Tag: dementia

Categories : Lab Tests and Imaging NeurologyTags :

Faster MRI Scans Offer New Hope for Dementia Diagnosis

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The time to carry out diagnostic MRI scans for dementia can be cut to one third of their standard length, according to a new study led by UCL researchers.

The findings, published in Alzheimer’s & Dementia, have been described as a step towards ending ‘the postcode lottery in dementia diagnosis’. Shorter scans would be easier and more comfortable for patients and also enable more people to be scanned at a lower cost. The team behind the study say this could at least double the number of dementia scans able to be done in one day.

Senior author Professor Nick Fox, Director of the UCL Dementia Research Centre at the UCL Queen Square Institute of Neurology, said: “As more treatments that can slow or change the course of dementia are being developed, it’s important to make sure MRI scans are available to everyone. This is because people living with dementia often need an MRI scan as part of their diagnosis before they can access these treatments.

“To help make this possible, our team carried out the first study looking at how new imaging techniques – called parallel imaging – could speed up MRI scans in clinics. Their goal is to move closer to a future where every person with dementia can get a diagnosis through a scan.”

MRI scans often play a key role in an accurate dementia diagnosis, including ruling out other causes of symptoms and assisting in diagnosing the type of dementia. Emerging disease-modifying treatments such as lecanemab and donanemab also require an MRI scan before starting treatment and for safety monitoring during the course of treatment. Reducing the cost of scanning would contribute to lowering the total cost of delivering for such treatments. 

The ADMIRA study (Accelerated Magnetic Resonance Imaging for Alzheimer’s disease), part funded by Alzheimer’s Society’s Heather Corrie Impact Fund, aimed to understand the reliability of fast MRI scans compared to standard-of-care clinical scans. The neurologists on the study were joined by co-authors from the UCL Hawkes Institute and the UCL Advanced Research Computing Centre in the faculty of Engineering.

The research team scanned 92 people in an outpatient setting where an MRI brain scan was planned as part of their routine clinical assessment. The accelerated scans were carried out and enhanced to increase the quality of the image using new scanning methods. Three neuroradiologists examined these scans, and weren’t aware if they were looking at fast or standard-of-care scans.

Co-author Professor Geoff Parker (UCL Hawkes Institute and UCL Medical Physics and Biomedical Engineering) said: “Our research has taken advantage of recent breakthroughs in scanner technology. Our task was to work out just how fast we could scan while maintaining image quality good enough for diagnosis.”

The team found that the quicker scans reduced time in the scanner by 63% and they were as reliable as the standard-of-care scans for diagnosis and visual ratings.

First author Dr Miguel Rosa-Grilo (UCL Queen Square Institute of Neurology) said: “We were confident that the new scan would prove non-inferior to the standard scan, given the high image quality – but it was remarkable how well it performed.”

Richard Oakley, Associate Director of Research and Innovation at Alzheimer’s Society, said: “Dementia is the UK’s biggest killer, but one in three people living with the condition haven’t had a diagnosis. An early and accurate diagnosis isn’t just a label, it’s the first step to getting vital care, support and treatment.

“While MRIs aren’t the only way to diagnosis dementia, very few people with concerns about their cognitive health are offered one as part of the diagnosis process, mainly because they are expensive and not widely available. These faster MRIs, which take less than half the time of standard scans, could help end this postcode lottery in dementia diagnosis, cut costs and potentially give more people access to them.

“MRI scans can be an uncomfortable and daunting experience for patients, so anything we can do to make it an easier process is really positive.

“So far, this shortened MRI scan has been tested at one specialist centre with one type of MRI scanner, so more research is needed to make sure this works across different types of scanners and a diverse range of people. We’re hugely encouraged by this progress and eager to see how it continues.”

The team will now build on their early results by making sure the approach works across different types of MRI machines, so it can benefit as many hospitals and clinics as possible.

Source: University College London

Categories : Ageing Metabolic DisordersTags :

Small Reductions in Cholesterol Could Slash Risk of Dementia for Those with Certain Genetics

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Low cholesterol can reduce the risk of dementia, a new University of Bristol-led study with more than a million participants has shown.

