logo
Three factors will stall dementia and the aging process, according to new U.S. study

Three factors will stall dementia and the aging process, according to new U.S. study

Yahoo6 days ago
By 2050, over 1.7 million Canadians are projected to be living with dementia. This represents an increase of 187 per cent compared to 2020, when approximately 597,300 Canadians were living with dementia, according to the Alzheimer's Society of Canada.
Dementia describes the decline of mental ability, while Alzheimer's Disease is the medical term for the brain disease that commonly causes dementia.
Researchers are now saying certain lifestyle changes can stave off mental decline. A new U.S. study sets out what Alzheimer's researchers are calling the strongest evidence yet regarding what is involved in slowing the aging process and improving cognition.
It comes down to three key factors: a diet heavy on leafy greens, berries and grains, regular moderate exercise and ongoing social interaction. Regular cardiovascular monitoring is also a factor.
Jessica Langbaum, senior director of research strategy at the Banner Alzheimer's Institute in Phoenix was not involved directly in the research but she presented the findings at an annual conference of experts in Toronto on Wednesday.
The Alzheimer's Association International Conference (AAIC) is the largest international meeting dedicated to advancing dementia science and clinical practice. This year's gathering brought together 8,000 scientists and clinicians from all over the world, with the goal of improving diagnosis, risk reduction and treatment.
The study pulled together diet, exercise and socialization in one substantial, structured study of 2,100 people in their 60s and 70s at risk of developing dementia, showing that bad habits 'can really slow down memory and thinking' in adults at risk for cognitive impairment and dementia, Langbaum told the PBS New Hour in an interview on Wednesday evening.
The subjects who participated in the study changed their habits, shifting from a sedentary lifestyle to an active one and improving their diet over a two-year period, resulting in cognitive function scores on par with people one or two years younger.
That might not sound like much, but Langbaum says the results are significant evidence that change can occur without medication. 'And so, it's showing that we can change the trajectory of aging,' she said.
There were two groups in the study. In one, lifestyle changes were structurally prescribed. In the other, the changes were self-directed. The results for the prescribed group were much better, but Langbaum says both groups showed improvement.
The biggest challenge that study participants faced was sustaining a new exercise regime. Langbaum recommends people find something that they enjoy doing.
'If (you're) frustrated by it, (you're) just going to give up. But do something that you enjoy. Better yet, do it with somebody else or others around you because socialization is key, and lastly, something that you can adhere to, if you can schedule it. It's something that you can stay committed to.'
Regarding nutrition she notes: 'We say what's good for the heart is good for the brain, so a nice balanced … nutritious diet with … those leafy greens, low in saturated fats, all of those things.'
The American Alzheimer's Association spent close to US$50 million on the study. The National Institutes of Health spent even more to ensure many of the participants underwent brain scans, blood tests and sleep studies aimed at provide additional information down the road.
Meanwhile, Langbaum expresses concern that structured intervention may not be sustainable in most communities. 'I think that's really the next stage of the research is, how do we make this scalable in communities so that people can implement these things into their daily lives?'
The American Alzheimer's Association is planning to spend another US$40 million on implementing the lessons of the study.
Langbaum says that will come with a change in the mindsets of doctors. They 'should be treating lifestyle interventions as they would a drug,' she told NPR. That would mean prescribing improved exercise and eating regimens and getting insurers to cover those prescriptions, she added.
Our website is the place for the latest breaking news, exclusive scoops, longreads and provocative commentary. Please bookmark nationalpost.com and sign up for our daily newsletter, Posted, here.
Orange background

Try Our AI Features

Explore what Daily8 AI can do for you:

Comments

No comments yet...

Related Articles

Genome BC Funds Research into the Respiratory Fallout of Wildfires
Genome BC Funds Research into the Respiratory Fallout of Wildfires

