Category: Ageing

Categories : Ageing Diet and NutritionTags :

In Humans, Reducing Calorie Intake Rejuvenates Muscles and Stimulates Anti-ageing Effects

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Reducing overall calorie intake may rejuvenate muscles and activate biological pathways important for good health, according new study, published in the journal Aging Cell. Calorie restriction, which cuts intake of calories but not essential nutrients, has long been known to delay the progression of age-related diseases in animal models. This finding, by researchers at the National Institutes of Health and their colleagues, suggests the same biological mechanisms may also apply to humans.

Researchers analysed data from participants in the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy (CALERIE), a study supported by the National Institute on Aging (NIA) that examined whether moderate calorie restriction conveys the same health benefits seen in animal studies. They found that during a two-year span, the goal for participants was to reduce their daily caloric intake by 25%, but the highest the group was able to reach was a 12% reduction. Even so, this slight reduction in calories was enough to activate most of the biological pathways that are important in healthy aging.

“A 12% reduction in calorie intake is very modest,” said corresponding author and NIA Scientific Director Luigi Ferrucci, MD, PhD. “This kind of small reduction in calorie intake is doable and may make a big difference in your health.”

The research team next sought to understand the molecular underpinnings of the benefits seen in limited, previous research of calorie restriction in humans. One study showed that individuals on calorie restriction lost muscle mass and an average of 20 pounds of weight over the first year and maintained their weight for the second year. However, despite losing muscle mass, calorie restriction participants did not lose muscle strength, indicating calorie restriction improved the amount of force generated by each unit of muscle mass, called muscle specific force.

For the current study, scientists used thigh muscle biopsies from CALERIE participants that were collected when individuals joined the study and at one-year and two-year follow ups.

To figure out which human genes were impacted during calorie restriction, the scientists isolated messenger RNA (mRNA), a molecule that contains the code for proteins, from muscle samples. The team determined the protein sequence of each mRNA and used the information to identify which genes originated specific mRNAs. Further analysis helped the scientists establish which genes during calorie restriction were upregulated, meaning the cells made more mRNA; and which were downregulated, meaning the cells produced less mRNA. The researchers confirmed calorie restriction affected the same gene pathways in humans as in mice and non-human primates. For example, a lower caloric intake upregulated genes responsible for energy generation and metabolism, and downregulated inflammatory genes leading to lower inflammation.

“Since inflammation and aging are strongly coupled, calorie restriction represents a powerful approach to preventing the pro-inflammatory state that is developed by many older people,” said Ferrucci.

Source: NIH/National Institute on Aging

Categories : Ageing NeurologyTags :

In Hearing Loss, How Hair Cells Lose Their ‘Hair’

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In some cases of hearing loss, a cochlear implant is required. Photo by Brett Sayles

With age, many people will eventually need hearing aids. In some cases, the reason for this may be a signalling pathway that controls auditory sensory cell function and is downregulated with age. In the journal iScience, researchers at the University of Basel report the clues they have uncovered about this process, which may yield potential therapies to slow its progression.

Nearly everyone eventually experiences hearing loss: loud noises or simple aging gradually cause the auditory sensory cells and their synapses in the inner ear to degenerate and die off. The only treatment option is a hearing aid or, in extreme cases, a cochlear implant.

“In order to develop new therapies, we need to better understand what the auditory sensory cells need for proper function,” explains Dr Maurizio Cortada from the Department of Biomedicine at the University of Basel and University Hospital Basel. In collaboration researchers at the Biozentrum, Cortada investigated which signalling pathways influence the sensory hair cells in the inner ear. In the process, the researchers discovered a central regulator.

This signaling pathway, known by researchers as the mTORC2-signaling pathway, plays an important role, among other things, for cell growth and the cytoskeleton. The role it plays for the hair cells in the inner ear has not previously been studied.

When the researchers removed a central gene of this signalling pathway in the hair cells of the inner ear of mice, the animals gradually lost their hearing. By the age of twelve weeks, they were completely deaf, the authors report in the study.

Shortening ‘hair’ and fewer synapses

Closer examination indicated that the sensory hair cells in the inner ear lost their sensors without the mTORC2 signalling pathway: the distinctive fibre bundles known as stereocilia. Through electron microscopes, the researchers observed the shortening of stereocilia. The number of synapses that transmit the signals to the auditory nerve was also reduced.

