New research may help explain why people with type 2 diabetes are more likely to develop dementia.
The findings could help identify risk factors for dementia in people with type 2 diabetes and inform interventions to help prevent or delay the condition.
The Imperial College London research emphasises the importance of carefully managing cardiometabolic factors such as blood pressure, cholesterol and glucose levels from the earliest stage.
The research, funded by Diabetes UK, analysed ‘cardiometabolic factors’ – such as blood pressure, blood sugars and cholesterol levels – in people with type 2 diabetes across two decades. The team identified changes in these factors during this period that were associated with developing dementia in later life.
Dr Eszter Vamos, Diabetes UK-funded researcher at Imperial, says: “Our results emphasise the importance of carefully managing cardiometabolic factors such as blood pressure, cholesterol and glucose levels early on, for people with type 2 diabetes.
“While this study cannot confirm causal associations, these results show that blood pressure and other cardiometabolic factors could be contributing to dementia development up to two decades before diagnosis.”
Dementia is known to be more common in people with type 2 diabetes, but the reason why people with type 2 are more at risk has not been clear.
High blood sugar levels, blood pressure and cholesterol in people with type 2 diabetes can damage blood vessels and lead to serious cardiovascular problems, such as heart attacks and strokes.
It has been suggested that these ‘cardiometabolic factors’ that are known to affect heart health might also affect brain health and could potentially play a role in the development of dementia in people with type 2 diabetes.
To explore this, a team of researchers, led by Dr Vamos, looked to see if the factors affecting heart health in people with type 2 diabetes could also impact their dementia risk.
They analysed data from 227,580 people with type 2 diabetes over the age of 42 years, around ten per cent of whom went on to develop dementia.
The team examined the participants’ medical history across the 20 years prior to their dementia diagnosis to look at changes in cardiometabolic factors and bodyweight, and compared these to people who didn’t develop dementia.
Over the 20-year period, changes in blood pressure differed between those who did and didn’t develop dementia.
People who developed dementia had higher blood pressure between 11 and 19 years before their dementia diagnosis, which then declined more steeply closer to their diagnosis, compared to those who didn’t develop dementia.
A decline in bodyweight starting at 11 years before a dementia diagnosis was found in people who developed the condition and this was steeper than in those who didn’t develop it.
Blood sugar and cholesterol levels were also found to be generally higher across the entire 20-year period among people with type 2 diabetes who developed dementia, compared to those who did not.
Eating healthily, keeping active, reducing alcohol intake and stopping smoking are all advised to help everyone reduce their risk of dementia. These findings suggest that by monitoring cardiometabolic factors and managing blood sugar, blood pressure, cholesterol and bodyweight, people with type 2 diabetes could be supported to lower their risk of dementia.
Dr Elizabeth Robertson, director of research at Diabetes UK, adds: “These crucial findings have uncovered how type 2 diabetes may contribute to dementia onset.
“Changes in the body that lead to dementia occur years before symptoms arise, and for the first time, researchers have uncovered a pattern of changes in people with type 2 diabetes that are associated with dementia.
“Knowing which factors contribute to the development of dementia, and when they have the biggest impact, is vital in giving people with type 2 diabetes the best possible care to prevent or delay dementia onset.”
Could a Mediterranean diet help beat dementia?
Eating a Mediterranean diet could help reduce the risk of dementia and cognitive decline, new research has found.
By following a dietary pattern with a greater intake of vegetables, fruit, cereals, fish and monounsaturated fatty acids – like that from olive oil – the risk of protein build-up and brain atrophy can be reduced.
Such a Mediterranean-led diet also has a low intake of dairy products, red meat and saturated fatty acids.
Previous research has revealed following such a diet can reduce risk of heart disease and support weight loss – but this new research from the DZNE German Centre for Neurodegenerative Diseases has revealed its efficacy in the fight against dementia.
“There was also a significant positive correlation between a closer adherence to a Mediterranean-like diet and a higher volume of the hippocampus,” says Tommaso Ballarini, lead author of the study.
“The hippocampus is an area of the brain that is considered the control centre of memory. It shrinks early and severely in Alzheimer’s disease.
”It is possible that the Mediterranean diet protects the brain from protein deposits and brain atrophy that can cause memory loss and dementia. Our study hints at this.”
In the study, a total of 512 people with an average age of around 70 were analysed – 169 of them were cognitively healthy, while 343 were identified as having a higher risk of developing Alzheimer’s disease.
“People in the second half of life have constant eating habits. We analysed whether the study participants regularly eat a Mediterranean diet – and whether this might have an impact on brain health,” says Professor Michael Wagner, who led the research group.
The participants first filled out a questionnaire in which they indicated which portions of 148 different foods they had eaten in the past months.
Those who frequently ate healthy foods typical of the Mediterranean diet, such as fish, vegetables and fruit, and only occasionally consumed foods such as red meat, scored highly on a scale.
The scientists then investigated brain atrophy through performing brain scans with magnetic resonance imaging (MRI) scanners to determine brain volume.
In addition, all subjects underwent various neuropsychological tests in which cognitive abilities such as memory functions were examined.
The research team also looked at biomarker levels (measured values) for amyloid beta proteins and tau proteins in the so-called cerebrospinal fluid (CSF) of 226 subjects.
The researchers, led by Prof Wagner, found that those who ate an unhealthy diet had more pathological levels of these biomarkers in the cerebrospinal fluid than those who regularly ate a Mediterranean-like diet.
In the memory tests, the participants who did not adhere to the Mediterranean diet also performed worse than those who regularly ate fish and vegetables.
“But the biological mechanism underlying this will have to be clarified in future studies,” adds Ballarini.
As a next step, the research team now plan to re-examine the same study participants in four to five years to explore how their nutrition – Mediterranean-like or unhealthy – affects brain ageing over time.
