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.
Research finds music therapy could be used on NHS wards as an alternative to medication
Photo by Sergio Capuzzimati on Unsplash
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
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.
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.
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.
Researchers from the University of Missouri have discovered that kaempferol, a natural antioxidant found in certain fruits and vegetables, such as kale, berries and endives, may support nerve cell health and holds promise as a potential treatment for ALS. Photo: Pixabay CC0
A natural compound found in everyday fruits and vegetables may hold the key to protecting nerve cells — and it’s showing promise as a potential treatment for ALS and dementia, according to new research from the University of Missouri.
“It’s exciting to discover a naturally occurring compound that may help people suffering from ALS or dementia,” Smita Saxena, a professor of physical medicine and rehabilitation at the School of Medicine and lead author of the study, said. “We found this compound had a strong impact in terms of maintaining motor and muscle function and reducing muscle atrophy.”
The study, which appears in Acta Neurologica, discovered that kaempferol, a natural antioxidant found in certain fruits and vegetables, such as kale, berries and endives, may support nerve cell health and holds promise as a potential treatment for ALS.
In lab-grown nerve cells from ALS patients, the compound helped the cells produce more energy and eased stress in the protein-processing center of the cell called the endoplasmic reticulum. Additionally, the compound improved overall cell function and slowed nerve cell damage. Researchers found that kaempferol worked by targeting a crucial pathway that helps control energy production and protein management — two functions that are disrupted in individuals with ALS.
“I believe this is one of the first compounds capable of targeting both the endoplasmic reticulum and mitochondria simultaneously,” Saxena said. “By interacting with both of these components within nerve cells, it has the potential to elicit a powerful neuroprotective effect.”
The challenge
The catch? The body doesn’t absorb kaempferol easily, and it could take a large amount to see real benefits in humans. For instance, an individual with ALS would need to consume at least 4.5kg of kale in a day to obtain a beneficial dose.
“Our bodies don’t absorb kaempferol very well from the vegetables we eat,” Saxena said. “Because of this, only a small amount reaches our tissues, limiting how effective it can be. We need to find ways to increase the dose of kaempferol or modify it so it’s absorbed into the bloodstream more easily.”
Another hurdle is getting the compound into the brain. The blood-brain barrier — a tightly locked layer of cells that blocks harmful substances — also makes it harder for larger molecules like kaempferol to pass through.
What’s next?
Despite its challenges, kaempferol remains a promising candidate for treating ALS, especially since it works even after symptoms start. It also shows potential for other neurodegenerative diseases including Alzheimer’s and Parkinson’s.
To make the compound easier for the body to absorb, Saxena’s team at the Roy Blunt NextGen Precision Health building is exploring ways to boost its uptake by neurons. One promising approach involves packaging lipid-based nanoparticles — tiny spherical particles made of fats that are commonly used in drug delivery.
“The idea is to encapsulate kaempferol within lipid-based nanoparticles that are easily absorbed by the neurons,” Saxena said. “This would target kaempferol to neurons to greatly increase its beneficial effect.”
The team is currently generating the nanoparticles with hopes of testing them by the end of the year.
An unusual public health policy in Wales may have produced the strongest evidence yet that a vaccine can reduce the risk of dementia. In a new study led by Stanford Medicine, researchers analysing the health records of Welsh older adults discovered that those who received the shingles vaccine were 20% less likely to develop dementia over the next seven years than those who did not receive the vaccine.
The remarkable findings, published April 2 in Nature, support an emerging theory that viruses that affect the nervous system can increase the risk of dementia. If further confirmed, the new findings suggest that a preventive intervention for dementia is already close at hand.
Lifelong infection
Shingles, a viral infection that produces a painful rash, is caused by the same virus that causes chicken pox — varicella-zoster. After people contract chicken pox, usually in childhood, the virus stays dormant in the nerve cells for life. In people who are older or have weakened immune systems, the dormant virus can reactivate and cause shingles.
Dementia affects more than 55 million people worldwide, with an estimated 10 million new cases every year. Decades of dementia research has largely focused on the accumulation of plaques and tangles in the brains of people with Alzheimer’s, the most common form of dementia. But with no breakthroughs in prevention or treatment, some researchers are exploring other avenues — including the role of certain viral infections.