“From other studies, we know that the production of key proteins in this signaling pathway decreases with age,” Cortada explains. There may be a connection to the loss of synapses and the reduced function of the auditory sensory cells in the inner ear that leads to hearing loss with increasing age.

“If this is confirmed, it would be a possible starting point for future therapies,” says the researcher. The middle and inner ear, for example, would be readily accessible for locally-administered medications or gene therapies. The results could pave the way for the development of such treatment options.

Source: University of Basel

Categories : AgeingTags :

Old Age Funding is Not Keeping Pace with Our Ageing Population, Report Finds

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South Africa’s population is ageing, yet government funding for community-based elder care services is not increasing to meet the demand.

This is a key finding by Family Caregiving, a programme at the University of Cape Town focused on the needs of older people, which has released two reports on funding for old age care and how care is experienced by older people in South Africa. 

“We want to work with the government and make useful suggestions about what is needed,” says Dr Elena Moore, who led the research together with Dr Gabrielle Kelly.

There are nearly 6 million people over the age of 60 in South Africa, about 10% of the population. The older population is expected to grow to over 15% of the total population by 2050. Also, 40% of older people have a significant need for care, says Moore.

The government currently provides subsidies to non-profit organisations that provide health and social services for older people. But according to Family Caregiving’s research, the overall amount spent on these subsidies by provincial governments, when adjusted for inflation and the growing ageing population, has decreased by 13% since 2007.

A lack of sufficient care for older people means that family members, often women, carry the burden of caring for older family members. The government does provide a Grant-in-Aid social grant of R510 a month, but few people who qualify for it know about it and the amount is too little to cover the cost of a full-time carer, according to the Family Caregiving report.

Family Caregiving is calling on the departments of social development and health to expand the implementation of the Older Persons Act of 2006. The Act provides for community-based care services, ensuring that older people can stay within their households and access the care they need in their communities.

According to the report, approximately 80 000 older people in South Africa receive care at a community centre and about 18 000 people receive state subsidies in care homes. But the report found that the subsidies do not come close to covering the running costs of these programmes and that existing programmes do not meet the growing demand.

Underfunding

Neighbourhood Old Age Home (NOAH), a non-profit organisation in the Western Cape, provides a variety of services. Its housing programme provides 94 beds. For this, it receives R440 000 from the provincial department for social development. But the actual cost of running the programme is nearly R850 000, so the organisation has to absorb almost half the running costs.

In Khayelitsha, NOAH runs a service centre that provides community-based care and support services to nearly 90 older people. The centre operates five days a week and offers meals, educational and skills development programmes, health and social services, and recreational opportunities.

The centre qualifies for an R2230 subsidy per person per year. It receives R190 000 from the government, but it costs R540 000 to run.

In Woodstock, the NOAH service centre has 29 beneficiaries. It operates three days a week and qualifies for a subsidy of R1419 per person per year. It received R59 300 in government funding, but it costs over R600 000 to run.

In KwaZulu-Natal, non-profit organisation The Association For The Aged (TAFTA) runs a variety of services for older persons. Its frail care services rely on a subsidy as well as the beneficiaries’ monthly old age grants, but this makes up only 40% of its running costs, creating a monthly shortfall of R6600 per person.

TAFTA’s assisted living programme is not subsidised. Beneficiaries contribute their old age grant (R2080) towards food and accommodation and TAFTA contributes another R2500 per person. TAFTA service centres receive R18 per person per day, leaving a shortfall of R35 per person per day.

According to Family Caregiving, smaller organisations that do not have the institutional networks of NOAH and TAFTA are often not able to absorb these shortfalls.

Esther Lewis, spokesperson for the Western Cape Department of Social Development, says the province subsidises 186 service centres, catering for 12 000 people. The province also supports financially struggling organisations with mentoring and training. This year, the Western Cape department provided additional grants to organisations for operational costs.

Although funding has increased in the Western Cape and KwaZulu-Natal since 2007, in most provinces subsidies are not paid or are not reported, Family Caregiving found.