The research, led by Dr Liv Tybjærg Nordestgaard while at the University of Bristol and the Department of Clinical Biochemistry at Copenhagen University Hospital – Herlev and Gentofte, found that people with certain genetic variants that naturally lower cholesterol have a lower risk of developing dementia.

The study, which is based on data from over a million people in Denmark, England, and Finland, has been published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. 

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs, such as statins and ezetimibe. To test the effect of cholesterol-lowering medication on the risk of dementia, the researchers used a method called Mendelian Randomisation – this genetic analysis technique allowed them to mimic the effects of these drugs to investigate how they influence the risk of dementia, while minimising the influence of confounding factors like weight, diet, and other lifestyle habits.

By comparing these individuals to individuals without these genetic variants, the researchers were able to measure differences in the risk of dementia. They found reducing the amount of cholesterol in the blood by a small amount (one millimole per litre) to be associated with up to 80% reduction in risk of developing dementia for certain drug targets.

“What our study indicates is that if you have these variants that lower your cholesterol, it looks like you have a significantly lower risk of developing dementia,” said Dr Nordestgaard, who now works in the Department of Clinical Biochemistry at Copenhagen University Hospital – Bispebjerg and Frederiksberg hospital.

The results suggest that having low cholesterol, whether due to genes or medical treatment, can help reduce the risk of dementia. However, the study does not say anything definitive about the effect of the medicine itself.  

One of the challenges is that dementia typically does not appear until late in life, and therefore research in the area typically requires a very long period of follow-up. 

It is still not known exactly why high cholesterol can increase the risk of dementia, but one possible explanation proposed by Dr Nordestgaard is that high cholesterol can lead to atherosclerosis. 

“Atherosclerosis is a result of the accumulation of cholesterol in your blood vessels,” Dr Nordestgaard said.  “It can be in both the body and the brain and increases the risk of forming small blood clots – one of the causes of dementia. 

“It would be a really good next step to carry out randomised clinical trials over 10 or 30 years, for example, where you give the participants cholesterol-lowering medication and then look at the risk of developing dementia,” Dr Nordestgaard added. 

The study used data from the UK Biobank, the Copenhagen General Population Study, the Copenhagen City Heart Study, the FinnGen study, and the Global Lipids Genetics Consortium.

Source: University of Bristol

Categories : NeurologyTags :

No ‘Beneficial’ Level of Alcohol Consumption for Dementia Risk

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Any amount of alcohol consumption may increase risk of dementia, according to the most comprehensive study of alcohol consumption and dementia risk to date.

Led by the University of Oxford, Yale University, and the University of Cambridge, the research challenges previous suggestions that light-to-moderate drinking may have a protective effect against dementia. The study is published in BMJ Evidence-Based Medicine.

Alcohol consumption is widespread and is linked with an increased risk of many diseases. Heavy drinking has previously been linked to higher risk of dementia. The connection between moderate levels of drinking and higher risk of dementia was uncertain with some studies suggesting that moderate drinking may even reduce dementia risk. However, recent studies involving brain scans have shown that drinking alcohol even at low levels may increase the risk of dementia.

This study combined observational data from more than half a million participants in two large and diverse population studies: the US Million Veteran Program and UK Biobank to assess whether self-reported alcohol use was linked with risk of developing a broad range of types of dementia.

The researchers also investigated links between genetically-predicted likelihood of drinking alcohol and alcohol use disorder for more than 2.4 million participants in 45 individual studies. This approach helped the researchers overcome some of the difficulties in distinguishing correlation from causation.