Previous studies based on health records have linked the shingles vaccine with lower dementia rates, but they could not account for a major source of bias: People who are vaccinated also tend to be more health conscious in myriad, difficult-to-measure ways. Behaviors such as diet and exercise, for instance, are known to influence dementia rates, but are not included in health records.
“All these associational studies suffer from the basic problem that people who get vaccinated have different health behaviours than those who don’t,” said Pascal Geldsetzer, MD, PhD, assistant professor of medicine and senior author of the new study. “In general, they’re seen as not being solid enough evidence to make any recommendations on.”
Markus Eyting, PhD, and Min Xie, PhD, postdoctoral scholars in primary care and population health, are the study’s co-lead authors.
A natural experiment
But two years ago, Geldsetzer recognized a fortuitous “natural experiment” in the rollout of the shingles vaccine in Wales that seemed to sidestep the bias. The vaccine used at that time contained a live-attenuated, or weakened, form of the virus.
The vaccination program, which began Sept. 1, 2013, specified that anyone who was 79 on that date was eligible for the vaccine for one year. (People who were 78 would become eligible the next year for one year, and so on.) People who were 80 or older on Sept. 1, 2013, were out of luck — they would never become eligible for the vaccine.
These rules, designed to ration the limited supply of the vaccine, also meant that the slight difference in age between 79- and 80-year-olds made all the difference in who had access to the vaccine. By comparing people who turned 80 just before Sept. 1, 2013, with people who turned 80 just after, the researchers could isolate the effect of being eligible for the vaccine.
The circumstances, well-documented in the country’s health records, were about as close to a randomized controlled trial as you could get without conducting one, Geldsetzer said.
The researchers looked at the health records of more than 280 000 older adults who were 71 to 88 years old and did not have dementia at the start of the vaccination program. They focused their analysis on those closest to either side of the eligibility threshold — comparing people who turned 80 in the week before with those who turned 80 in the week after.
“We know that if you take a thousand people at random born in one week and a thousand people at random born a week later, there shouldn’t be anything different about them on average,” Geldsetzer said. “They are similar to each other apart from this tiny difference in age.”
The same proportion of both groups likely would have wanted to get the vaccine, but only half, those almost 80, were allowed to by the eligibility rules.
“What makes the study so powerful is that it’s essentially like a randomised trial with a control group — those a little bit too old to be eligible for the vaccine — and an intervention group — those just young enough to be eligible,” Geldsetzer said.
Protection against dementia
Over the next seven years, the researchers compared the health outcomes of people closest in age who were eligible and ineligible to receive the vaccine. By factoring in actual vaccination rates — about half of the population who were eligible received the vaccine, compared with almost none of the people who were ineligible — they could derive the effects of receiving the vaccine.
As expected, the vaccine reduced the occurrence over that seven-year period of shingles by about 37% for people who received the vaccine, similar to what had been found in clinical trials of the vaccine. (The live-attenuated vaccine’s effectiveness wanes over time.)
This huge protective signal was there, any which way you looked at the data.”
By 2020, one in eight older adults, who were by then 86 and 87, had been diagnosed with dementia. But those who received the shingles vaccine were 20% less likely to develop dementia than the unvaccinated.
“It was a really striking finding,” Geldsetzer said. “This huge protective signal was there, any which way you looked at the data.”
The scientists searched high and low for other variables that might have influenced dementia risk but found the two groups to be indistinguishable in all characteristics. There was no difference in the level of education between the people who were eligible and ineligible, for example. Those who were eligible were not more likely to get other vaccinations or preventive treatments, nor were they less likely to be diagnosed with other common health conditions, such as diabetes, heart disease and cancer.
The only difference was the drop in dementia diagnoses.
“Because of the unique way in which the vaccine was rolled out, bias in the analysis is much less likely than would usually be the case,” Geldsetzer said.
Nevertheless, his team analyzed the data in alternate ways — using different age ranges or looking only at deaths attributed to dementia, for example — but the link between vaccination and lower dementia rates remained.