Rugby stars join Shearer in dementia in sport fight
Two world-renowned former rugby stars have joined with Alan Shearer in stepping up the fight against dementia in sport.
Shane Williams, the all-time record try scorer for Wales, and World Cup-winning England lock Ben Kay are among 50 former elite rugby players to have backed the prevent PREVENT:RFC project, the latest phase of the Sport United Against Dementia campaign.
It builds on the existing UK and Ireland-wide PREVENT project, which also includes an informal pilot study with footballer players, including Alan Shearer, the Premier League’s record goalscorer turned BBC pundit.
Recently, the former England captain presented the BBC documentary ‘Alan Shearer: Dementia, Football and Me’, which investigated the link between the game and brain injury.
The large-scale PREVENT:RFC research, funded by the Alzheimer’s Society, will look at vital unanswered questions, such as whether elite rugby players show more early warning signs of dementia than the general population, and if so, why this is the case.
“It was really important to me as a rugby player to take part in this study. There has been a lot of media coverage around this topic lately and as a result, I know lots of players are worried about their dementia risk,” says Kay.
“Hopefully, by doing this research now, we can get a better understanding of this issue and make a real difference for the future.”
Shearer adds: “I’ve been following the sport and dementia conversation for years now – and there’s still more I want to learn about the science behind the stories in the news.
“I know the risk of dementia is something that worries many players, so work directed to understanding the earliest stage of dementia is incredibly important, and this study in rugby players will add to our understanding of that in sport.”
PREVENT:RFC will be based in Edinburgh with Professor Craig Ritchie, PREVENT’s principal investigator, working in collaboration with Professor William Stewart from the University of Glasgow. Previous research led by Professor Stewart revealed that professional footballers appear to be five times more likely to die from Alzheimer’s disease than the general population.
Through committing a further £250,000 to research, the PREVENT:RFC project involves further participants to the 700 people already enrolled in PREVENT, and will undergo an initial assessment—involving physical health checks, brain scans, memory assessments, lifestyle questionnaires and sample collections – and then return for another visit two years later.
PREVENT – part of the groundbreaking Sport United Against Dementia campaign, which continues to unite the collective power and reach of sport for the first time to improve the lives of current and former players of all levels – is funded by the Alzheimer’s Society for over seven years and follows people aged 40 to 59, aiming to find ways of detecting dementia before symptoms appear, and stopping people from developing the disease.
It takes place at the University of Edinburgh, Imperial College London, Trinity College Dublin, University of Cambridge and University of Oxford.
Dr Richard Oakley, head of research at Alzheimer’s Society, funder of the PREVENT study, says:
“This is a desperately needed, exciting world-class research study looking to answer questions around brain health in elite rugby players.
“There’s been a lot of attention focused on sports players who’ve developed dementia, and that’s raised important questions about whether playing sports like football and rugby increases the risk of developing the condition.
“While we’re seeing some evidence of a potential link, the latest findings don’t explain why sports players may be at a greater risk of developing dementia.
“Alongside launching Sport United Against Dementia, we’re really excited to fund this new phase of the PREVENT study – we hope it’ll provide the answers so many people are looking for.”
Professor Stewart, consultant neuropathologist and honorary professor at the University of Glasgow, adds: “It is vitally important we better understand the links between sports such as football and rugby and dementia, so we can better protect players from any risks they may face.
“Previous research led by our team at the University of Glasgow demonstrated the increased risk of neurodegenerative disease in former professional football players.
“I am delighted to be a part of this latest PREVENT study into professional rugby players, and the adjoining pilot looking at professional football players, so we can bring more insight to this important research area.”
Toxic gas reduction linked to dementia treatment
A potential treatment for dementia could be designed on the back of new findings that show the benefits of reducing toxic gas levels in the brain.
The study analysed the impact of reducing the levels in the brain of hydrogen sulfide (H2S), which is potentially harmful to neurons.
Researchers found that H2S was blocking the activity of some cells’ potassium channels, which allow electrically charged atoms to pass through.
This caused an increase in activity when these pathways were disrupted and researchers believe this overactivity is a cause of cell death.
Cells were taken from rat brains and the team of scientists from the universities of Reading, Leeds and John Hopkins charged them with an H2S donor molecule.
They were able to establish that this change in activity was controlled by the potassium channel after comparing it with mutated cells.
These findings could be significant in terms of developing dementia treatments, as these mutated channels have previously shown they can protect against the build up of toxic proteins.
This includes the amyloid beta protein, which has been found to build up in dementia patient’s brains causing damage to neurons.
Dr Mark Dallas, associate professor in neuroscience at the University of Reading, said: “this is an exciting finding as it gives us new insights about the role of hydrogen sulfide in various brain diseases.
“There has been growing interest in the effect of hydrogen sulfide on the brain and this study shows how important the implications of its build-up on proper brain functioning may be.
“We saw that hydrogen sulfide acts to disrupt the normal functioning of potassium channels. These channels regulate electrical activity across the connections between brain cells, and when these channels are blocked from working properly we see overexcitable brain cells which we believe is leading to nerve cell death.
“The implication for potential treatments is particularly exciting because finding drugs that target hydrogen sulfide production in our brains may have a host of benefits for diseases, and there are clear links between hydrogen sulfide build up and other warning signs for diseases such as Alzheimer’s.”
The paper – published in Scientific Reports – noted that the findings could also help develop treatments for epilepsy.
Dr Moza Al-Owais, research fellow at the University of Leeds, said: “This exciting study demonstrates the growing evidence that gasotransmitters play an important role as signalling molecules in the regulation of the physiological processes underlying Alzheimer’s disease, which are relatively poorly understood, opening new avenues for investigation and drug discovery.”
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