Key findings:

  • Observational analyses seemed to support previous findings that current low and moderate drinking is associated with lower risk of dementia when compared with non-drinking and heavy drinking; however, some current non-drinkers were previously heavy drinkers, which could account for their increased dementia risk compared to consistently low drinkers;
  • Genetic analyses, however, revealed a continuously increasing trend of higher dementia risk with greater alcohol intakes, suggesting that any level of alcohol consumption increases the risk of dementia, with no evidence that drinking alcohol may have a protective effect;
  • A doubled increase in a person’s genetically-predicted risk of alcohol use disorder was associated with a 16% higher risk of dementia, while a three times higher increase in number of alcoholic drinks per week increased the risk of dementia risk by 15%;
  • The study also showed that people who later developed dementia reduced their alcohol intake before diagnosis, another explanation for prior findings of protective effects of alcohol, rather than true benefit.

Dr Anya Topiwala, Senior Clinical Researcher at Oxford Population Health, Consultant Psychiatrist, and lead author of the study, said ‘Our findings challenge the common belief that low levels of alcohol are beneficial for brain health. Genetic evidence offers no support for a protective effect – in fact, it suggests the opposite. Even light or moderate drinking may increase the risk of dementia, indicating that reducing alcohol consumption across the population could play a significant role in dementia prevention.’

Dr Stephen Burgess, Statistician at the University of Cambridge, said ‘The random nature of genetic inheritance allows us to compare groups with higher and lower levels of alcohol drinking in a way that allows us to make conclusions that untangle the confusion between correlation and causation. Our findings do not only hold for those who have a particular genetic predisposition, but for anyone who chooses to drink, our study suggests that greater alcohol consumption leads to higher risk of dementia.’

Dr Joel Gelernter, Professor at Yale University and senior author of the study, said ‘These results, which add to our understanding of the relationship between alcohol and dementia, have clinical implications – there was a time when medical knowledge seemed to support that light drinking would be beneficial to brain health, and this work adds to the evidence that this is not correct’.

This study adds to growing evidence that alcohol use, even at moderate levels, may have no safe threshold when it comes to brain health, reinforcing the case for preventive strategies that reduce alcohol consumption in the general population.

The study, ‘Alcohol use and risk of dementia in diverse populations: evidence from cohort, case–control and Mendelian randomisation approaches‘, is published in BMJ Evidence-Based Medicine.

Source: Oxford University

Categories : Ageing Neurodegenerative DiseasesTags :

Is Physical Frailty a Cause of Dementia?

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A new study suggests that physical frailty may contribute to the development of dementia. The study was published on September 17, 2025, in Neurology®, the medical journal of the American Academy of Neurology.

Physical frailty is defined as having three or more of these five symptoms: often feeling tired; little or no physical activity; slow walking speed; low grip strength; and unintentional weight loss.

“We’ve known that frailty is associated with a higher risk of dementia, but our study provides evidence that frailty may be an actual cause of dementia,” said study author Yacong Bo, PhD, of Zhengzhou University in China. “On the other hand, despite this new evidence, we can’t rule out the possibility that frailty is instead a marker of the early changes in the disease process.”

The study involved 489 573 people with an average age of 57 who were followed for an average of 14 years. A total of 4.6% of the participants met the definition for frailty, with three or more of the symptoms. Another 43.9% who had one or two symptoms were categorised as pre-frailty and 51.5% had no symptoms and were categorised as not frail.

During the study, 8900 people developed dementia. A total of 4.6% of those with frailty developed dementia, compared to 2.2% of those with pre-frailty and 1.3% of those without frailty. After researchers adjusted for other factors that could affect the risk of dementia, such as age, education level and physical activity, they found that the people who met the definition for frailty were nearly three times more likely to develop dementia than those who had no symptoms of frailty.

Those categorised as pre-frailty were 50% more likely to develop dementia. People with frailty who also had genes linked to dementia were nearly four times more likely to develop dementia than those without frailty or the genetic risk. The researchers also analysed the data and found evidence suggesting that frailty may potentially be a factor in causing dementia.

“These findings reinforce the importance of identifying and managing frailty as a strategy for preventing dementia,” Bo said.

Looking at the data from the other direction, the researchers found that dementia is unlikely to increase the risk of frailty. The researchers also looked at brain imaging and biological biomarkers and found that people with frailty were more likely to have changes in their brain structure related to dementia.