Looking forward

Family Caregiving is calling for more funding for old-age care, from subsidies for care organisations to increased funding for health facilities for old age care.

Moore says a multi-disciplinary team is needed to address the challenges facing older people. The team should include representatives from the government departments and organisations as well as a range of experts, from economists to healthcare practitioners.

The Family Caregiving report recommends that the government take steps to ensure that all provinces provide subsidies for old age care and that subsidies increase to meet the growing demand. It recommends that while subsidies focus on service centres and residential care, government support for home-based care services be expanded. Also, existing healthcare facilities, such as clinics and hospitals, can be better optimised to care for older people. Health workers should receive training and information on caring for older people, the report says.

Republished from GroundUp under a Creative Commons Attribution-NoDerivatives 4.0 International License.

Source: GroundUp

Categories : Ageing GenderTags :

Women Who Reach Their 90s Tend to Have Maintained Stable Weight

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Reaching the age of 90, 95 or 100, known as exceptional longevity, was more likely for women who maintained their body weight after age 60, according to a multi-institutional study led by University of California San Diego. Older women who sustained a stable weight were 1.2 to 2 times more likely to achieve longevity compared to those who lost 5% of their weight or more.

In this study published in the Journal of Gerontology: Medical Sciences, researchers investigated the link between weight changes later in life with exceptional longevity among 54 437 women who enrolled in the Women’s Health Initiative, a prospective study investigating causes of chronic diseases among postmenopausal women. Throughout the follow up period, 30 647 (56%) of the participants survived to the age of 90 or beyond.

Women who lost at least 5% weight were less likely to achieve longevity compared to those who achieved stable weight. For example, women who unintentionally lost weight were 51% less likely to survive to the age of 90. However, gaining 5% or more weight, compared to stable weight, was not associated with exceptional longevity.

“It is very common for older women in the United States to experience overweight or obesity with a body mass index range of 25 to 35. Our findings support stable weight as a goal for longevity in older women,” said first author Aladdin H. Shadyab, PhD, MPH, associate professor at UC San Diego.

“If aging women find themselves losing weight when they are not trying to lose weight, this could be a warning sign of ill health and a predictor of decreased longevity.”

The findings suggest that general recommendations for weight loss in older women may not help them live longer. Nevertheless, the authors caution that women should heed medical advice if moderate weight loss is recommended to improve their health or quality of life.

The data adds to research connecting weight change and mortality and is notably the first large study to examine weight change later in life and its relation to exceptional longevity.

Source: University of California – San Diego

Categories : Ageing Cardiovascular DiseaseTags :

Stressful Life Events Contribute to Atrial Fibrillation Risk in Postmenopausal Women

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An estimated 1 in 4 postmenopausal women may develop atrial fibrillation in their lifetime, with stressful life events and insomnia being major contributing factors, according to new research published in the Journal of the American Heart Association.

Atrial fibrillation may lead to blood clots, stroke, heart failure or other cardiovascular complications. It primarily affects older adults.

“In my general cardiology practice, I see many postmenopausal women with picture perfect physical health who struggle with poor sleep and negative psychological emotional feelings or experience, which we now know may put them at risk for developing atrial fibrillation,” said lead study author Susan X. Zhao, M.D., a cardiologist at Santa Clara Valley Medical Center in California. “I strongly believe that in addition to age, genetic and other heart-health related risk factors, psychosocial factors are the missing piece to the puzzle of the genesis of atrial fibrillation.“

Researchers reviewed data from more than 83 000 questionnaires by women ages 50-79 from the Women’s Health Initiative, a major US study. Participants were asked a series of questions in key categories: stressful life events, their sense of optimism, social support and insomnia. Questions about stressful life events addressed topics such as loss of a loved one; illness; divorce; financial pressure; and domestic, verbal, physical or sexual abuse. Questions about sleeping habits focused on if participants had trouble falling asleep, wake up several times during the night and  overall sleep quality, for example. Questions about participants’ outlook on life and social supports addressed having friends to talk with during and about difficult or stressful situations; a sense of optimism such as believing good things are on the horizon; and having help with daily chores.