“The signal in our data was so strong, so clear and so persistent,” he said.
Stronger response in women
In a further finding, the study showed that protection against dementia was much more pronounced in women than in men. This could be due to sex differences in immune response or in the way dementia develops, Geldsetzer said. Women on average have higher antibody responses to vaccination, for example, and shingles is more common in women than in men.
Whether the vaccine protects against dementia by revving up the immune system overall, by specifically reducing reactivations of the virus or by some other mechanism is still unknown.
Also unknown is whether a newer version of the vaccine, which contains only certain proteins from the virus and is more effective at preventing shingles, may have a similar or even greater impact on dementia.
Geldsetzer hopes the new findings will inspire more funding for this line of research.
“At least investing a subset of our resources into investigating these pathways could lead to breakthroughs in terms of treatment and prevention,” he said.
In the past two years, his team has replicated the Wales findings in health records from other countries, including England, Australia, New Zealand and Canada, that had similar rollouts of the vaccine. “We just keep seeing this strong protective signal for dementia in dataset after dataset,” he said.
But Geldsetzer has set his sights on a large, randomized controlled trial, which would provide the strongest proof of cause and effect. Participants would be randomly assigned to receive the live-attenuated vaccine or a placebo shot.
“It would be a very simple, pragmatic trial because we have a one-off intervention that we know is safe,” he said.
Geldsetzer is seeking philanthropic funding for the trial as the live-attenuated vaccine is no longer manufactured by pharmaceutical companies.
And such a trial might not take long to see results. He pointed to a graph of the Wales data tracking the dementia rates of those who were eligible and ineligible for the vaccine. The two curves began to separate in about a year and a half.
Researchers at Karolinska Institutet have demonstrated how specific biomarkers in the blood can predict the development of dementia up to 10 years before diagnosis with high accuracy, among older adults living independently in the community.
A new study, published in Nature Medicine, has investigated the potential of specific biomarkers such as tau217, Neurofilament Light (NfL), and Glial Fibrillary Acidic Protein (GFAP) to predict the occurrence of dementia, including Alzheimer’s disease, up to ten years before an actual diagnosis in cognitively healthy older adults living in the community.
Blood samples from more than two thousand
Previous research has suggested that these biomarkers could be useful in early dementia diagnostics, but most studies involved individuals who have already sought medical care for cognitive issues, due to cognitive concerns or cognitive symptoms, such as memory difficulties.
A larger, community-based study, was necessary to determine the predictive value of biomarkers in the general population.
Led by researchers from the Aging Research Center of Karolinska Institutet in collaboration with SciLifeLab and KTH Royal Institute of Technology in Stockholm, the study analysed blood biomarkers in more than 2100 adults aged 60+, who were followed over time to determine if they developed dementia.
At a follow-up ten years later, 17% of participants had developed dementia. The accuracy of the biomarkers used in the study was found to be up to 83%.
“This is an encouraging result, especially considering the 10-year predictive window between testing and diagnosis. It shows that it is possible to reliably identify individuals who develop dementia and those who will remain healthy,” says Giulia Grande, assistant professor at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and first author of the study.
Promising biomarkers
“Our findings imply that if an individual has low levels of these biomarkers, their risk of developing dementia over the next decade is minimal”, explains Davide Vetrano, associate professor at the same department and the study’s senior author. “This information could offer reassurance to individuals worried about their cognitive health, as it potentially rules out the future development of dementia.”
However, the researchers also observed that these biomarkers had low positive predictive values, meaning elevated biomarker levels alone could not reliably identify individuals who would surely develop dementia within the next ten years. Therefore, the study authors advise against widespread use of these biomarkers as screening tools in the population at this stage.
“These biomarkers are promising, but they are currently not suitable as standalone screening tests to identify dementia risk in the general population,” says Davide Vetrano.
The researchers also noted that a combination of the three most relevant biomarkers – p-tau217 with NfL or GFAP – could improve predictive accuracy.
“Further research is needed to determine how these biomarkers can be effectively used in real-world settings, especially for elderly living in the community or in primary health care services,” says Grande.