“These biomarkers may be a mechanism underlying the pathway from frailty to dementia,” said Bo. A limitation of the study was that four of the five symptoms of frailty were reported by the participants, so they may not have provided accurate information.

Source: American Academy of Neurology

Categories : NeurologyTags :

How ‘Brain Cleaning’ While We Sleep May Lower Our Risk of Dementia

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Julia Chapman, Macquarie University; Camilla Hoyos, Macquarie University, and Craig Phillips, Macquarie University

The brain has its own waste disposal system – known as the glymphatic system – that’s thought to be more active when we sleep.

But disrupted sleep might hinder this waste disposal system and slow the clearance of waste products or toxins from the brain. And researchers are proposing a build-up of these toxins due to lost sleep could increase someone’s risk of dementia.

There is still some debate about how this glymphatic system works in humans, with most research so far in mice.

But it raises the possibility that better sleep might boost clearance of these toxins from the human brain and so reduce the risk of dementia.

Here’s what we know so far about this emerging area of research.

Why waste matters

All cells in the body create waste. Outside the brain, the lymphatic system carries this waste from the spaces between cells to the blood via a network of lymphatic vessels.

But the brain has no lymphatic vessels. And until about 12 years ago, how the brain clears its waste was a mystery. That’s when scientists discovered the “glymphatic system” and described how it “flushes out” brain toxins.

Let’s start with cerebrospinal fluid, the fluid that surrounds the brain and spinal cord. This fluid flows in the areas surrounding the brain’s blood vessels. It then enters the spaces between the brain cells, collecting waste, then carries it out of the brain via large draining veins.

Scientists then showed in mice that this glymphatic system was most active – with increased flushing of waste products – during sleep.

One such waste product is amyloid beta (Aβ) protein. Aβ that accumulates in the brain can form clumps called plaques. These, along with tangles of tau protein found in neurons (brain cells), are a hallmark of Alzheimer’s disease, the most common type of dementia.

In humans and mice, studies have shown that levels of Aβ detected in the cerebrospinal fluid increase when awake and then rapidly fall during sleep.

But more recently, another study (in mice) showed pretty much the opposite – suggesting the glymphatic system is more active in the daytime. Researchers are debating what might explain the findings.

So we still have some way to go before we can say exactly how the glymphatic system works – in mice or humans – to clear the brain of toxins that might otherwise increase the risk of dementia.

Does this happen in humans too?

We know sleeping well is good for us, particularly our brain health. We are all aware of the short-term effects of sleep deprivation on our brain’s ability to function, and we know sleep helps improve memory.

In one experiment, a single night of complete sleep deprivation in healthy adults increased the amount of Aβ in the hippocampus, an area of the brain implicated in Alzheimer’s disease. This suggests sleep can influence the clearance of Aβ from the human brain, supporting the idea that the human glymphatic system is more active while we sleep.

This also raises the question of whether good sleep might lead to better clearance of toxins such as Aβ from the brain, and so be a potential target to prevent dementia.

How about sleep apnoea or insomnia?

What is less clear is what long-term disrupted sleep, for instance if someone has a sleep disorder, means for the body’s ability to clear Aβ from the brain.

Sleep apnoea is a common sleep disorder when someone’s breathing stops multiple times as they sleep. This can lead to chronic (long-term) sleep deprivation, and reduced oxygen in the blood. Both may be implicated in the accumulation of toxins in the brain.

Sleep apnoea has also been linked with an increased risk of dementia. And we now know that after people are treated for sleep apnoea more Aβ is cleared from the brain.

Insomnia is when someone has difficulty falling asleep and/or staying asleep. When this happens in the long term, there’s also an increased risk of dementia. However, we don’t know the effect of treating insomnia on toxins associated with dementia.

So again, it’s still too early to say for sure that treating a sleep disorder reduces your risk of dementia because of reduced levels of toxins in the brain.

So where does this leave us?

Collectively, these studies suggest enough good quality sleep is important for a healthy brain, and in particular for clearing toxins associated with dementia from the brain.

But we still don’t know if treating a sleep disorder or improving sleep more broadly affects the brain’s ability to remove toxins, and whether this reduces the risk of dementia. It’s an area researchers, including us, are actively working on.