Yahoo

time10 minutes ago

  • Yahoo

Genome BC Funds Research into the Respiratory Fallout of Wildfires

VANCOUVER, BC, Aug. 6, 2025 /CNW/ - British Columbians know the stark realities of climate change, as wildfires surge across the province. Over a million hectares burned across BC in 2024, blanketing communities in thick smoke and dramatically increasing the number of hazy, lung-choking days. As summer becomes a season of smoke, this escalating environmental challenge also has a hidden, insidious impact: a profound and lasting toll on our respiratory health. Wildfire smoke is more than just an inconvenience; it's a dangerous cocktail of particulate matter that infiltrates our lungs and bodies, exacerbating existing conditions and potentially triggering new ones. The costs are staggering, both in human lives and healthcare dollars, with Health Canada estimating up to 240 deaths and $1.8 billion in annual costs due to short-term health effects alone. In response to this challenge, Genome BC is funding three research projects that will delve into the genetic-level impacts of wildfire smoke exposure. "These projects are specifically designed to uncover what makes our vulnerable populations – from newborns to those with chronic lung conditions – more susceptible to wildfire-related respiratory issues," said Suzanne Gill, Genome BC's President and CEO. "We hope this knowledge can both inform treatment and care within our healthcare system and reduce the overall economic toll of wildfires." PROJECT 1: Wildfire Exposure and Early Childhood Health The next generation of British Columbians could be feeling the effects of wildfires before they even take their first breath. This project uses a holistic approach to study the impact of disaster exposure during pregnancy, including if it can have lasting effects on how genes are expressed in developing children. This may increase the risk of respiratory diagnoses such as asthma, bronchitis, wheezing, hives, eczema and other allergic reactions. Lead Researcher, Dr. Michael Kobor of the University of British Columbia believes the results can inform public health policies about respiratory health, especially vulnerable groups such as infants and pregnant people. "With this research, we aim to better our understanding of the impacts of prenatal wildfire disaster exposure on the next generation," he said. "Early-life environments can have a lasting impact on people throughout the course of their lives, including on their health outcomes. We hope this work will help shape healthy futures for children as global temperatures rise and wildfires become increasingly common." PROJECT 2: How Wildfire Smoke Affects People with Chronic Obstructive Pulmonary Disease (COPD) For the over 2 million Canadians living with Chronic Obstructive Pulmonary Disease (COPD), wildfire smoke presents a particularly grave threat. COPD is already the leading cause of hospitalization in Canada, costing our healthcare system an estimated $1.5 billion annually. Wildfire smoke can significantly worsen symptoms and lead to severe complications for COPD patients. Dr. Graeme Koelwyn from Simon Fraser University and and Dr. Don Sin from the University of British Columbia are studying the genomic changes in innate immune cells — our first line of defense against inhaled particles — of COPD patients. Their research aims to understand how these immune cells respond to wildfire smoke in patients at the genetic level as symptoms become worse, and to identify effective treatments. "This information is critical to develop disease management and exposure mitigation strategies for people living with COPD," Dr. Koelwyn said, "especially in this time of increasing societal and financial burden within our changing world and environment." PROJECT 3: How Wildfire Smoke and Aeroallergens Affect Lung Health Dr. Emilia Lim and Dr. Min Hyung Ryu from the University of British Columbia are focusing on airborne allergens (aeroallergens) triggered by the increase of atmospheric carbon dioxide and high temperatures that happen when there are frequent wildfires. These situations also tend to prolong allergy seasons. Our bodies generate an immune response to protect us when aeroallergens enter our lungs. "Aeroallergens are harmful to everyone, but people with lung conditions such as asthma, COPD and lung cancer survivors are at higher risk," because their immune systems are theoretically less robust, Dr. Lim explains. "It's important to know how these groups are affected differently." The researchers want to understand the links between our individual genetic differences and environmental triggers. Dr. Ryu noted, "identifying populations that are susceptible to these changes can help us find better ways to prevent and treat respiratory diseases." The Value of Proactive Research The escalating financial burden of wildfire recovery underscores the urgent need for proactive strategies. These three projects exemplify how genomics research is providing critical insights into the complex interplay between our environment and our health. "With our proximity to wildfires and access to interdisciplinary teams, Canadian researchers are uniquely equipped to tackle these questions first-hand," said Gill. "The fundamental knowledge gained will lay the groundwork for better policy decisions and more efficient treatments in the future. Any breakthroughs in respiratory health or disease prevention will translate into economic benefits for British Columbians and beyond." About Genome British Columbia: Genome BC is a not-for-profit organization that has advanced genomics research and innovation for 25 years, growing a world-class life sciences sector in BC and delivering sustainable benefits for British Columbia, Canada and beyond. Genome BC has attracted over $1.1 billion in direct co-investment to the province, which has contributed to funding more than 600 genomics research and innovation projects. These initiatives enhance healthcare and address environmental and natural resource challenges, improving the lives of British Columbians. Genome BC also integrates genomics into society by supporting responsible research and innovation and fostering an understanding and appreciation of the life sciences among educators, students and the public. SOURCE Genome British Columbia View original content to download multimedia: Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data