During approximately a decade of follow-up, the study found:

  • About 25% or 23 954 women developed atrial fibrillation.
  • A two-cluster system (the stress cluster and the strain cluster).
  • For each additional point on the insomnia scale, there is a 4% higher likelihood of developing atrial fibrillation. Similarly, for each additional point on the stressful life event scale, there is a 2% higher likelihood of having atrial fibrillation.

“The heart and brain connection has been long established in many conditions,” Zhao said. “Atrial fibrillation is a disease of the electrical conduction system and is prone to hormonal changes stemming from stress and poor sleep. These common pathways likely underpin the association between stress and insomnia with atrial fibrillation.”

Researchers noted that stressful life events, poor sleep and feelings, such as depression, anxiety or feeling overwhelmed by one’s circumstances, are often interrelated. It’s difficult to know whether these factors accumulate gradually over the years to increase the risk of atrial fibrillation as women age.

Chronic stress has not been consistently associated with atrial fibrillation, and the researchers note that a limitation of their study is that it relied on patient questionnaires from the start of the study. Stressful life events, however, though significant and traumatic, may not be long lasting, Zhao notes. Further research is needed to confirm these associations and evaluate whether customised stress-relieving interventions may modify atrial fibrillation risk.

Source: EurekAlert!

Categories : Ageing Diet and NutritionTags :

Yeast Studies Suggest that Early Diet may be Key for Lifelong Health

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Researchers at the Babraham Institute are proposing an alternative link between diet and ageing based on studies in yeast. In a study using yeast, a useful model organism to study ageing, researchers showed that a ‘healthier’ galactose diet in early life led to reduced senescence in those cells. The findings, published in PLOS Biology, suggest that dietary makeup at a young age may have a long-lasting impact on health throughout the lifespan.

Dr Jon Houseley and his team have published their experiments, showing that healthy ageing is achievable through dietary change without restriction by potentially optimising diet, and that ill-health is not an inevitable part of the ageing process.

Scientists have long known that caloric restriction improves health in later life and may even extend life. However, studies in mice show that caloric restriction really needs to be maintained throughout life to achieve this impact, and the health benefits disappear when a normal diet is resumed. Dr Houseley’s new research conducted in yeast suggests an alternative to calorie restriction can lead to improved health through the lifecycle.

“We show that diet in early life can switch yeast onto a healthier trajectory. By giving yeast a different diet without restricting calories we were able to suppress senescence, when cells no longer divide, and loss of fitness in aged cells.” Said Dr Dorottya Horkai, lead researcher on the study.

Rather than growing yeast on their usual glucose-rich diet, the researchers swapped their diet to galactose and observed that many molecular changes which normally accompany ageing did not occur. The cells grown on galactose remained just as fit as young cells even late in life, despite not living any longer, showing that the period of ill-health towards the end of life was dramatically reduced.

“Crucially, the dietary change only works when cells are young, and actually diet makes little difference in old yeast. It is hard to translate what youth means between yeast and humans, but all these studies point to the same trend – to live a long and healthy life, a healthy diet from an early age makes a difference.” explains Dr Houseley.

Yeast are good model organisms for studying ageing as they share many of the same cellular machinery as animals and humans. This avenue of research in yeast helps us to seek a more achievable way to improve healthy ageing though diet compared to sustained and severe calorie restriction, although more research is needed.

Source: Babraham Institute

Categories : Ageing GeneticsTags :

Mice Live Longer when Given a Longevity Gene from Naked Mole Rats

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CRISPR-Cas9 is a customisable tool that lets scientists cut and insert small pieces of DNA at precise areas along a DNA strand. This lets scientists study our genes in a specific, targeted way. Credit: Ernesto del Aguila III, National Human Genome Research Institute, NIH

In a ground-breaking advance in aging research, scientists have successfully transferred a longevity gene from naked mole rats to mice, resulting in improved health and an extension of the mouse’s lifespan.

Naked mole rats are known for their long lifespans and exceptional resistance to age-related diseases. By introducing a specific gene responsible for enhanced cellular repair and protection into mice, the researchers have opened exciting possibilities for unlocking the secrets of aging and extending human lifespan.

“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, professor at Rochester University. Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, report in a study published in Nature that they successfully transferred a gene responsible for making high molecular weight hyaluronic acid (HMW-HA) from a naked mole rat to mice. This led to improved health and an approximate 4.4 percent increase in median lifespan for the mice.