For instance, we’re investigating the concentration of Aβ and tau measured in blood across the 24-hour sleep-wake cycle in people with sleep apnoea, on and off treatment, to better understand how sleep apnoea affects brain cleaning.

Researchers are also looking into the potential for treating insomnia with a class of drugs known as orexin receptor antagonists to see if this affects the clearance of Aβ from the brain.

If you’re concerned

This is an emerging field and we don’t yet have all the answers about the link between disrupted sleep and dementia, or whether better sleep can boost the glymphatic system and so prevent cognitive decline.

So if you are concerned about your sleep or cognition, please see your doctor.

Julia Chapman, Clinical Trials Lead and Postdoctoral Research Fellow, Woolcock Institute of Medical Research and Conjoint Lecturer, Macquarie University; Camilla Hoyos, Senior Lecturer in the Centre for Sleep and Chronobiology, Macquarie University, and Craig Phillips, Associate Professor, Macquarie Medical School, Macquarie University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : Metabolic Disorders Neurodegenerative DiseasesTags :

Does Metformin Possibly Help Prevent Dementia?

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New research in Diabetes, Obesity and Metabolism reveals that metformin, a medication traditionally prescribed to treat diabetes, is linked to lower risks of dementia and early death.

In the study by investigators at Taipei Medical University that included 452,777 adults with varying degrees of overweight and obesity, 35,784 cases of dementia and 76,048 deaths occurred over 10 years. Metformin users exhibited significantly lower risks of both dementia and all-cause death than nonusers.

The benefits of metformin were seen across all categories of overweight, obesity, and severe obesity, with 8–12% lower risks of dementia and 26–28% lower risks of death.

“Although our study results are promising for metformin’s effects on dementia and mortality, further research is required to explore the mechanisms involved,” said co-corresponding author Chiehfeng Chen, MD, PhD, MPH.

Source: Wiley

Categories : Ageing Mental HealthTags :

Music May Reduce Distress for Dementia Patients

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Research finds music therapy could be used on NHS wards as an alternative to medication

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A new treatment that uses music therapy on dementia wards could improve care and support for some of the NHS’s most vulnerable patients.

Researchers at Anglia Ruskin University (ARU) and Cambridgeshire and Peterborough NHS Foundation Trust have piloted a music therapy approach called MELODIC, across two NHS dementia wards.

More alternatives to psychotropic medication are needed to support dementia patients who experience severe distress.

The pilot study involved a music therapist being embedded on hospital wards, the delivery of clinical music sessions and the implementation of musical care plans for each patient, and results from the research have been published in Frontiers of Psychiatry.

Music therapy, delivered by trained therapists, can include singing, playing or listening to music. The therapist can also identify specific ways that music can be used by families and carers in an individual’s daily care routine.

During the study, patient data suggested a slight improvement in quality-of-life scores among patients and a reduction in the severity of distress symptoms and disruptiveness, although agitation scores increased slightly.

There were no increases in routinely reported incidents, and no adverse events related to music therapy interventions were reported. This is relevant for future research on mental health dementia wards where limited studies have been conducted to date.

“People with dementia on inpatient mental health wards are often experiencing very high levels of distress, and staff are under immense pressure to manage this in ways that are safe and compassionate.

“Our study yielded promising results and importantly showed that the MELODIC tool can be used effectively in these highly complex settings, giving an alternative option to current ways of managing severe distress, such as psychotropic medication.”Lead author Naomi Thompson, a researcher at ARU’s Cambridge Institute for Music Therapy Research

The approach was shaped by interviews with 49 healthcare professionals, patients, and their families about their experiences managing distress on dementia wards and using music in everyday care and life to help develop the intervention. Results were published in the Journal of Geriatric Psychiatry.

Importantly, the intervention, co-designed by clinicians, researchers, and people with lived experience, cost just £2025 per month for the therapist and £400 initial outlay for equipment, suggesting a low-cost, scalable model.

