens when they put Tau proteins next to cells which have been cloned from human neuroblastoma cells – a type of cell that develops into nerve cells (neurons) during pregnancy
- what happens when ‘washed’ neuroblastoma cells with abnormal Tau protein clumps in them are put next to normal neuroblastoma cells in a substance that did not contain any Tau protein
What were the basic results?
Slightly changing the molecular structure of the Tau proteins so they could be studied did not change their ability to form clumps that looked like neurofibrillary tangles when they were put in different chemical solutions.
Neuron-like cells rapidly absorbed the Tau proteins that surrounded them. This triggered the Tau proteins to group together within the cell, forming neurofibrillary tangles.
Cells released these neurofibrillary tangles which were a combination of the normal cell Tau protein and the changed Tau protein that had been outside the cell to start with.
These Tau protein clumps were then taken up by normal neuron-like cells and caused Tau clumps to form, thus spreading the process.
How did the researchers interpret the results?
The researchers reported that “short exposure to …Tau proteins outside the cell leads to infection of healthy cells and initiates the nucleation of aggregate seeds that incorporate and rapidly progress the aggregation of endogenous Tau. The resulting co-aggregates are furthermore seen to be released into the extracellular medium and are capable of infecting other cells.”
This study shows that in laboratory conditions, a Tau protein outside a neuron can be rapidly absorbed by the cell and can trigger Tau proteins inside the cell to form clumps instead of their usual function.
The study then shows that the cell can release the Tau clumps and they can be absorbed by other neurones and cause Tau protein clumps to form.
This gives a clue as to how neurofibrillary tangles might spread in the brain of people with Alzheimer’s disease.
However, there are limitations to this research, including:
- The research shows that in a laboratory setting, formation of chains of Tau proteins in one neuron-like cell can trigger the process in cells nearby. Other mechanisms might be in place in the brain which stops this ability to spread.
- The research does not explain why some Tau proteins start to clump together in the first place, but it does show that once it has started, it can potentially spread.
Whilst this research is valuable in furthering our understanding of the potential mechanisms that cause Alzheimer’s disease, it does not show any association or link with brain injuries.