A unique mechanism for cancer resistance

Naked mole rats are mouse-sized rodents that have exceptional longevity for rodents of their size; they can live up to 41 years, nearly ten times as long as similar-size rodents. Unlike many other species, naked mole rats do not often contract age-related diseases such neurodegeneration, cardiovascular disease, arthritis, and cancer. Gorbunova and Seluanov have devoted decades of research to understanding the unique mechanisms that naked mole rats use to protect themselves against aging and diseases.

The researchers previously discovered that HMW-HA is one mechanism responsible for naked mole rats’ unusual resistance to cancer. Compared to mice and humans, naked mole rats have about ten times more HMW-HA in their bodies. When the researchers removed HMW-HA from naked mole rat cells, the cells were more likely to form tumours.

Gorbunova, Seluanov, and their colleagues wanted to see if the positive effects of HMW-HA could also be reproduced in other animals.

Transferring an HMW-HA-producing gene

The team genetically modified a mouse model to produce the naked mole rat version of the hyaluronan synthase 2 gene, which is the gene responsible for making a protein that produces HMW-HA. While all mammals have the hyaluronan synthase 2 gene, the naked mole rat version seems to be enhanced to drive stronger gene expression.

The researchers found that the mice that had the naked mole rat version of the gene had better protection against both spontaneous tumors and chemically induced skin cancer. The mice also had improved overall health and lived longer compared to regular mice. As the mice with the naked mole rat version of the gene aged, they had less inflammation in different parts of their bodies — inflammation being a hallmark of aging — and maintained a healthier gut.

While more research is needed on exactly why HMW-HA has such beneficial effects, the researchers believe it is due to HMW-HA’s ability to directly regulate the immune system.

A fountain of youth for humans?

“It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice,” Gorbunova says. “Our next goal is to transfer this benefit to humans.”

They believe they can accomplish this through two routes: either by slowing down degradation of HMW-HA or by enhancing HMW-HA synthesis.

“We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials,” Seluanov says. “We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health.”

Source: University of Rochester

Categories : Ageing Metabolic DisordersTags :

In Animal Studies, Metformin Extends Lifespan

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Researchers have discovered that the common antidiabetic drug metformin not only lowers blood sugar levels but has revealed to extend lifespan in C. Elegans, an animal model that shares similar metabolic systems with humans and are often used to model human diseases.

This study, led by investigators at Massachusetts General Hospital (MGH), reveals that metformin promotes longevity by stimulating the body’s production of ether lipids, a major structural component of cell membranes.

The findings, which are published in eLife, suggest that boosting production of ether lipids in humans may support healthy aging and reduce the impact of aging-related diseases.

To identify the genes required to enable lifespan extension in response to metformin and its sister drug phenformin (drugs called biguanides), the scientists silenced individual genes in the roundworm Caenorhabditis elegans (which shares over 80% of its proteins with humans and has an average lifespan of about two weeks) and examined what happens to the altered worms after exposure to the medications.

The experiments reveal that genes that increase production of ether lipids are required to extend lifespan in response to the biguanides. Inactivation of the genes that encode for these enzymes completely prevented the longevity-promoting effects of biguanides. Importantly, inactivation of these genes prevented lifespan extension in a variety of situations that are also known to promote longevity, including dietary restriction.

The team also found that increasing ether lipid synthesis alone (by overexpressing a single, key ether lipid biosynthetic enzyme called fard-1) was sufficient to extend C. elegans’ lifespan, orchestrating a metabolic stress defense response through a factor called SKN-1, which is the worm counterpart to the mammalian protein Nrf. This response altered metabolism to promote a longer lifespan.

“Our study implicates promotion of ether lipid biosynthesis as a novel therapeutic target to promote healthy aging. This suggests that dietary or pharmacologic intervention to promote ether lipid synthesis might one day represent a strategy to treat aging and aging-related diseases,” says senior author Alexander A. Soukas, MD, PhD, an Associate Professor at Harvard Medical School.

“Because our studies focused solely on interventions in C. elegans, further studies in mammalian models (such as human cells and mice), epidemiological observation, and rigorous clinical trials are required to determine the viability of promoting ether lipid synthesis to promote human health-span and lifespan.”