“Some people with dementia can get so confused and distressed that we need to admit them to hospital to keep them safe. It can be difficult to manage distress in a ward environment and hard for patients, families and staff.

“I am very excited that it may now be possible for NHS staff to improve their experience on dementia wards using the power of music, and we look forward to working with ARU to develop this further.”

Dr Ben Underwood, Research and Development Director and Honorary Consultant Psychiatrist at CPFT

Source: Anglia Ruskin University

Categories : Neurodegenerative DiseasesTags :

A Cough Medicine Shows Potential to Slow Parkinson’s-related Dementia

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Dementia poses a major health challenge with no safe, affordable treatments to slow its progression. Researchers at Lawson Research Institute (Lawson), the research arm of St. Joseph’s Health Care London, are investigating whether Ambroxol – a cough medicine used safely for decades in Europe – can slow dementia in people with Parkinson’s disease.  

Published in JAMA Neurology, this 12-month clinical trial involving 55 participants with Parkinson’s disease dementia (PDD) monitored memory, psychiatric symptoms and GFAP, a blood marker linked to brain damage. 

Parkinson’s disease dementia causes memory loss, confusion, hallucinations and mood changes. About half of those diagnosed with Parkinson’s develop dementia within 10 years, profoundly affecting patients, families and the health care system. 

Led by Cognitive Neurologist Dr Stephen Pasternak, the study gave one group daily Ambroxol while the other group received a placebo.  

“Our goal was to change the course of Parkinson’s dementia,” says Pasternak. “This early trial offers hope and provides a strong foundation for larger studies.” 

Key findings from the clinical trial include: 

  • Ambroxol was safe, well-tolerated and reached therapeutic levels in the brain. 
  • Psychiatric symptoms worsened in the placebo group but remained stable in those taking Ambroxol. 
  • Participants with high-risk GBA1 gene variants showed improved cognitive performance on Ambroxol. 
  • A marker of brain cell damage (GFAP) increased in the placebo group but stayed stable with Ambroxol, suggesting potential brain protection.

Although Ambroxol is approved in Europe for treating respiratory conditions and has a long-standing safety record – including use at high doses and during pregnancy – it is not approved for any use in Canada or the U.S. 

“Current therapies for Parkinson’s disease and dementia address symptoms but do not stop the underlying disease,” explains Pasternak. “These findings suggest Ambroxol may protect brain function, especially in those genetically at risk. It offers a promising new treatment avenue where few currently exist.” 

An old drug with new possibilities  

Ambroxol supports a key enzyme called glucocerebrosidase (GCase), which is produced by the GBA1 gene. In people with Parkinson’s disease, GCase levels are often low. When this enzyme doesn’t work properly, waste builds up in brain cells, leading to damage. 

Pasternak learned about Ambroxol during a fellowship at The Hospital for Sick Children (SickKids) in Toronto, where it was identified as a treatment for Gaucher disease – a rare genetic disorder in children caused by a deficiency of GCase. He is now applying that research to explore whether boosting GCase with Ambroxol could help protect the brain in Parkinson’s related diseases. 

“This research is vital because Parkinson’s dementia profoundly affects patients and families,” says Pasternak. “If a drug like Ambroxol can help, it could offer real hope and improve lives.” 

Funded by the Weston Family Foundation, this study is an important step toward developing new treatments for Parkinson’s disease and other cognitive disorders, including dementia with Lewy bodies. Pasternak and his team plan to start a follow-up clinical trial focused specifically on cognition later this year. 

Source: St. Joseph’s Health Care London

Categories : Genetics Neurodegenerative DiseasesTags :

Common Gene Variant Doubles Dementia Risk for Men

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New research has found that men who carry a common genetic variant are twice as likely to develop dementia in their lifetime compared to women. The research, published in Neurology, used data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial to investigate whether people who had variants in the haemochromatosis (HFE) gene, which is critical for regulating iron levels in the body, might be at increased risk of dementia.

Co-author Professor John Olynyk, from the Curtin Medical School, said one in three people carry one copy of the variant, known as H63D, while one in 36 carry two copies.