Breakthrough study finds deficiency of this common nutrient could contribute to Alzheimer's
Breakthrough study finds deficiency of this common nutrient could contribute to Alzheimer's

Yahoo

time3 hours ago

  • Yahoo

Breakthrough study finds deficiency of this common nutrient could contribute to Alzheimer's

A deficiency of the metal lithium in the body could be a key factor contributing to the development of dementia in Alzherimer's patients, a groundbreaking new study reveals. The decade-long research, published in the journal Nature, shows for the first time that lithium occurs naturally in the brain and maintains the normal function of all its major cell types, preventing nerves from degradation. Scientists from Harvard Medical School found that lithium loss in the human brain is one of the earliest changes leading to Alzheimer's, while in mice, a similar lithium depletion accelerated memory decline. A reduced lithium level was found in some cases due to the metal's impaired uptake and its binding to amyloid plaques, which are known to be smoking gun signs of Alzheimer's. Researchers also showed that a new type of lithium compound – lithium orotate – can avoid capture by amyloid plaques and restore memory in mice. In the study, scientists used an advanced type of mass spectroscopy chemical analysis method to measure trace levels of about 30 different metals in the brain and blood samples from a range of people, including cognitively healthy people, those in an early stage of dementia, and those with advanced Alzheimer's. The analysis revealed that lithium was the only metal with markedly different levels across groups, which also seemed to change at the earliest stages of memory loss. 'Lithium turns out to be like other nutrients we get from the environment, such as iron and vitamin C,' study senior author Bruce Yankner said. 'It's the first time anyone's shown that lithium exists at a natural level that's biologically meaningful without giving it as a drug,' Dr Yankner said. Although lithium compounds have been historically in use to treat a range of mental conditions like bipolar disorder and major depressive disorder, in these cases, they are given at much higher concentrations that could even be toxic to older people. Scientists have now found that lithium orotate is effective at one-thousandth this dose – enough to mimic the natural level of lithium in the brain. The latest findings with lithium orotate, however, needs to be confirmed in humans via clinical trials. Yet, researchers suspect that measuring lithium levels could help screen people for early Alzheimer's. The findings revise the theory of Alzheimer's disease, which affects nearly 400 million people worldwide, offering a new strategy for early diagnosis, prevention, and treatment. Decades of studies have shown that Alzheimer's disease involves an array of brain abnormalities, including clumps of the protein amyloid beta, tangles of the protein tau, and a loss of the brain's protective protein REST. However, these abnormalities have never fully explained the condition. For instance, it remains unclear why some people with Alzheimer's-like changes in the brain never go on to develop dementia or cognitive decline. Recent treatments developed to target amyloid beta plaques also don't seem to reverse memory loss, only modestly reducing the rate of cognitive decline. Now, scientists say lithium could be the critical missing link. 'The idea that lithium deficiency could be a cause of Alzheimer's disease is new and suggests a different therapeutic approach,' Dr Yankner said. 'You have to be careful about extrapolating from mouse models, and you never know until you try it in a controlled human clinical trial... But so far the results are very encouraging,' he added.

Research on reversing Alzheimer's reveals lithium as potential key
Research on reversing Alzheimer's reveals lithium as potential key