Source: Massachusetts General Hospital

Categories : Ageing NeurologyTags :

Social Isolation Linked to Reduced Brain Volume in Older People

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A study of nearly 9000 older people in Japan found that those who have little social contact with others may be more likely to have reduction of overall brain volume, and in areas of the brain affected by dementia, compared with those who have more frequent social contact. The study results were published in Neurology.

“Social isolation is a growing problem for older adults,” said study author Toshiharu Ninomiya, MD, PhD, of Kyushu University in Fukuoka, Japan. “These results suggest that providing support for people to help them start and maintain their connections to others may be beneficial for preventing brain atrophy and the development of dementia.”

The study involved 8896 people without dementia, average age 73. They had MRI brain scans and health exams, and were asked how often they were in contact with friends or relatives that did not live with them.

The people with the lowest amount of social contact had overall brain volume that was significantly lower than those with the most social contact. The total brain volume, or the sum of white and grey matter, as a percentage of the total intracranial volume, or the volume within the cranium, including the brain, meninges, and cerebrospinal fluid, was 67.3% in the lowest contact group compared to 67.8% in the highest contact group. They also had lower volumes in areas of the brain such as the hippocampus and amygdala that play a role in memory and are affected by dementia.

The researchers took into account other factors that could affect brain volume, such as age, diabetes, smoking and exercise.

The socially isolated people also had more small areas of damage in the brain, called white matter lesions, than the people with frequent social contact. The percentage of intracranial volume made up of white matter lesions was 0.30 for the socially isolated group, compared to 0.26 for the most socially connected group.

The researchers found that symptoms of depression partly explained the relationship between social isolation and brain volumes. However, symptoms of depression accounted for only 15% to 29% of the association.

“While this study is a snapshot in time and does not determine that social isolation causes brain atrophy, some studies have shown that exposing older people to socially stimulating groups stopped or even reversed declines in brain volume and improved thinking and memory skills, so it’s possible that interventions to improve people’s social isolation could prevent brain volume loss and the dementia that often follows,” Ninomiya said.

Since the study involved only older Japanese people, a limitation is that the findings may not be generalisable to people of other ethnicities and younger people.

Source: American Academy of Neurology

Categories : Ageing Skeletal SystemTags :

Does Low Bone Density Predict an Increased Risk of Dementia?

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People who have low bone density may have an increased risk of developing dementia compared to people who have higher bone density, according to a study of over 3500 people published in Neurology. As an observational study, it only shows an association and cannot prove that low bone density causes dementia.

“Low bone density and dementia are two conditions that commonly affect older people simultaneously, especially as bone loss often increases due to physical inactivity and poor nutrition during dementia,” said study author Mohammad Arfan Ikram, MD, PhD, of the Erasmus University Medical Center in Rotterdam, Netherlands. “However, little is known about bone loss that occurs in the period leading up to dementia. Our study found that bone loss indeed already occurs before dementia and thus is linked to a higher risk of dementia.”

The study involved 3651 people in the Netherlands with an average age of 72 who did not have dementia at the start of the study. Over an average of 11 years of follow-up, 688 people or 19% developed dementia.

X-rays were used to identify bone density, and participants were interviewed every four to five years and completed physical tests such as bone scans and tests for dementia.

Of the 1211 people with the lowest total body bone density, 90 people developed dementia within 10 years, compared to 57 of the 1211 people with the highest bone density.

After adjusting for factors such as age, sex, education, other illnesses and medication use, and a family history of dementia, researchers found that within 10 years, people with the lowest total body bone density were 42% more likely to develop dementia than people in the highest group.

“Previous research has found factors like diet and exercise may impact bones differently as well as the risk of dementia,” Ikram added. “Our research has found a link between bone loss and dementia, but further studies are needed to better understand this connection between bone density and memory loss. It’s possible that bone loss may occur already in the earliest phases of dementia, years before any clinical symptoms manifest themselves. If that were the case, bone loss could be an indicator of risk for dementia and people with bone loss could be targeted for screening and improved care.”

A limitation of the study is that participants were primarily of European origin and age 70 or older at the start of the study, so these findings may vary in different races, ethnicities, and younger age groups.

Source: American Academy of Neurology