“Having just one copy of this gene variant does not impact someone’s health or increase their risk of dementia. However, having two copies of the variant more than doubled the risk of dementia in men, but not women,” Professor Olynyk said.

“While the genetic variant itself cannot be changed, the brain pathways which it affects – leading to the damage that causes dementia – could potentially be treated if we understood more about it.”

Professor Olynyk said further research was needed to investigate why this genetic variant increased the risk of dementia for males but not females.

“The HFE gene is routinely tested for in most Western countries including Australia when assessing people for haemochromatosis – a disorder that causes the body to absorb too much iron. Our findings suggest that perhaps this testing could be offered to men more broadly,” Professor Olynyk said.

“While the HFE gene is critical for controlling iron levels in the body, we found no direct link between iron levels in the blood and increased dementia risk in affected men.

“This points to other mechanisms at play, possibly involving the increased risk of brain injury from inflammation and cell damage in the body.”

The ASPREE trial was a double-blind, randomised, placebo-controlled trial of daily low-aspirin in 19 114 healthy older people in Australia and the USA. Primarily undertaken to evaluate the risks versus benefits of daily low-dose aspirin in this cohort, it created a treasure trove of healthy ageing data that has underpinned a wealth of research studies.

Source: Curtin University

Categories : Mental Health Metabolic DisordersTags :

Metabolic Syndrome Linked to Increased Risk of Young-onset Dementia

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Having a larger waistline, high blood pressure and other risk factors that make up metabolic syndrome is associated with an increased risk of young-onset dementia, according to a study published on April 23, 2025, online in Neurology®, the medical journal of the American Academy of Neurology. Young-onset dementia is diagnosed before the age of 65. The study does not prove that metabolic syndrome causes young-onset dementia, it only shows an association.

Metabolic syndrome is defined as having excess belly fat plus two or more of the following risk factors: high blood pressure, high blood sugar, higher than normal triglycerides, which are a type of fat found in the blood, and low high-density lipoprotein (HDL) cholesterol, or “good” cholesterol.

“While most dementia is diagnosed in older age, young-onset dementia occurs while a person is still working and perhaps raising a family,” said study author Minwoo Lee, MD, PhD, of Hallym University Sacred Heart Hospital in Anyang, South Korea. “Our study found having metabolic syndrome in middle age is a risk factor for young-onset dementia.”

For the study, researchers reviewed national health insurance data in South Korea to identify nearly two million people between the ages of 40 and 60 who had a health check-up. The check-up included measurements of waist circumference, blood pressure, blood sugar, triglyceride and cholesterol levels. Of all participants, 25% had metabolic syndrome.

Over an average follow-up period of eight years, 8921 people, or 0.45% of all participants, developed dementia. For those with metabolic syndrome, the incidence rate was 0.86 cases per 1000 person-years, compared to 0.49 cases for those without metabolic syndrome. Person-years represent both the number of people in the study and the amount of time each person spends in the study.

After adjusting for age, education and health factors such as level of physical activity, depression and stroke, researchers found metabolic syndrome was associated with a 24% higher risk of dementia. When looking at specific types of dementia, it was associated with a 12% increased risk of Alzheimer’s disease and a 21% increased risk of vascular dementia.

Researchers found female participants with metabolic syndrome had a 34% increased risk of dementia compared to male participants who had a 15% increased risk. People in their 40s had a greater risk than people in their 50s.

Researchers found each component of metabolic syndrome was associated with an increased risk of dementia, which was cumulative. People with all five components had a 70% increased risk of dementia.

“Our findings suggest that lifestyle changes to reduce the risk of metabolic syndrome, such as eating a healthy diet, exercising regularly, maintaining a healthy weight, quitting smoking and reducing stress, may help reduce the risk of young-onset dementia,” said Lee. “Future research that follows people over longer periods of time and uses brain scans to look for biomarkers of dementia is needed to confirm and expand upon our findings.”

A limitation of the study was that researchers did not review genetic risk factors for Alzheimer’s disease.

The study was supported by the Korean National Research Foundation.

Source: American Academy of Neurology