Yahoo

time7 hours ago

  • Yahoo

Research on reversing Alzheimer's reveals lithium as potential key

Seven years of investigation by scientists at Harvard Medical School has revealed that the loss of the metal lithium plays a powerful role in Alzheimer's disease, a finding that could lead to earlier detection, new treatments and a broader understanding of how the brain ages. Researchers led by Bruce A. Yankner, a professor of genetics and neurology at Harvard Medical School, reported that they were able to reverse the disease in mice and restore brain function with small amounts of the compound lithium orotate, enough to mimic the metal's natural level in the brain. Their study appeared Wednesday in the journal Nature. Subscribe to The Post Most newsletter for the most important and interesting stories from The Washington Post. 'The obvious impact is that because lithium orotate is dirt cheap, hopefully we will get rigorous, randomized trials testing this very, very quickly,' said Matt Kaeberlein, former director of the Healthy Aging and Longevity Research Institute at the University of Washington, who did not participate in the study. 'And I would say that it will be an embarrassment to the Alzheimer's clinical community if that doesn't happen right away.' Yankner, who is also the co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard, said: 'I do not recommend that people take lithium at this point, because it has not been validated as a treatment in humans. We always have to be cautious because things can change as you go from mice to humans.' He added that the findings still need to be validated by other labs. Although there have been recent breakthroughs in the treatment of Alzheimer's, no medication has succeeded in stopping or reversing the disease that afflicts more than 7 million Americans, a number projected to reach almost 13 million by 2050, according to the Alzheimer's Association. Lithium is widely prescribed for patients with bipolar disorder, and previous research indicated that it held potential as an Alzheimer's treatment and an antiaging medication. A 2017 study in Denmark suggested the presence of lithium in drinking water might be associated with a lower incidence of dementia. However, the new work is the first to describe the specific roles that lithium plays in the brain, its influence on all of the brain's major cell types and the effect that its deficiency later in life has on aging. Results of the study by Yankner's lab and researchers at Boston Children's Hospital and the Rush Alzheimer's Disease Center in Chicago also suggest that measuring lithium levels might help doctors screen people for signs of Alzheimer's years before the first symptoms begin to appear. Yankner said doctors might be able to measure lithium levels in the cerebrospinal fluid or blood, or through brain imaging. - - - How our brains use lithium In a healthy brain, lithium maintains the connections and communication lines that allow neurons to talk with one another. The metal also helps form the myelin that coats and insulates the communication lines and helps microglial cells clear cellular debris that can impede brain function. 'In normal aging mice,' Yankner said, 'lithium promotes good memory function. In normal aging humans,' higher lithium levels also correspond to better memory function. The depletion of lithium in the brain plays a role in most of the deterioration in several mouse models of Alzheimer's disease. Loss of lithium accelerates the development of harmful clumps of the protein amyloid beta and tangles of the protein tau that resemble the structures found in people with Alzheimer's. Amyloid plaques and tau tangles disrupt communication between nerve cells. The plaques in turn undermine lithium by trapping it, weakening its ability to help the brain function. Lithium depletion is involved in other destructive processes of Alzheimer's: decay of brain synapses, damage to the myelin that protects nerve fibers and reduced capacity of microglial cells to break down amyloid plaques. Lithium's pervasive role comes despite the fact that our brains contain only a small amount of it. After examining more than 500 human brains from Rush and other brain banks, Yankner's team discovered the naturally occurring lithium in the brain is 1,000 times less than the lithium provided in medications to treat bipolar disorder. Li-Huei Tsai, director of the Picower Institute for Learning and Memory at Massachusetts Institute of Technology and who was not involved in the study, called it 'very exciting,' especially when many in the field, including her own lab, have focused on genetic risk factors for Alzheimer's. 'But clearly genetic risk factors are not the only things,' said Tsai, who is also Picower professor of neuroscience. 'There are a lot of people walking around carrying these risk genes, but they are not affected by Alzheimer's disease. I feel this study provides a very important piece of the puzzle.' - - - Pathways for treatment Alzheimer's treatments mostly help to manage symptoms and slow the decline it causes in thinking and functioning. Aducanumab, lecanemab, and donanemab, all lab-made antibodies, bind to the harmful amyloid plaques and help remove them. Donepezil, rivastigmine and galantamine ― all in the class of medications known as cholinesterase inhibitors ― work by replenishing a chemical messenger called acetylcholine, which is diminished in Alzheimer's. Acetylcholine plays an important role in memory, muscle movement and attention. Yankner and his team found that when they gave otherwise healthy mice a reduced-lithium diet, the mice lost brain synapses and began to lose memory. 'We found that when we administered lithium orotate to aging mice [that had] started losing their memory, the lithium orotate actually reverted their memory to the young adult, six month level,' he said. Lithium orotate helped the mice reduce production of the amyloid plaques and tau tangles, and allowed the microglial cells to remove the plaques much more effectively. Yankner said one factor that might help lithium orotate reach clinical trials sooner is the small amount of the treatment needed, which could greatly reduce the risk of harmful side effects, such as kidney dysfunction and thyroid toxicity. Aside from its potential in treating Alzheimer's, Yankner said lithium orotate might also have implications for the treatment of Parkinson's disease, an area his lab is investigating. 'That needs to be rigorously examined,' he said. 'But we're looking at a whole slew of disorders.' Related Content Trump is threatening to take over D.C. Here's what he can and can't do. They once shared recipes. Now her family is going hungry in Gaza. Pets are being abandoned, surrendered amid Trump's immigration crackdown Solve the daily Crossword

DOWNLOAD THE APP

Get Started Now: Download the App

Ready to dive into a world of global content with local flavor? Download Daily8 app today from your preferred app store and start exploring.
app-storeplay-store