“We need to move a step further and see whether the combination of these biomarkers with other clinical, biological or functional information could improve the possibility of these biomarkers to be used as screening tools for the general population”, Grande continues.
The study was mainly funded by the Swedish Research Council, The Swedish Brain Foundation and The Strategic Research Area in Epidemiology and Biostatistics at Karolinska Institutet. The researchers declare that there are no conflicts of interest.
Past research has suggested that inflammation may contribute to the development and progression of dementia and that non-steroidal anti-inflammatory (NSAID) medications may help protect against dementia due to their anti-inflammatory effects. A new large prospective study published in the Journal of the American Geriatrics Society provides additional evidence, showing that long-term NSAID use is linked to a decreased risk of developing dementia.
In the population-based study of 11 745 adults with an average follow-up of 14.5 years, 9520 participants had used NSAIDs at any given time, and 2091 participants developed dementia. Long-term NSAID use was associated with a 12% reduced risk of developing dementia. Short- and intermediate-term use did not provide benefits. Also, the cumulative dose of NSAIDs was not associated with decreased dementia risk.
The findings suggest that prolonged, rather than intensive, use of anti-inflammatory medications may help protect against dementia.
“Our study provides evidence on possible preventive effects of anti-inflammatory medication against the dementia process. There is a need for more studies to further consolidate this evidence and possibly develop preventive strategies,” said corresponding author M. Arfan Ikram, MSc, MD, PhD, of Erasmus MC University Medical Center Rotterdam, in the Netherlands.
Meeting the minimum requirement for vitamin B12, needed to make DNA, red blood cells and nerve tissue, may not actually be enough – particularly if for older adults. It may even put them at risk for cognitive impairment, according to a study published in Annals of Neurology.
The research found that older, healthy volunteers, with lower concentrations of B12, but still in the normal range, showed signs of neurological and cognitive deficiency. These levels were associated with more damage to the brain’s white matter – the nerve fibres that enable communication between areas of the brain – and test scores associated with slower cognitive and visual processing speeds, compared to those with higher B12.
The UC San Francisco researchers, led by senior author Ari J. Green, MD, of the Departments of Neurology and Ophthalmology and the Weill Institute for Neurosciences, said that the results raise questions about current B12 requirements and suggest the recommendations need updating.
“Previous studies that defined healthy amounts of B12 may have missed subtle functional manifestations of high or low levels that can affect people without causing overt symptoms,” said Green, noting that clear deficiencies of the vitamin are commonly associated with a type of anaemia. “Revisiting the definition of B12 deficiency to incorporate functional biomarkers could lead to earlier intervention and prevention of cognitive decline.”
Lower B12 correlates with slower processing speeds, brain lesions
In the study, researchers enrolled 231 healthy participants without dementia or mild cognitive impairment, whose average age was 71. They were recruited through the Brain Aging Network for Cognitive Health (BrANCH) study at UCSF.
Their blood B12 amounts averaged 414.8pmol/L, well above the U.S. minimum of 148pmol/L. Adjusted for factors like age, sex, education and cardiovascular risks, researchers looked at the biologically active component of B12, which provides a more accurate measure of the amount of the vitamin that the body can utilize. In cognitive testing, participants with lower active B12 were found to have slower processing speed, relating to subtle cognitive decline. Its impact was amplified by older age. They also showed significant delays responding to visual stimuli, indicating slower visual processing speeds and general slower brain conductivity.
MRIs revealed a higher volume of lesions in the participants’ white matter, which may be associated with cognitive decline, dementia or stroke.
While the study volunteers were older adults, who may have a specific vulnerability to lower levels of B12, co-first author Alexandra Beaudry-Richard, MSc, said that these lower levels could “impact cognition to a greater extent than what we previously thought, and may affect a much larger proportion of the population than we realize.” Beaudry-Richard is currently completing her doctorate in research and medicine at the UCSF Department of Neurology and the Department of Microbiology and Immunology at the University of Ottawa.
“In addition to redefining B12 deficiency, clinicians should consider supplementation in older patients with neurological symptoms even if their levels are within normal limits,” she said. “Ultimately, we need to invest in more research about the underlying biology of B12 insufficiency, since it may be a preventable cause of cognitive decline.”
