Anxiety associated with faster Alzheimer's disease onset

November 24, 2020

Science Daily/Radiological Society of North America

Anxiety is associated with an increased rate of progression from mild cognitive impairment to Alzheimer's disease, according to a study being presented at the annual meeting of the Radiological Society of North America (RSNA).

Alzheimer's disease represents a major public health crisis worldwide. The number of deaths from the disease has more than doubled since 2000, and it is currently the fifth-leading cause of death among individuals over 65 in the U.S.

Many people with Alzheimer's disease first suffer from mild cognitive impairment, a decline in cognitive abilities like memory and thinking skills that is more rapid than normally associated with aging. Anxiety has been frequently observed in patients with mild cognitive impairment, although its role in disease progression is not well understood.

"We know that volume loss in certain areas of the brain is a factor that predicts progression to Alzheimer's disease," said study senior author Maria Vittoria Spampinato, M.D., professor of radiology at the Medical University of South Carolina (MUSC) in Charleston. "In this study, we wanted to see if anxiety had an effect on brain structure, or if the effect of anxiety was independent from brain structure in favoring the progression of disease."

The study group included 339 patients, average age of 72 years, from the Alzheimer's Disease Neuroimaging Initiative 2 cohort. Each person had a baseline diagnosis of mild cognitive impairment; 72 progressed to Alzheimer's disease while 267 remained stable.

The researchers obtained brain MRIs to determine the baseline volumes of the hippocampus and the entorhinal cortex, two areas important to forming memories. They also tested for the presence of the ApoE4 allele, the most prevalent genetic risk factor for Alzheimer's disease. Anxiety was measured with established clinical surveys.

As expected, patients who progressed to Alzheimer's disease had significantly lower volumes in the hippocampus and the entorhinal cortex and greater frequency of the ApoE4 allele. Most notably though, the researchers found that anxiety was independently associated with cognitive decline.

"Mild cognitive impairment patients with anxiety symptoms developed Alzheimer's disease faster than individuals without anxiety, independently of whether they had a genetic risk factor for Alzheimer's disease or brain volume loss," said study first author Jenny L. Ulber, a medical student at MUSC.

The link between anxiety symptoms and a faster progression to Alzheimer's disease presents an opportunity for improving the screening and management of patients with early mild cognitive impairment, the researchers said.

"We need to better understand the association between anxiety disorders and cognitive decline," Dr. Spampinato said. "We don't know yet if the anxiety is a symptom -- in other words, their memory is getting worse and they become anxious -- or if anxiety contributes to cognitive decline. If we were able in the future to find that anxiety is actually causing progression, then we should more aggressively screen for anxiety disorders in the elderly."

"The geriatric population is routinely screened for depression in many hospitals, but perhaps this vulnerable population should also be assessed for anxiety disorders," Ulber added. "Middle-aged and elderly individuals with high level of anxiety may benefit from intervention, whether it be pharmacological or cognitive behavioral therapy, with the goal of slowing cognitive decline."

The study was based on MRI scans done at one point in time. For future research, the team would like to study MRIs obtained after the initial scan to better understand the connection between anxiety and brain structure.

"We're now interested in looking at changes over time to see if anxiety has an effect one way or the other on how fast the brain damage progresses," Dr. Spampinato said. "We will also take a closer look at gender differences in the association between anxiety and cognitive decline."

https://www.sciencedaily.com/releases/2020/11/201124092156.htm

Cocoa flavanols boost brain oxygenation, cognition in healthy adults

November 24, 2020

Science Daily/University of Illinois at Urbana-Champaign, News Bureau

The brains of healthy adults recovered faster from a mild vascular challenge and performed better on complex tests if the participants consumed cocoa flavanols beforehand, researchers report in the journal Scientific Reports. In the study, 14 of 18 participants saw these improvements after ingesting the flavanols.

Previous studies have shown that eating foods rich in flavanols can benefit vascular function, but this is the first to find a positive effect on brain vascular function and cognitive performance in young healthy adults, said Catarina Rendeiro, a researcher and lecturer in nutritional sciences at the University of Birmingham who led the research with University of Illinois at Urbana-Champaign psychology professors Monica Fabiani and Gabriele Gratton.

"Flavanols are small molecules found in many fruits and vegetables, and cocoa, too," Rendeiro said. "They give fruits and vegetables their bright colors, and they are known to benefit vascular function. We wanted to know whether flavanols also benefit the brain vasculature, and whether that could have a positive impact on cognitive function."

The team recruited adult nonsmokers with no known brain, heart, vascular or respiratory disease, reasoning that any effects seen in this population would provide robust evidence that dietary flavanols can improve brain function in healthy people.

The team tested the 18 participants before their intake of cocoa flavanols and in two separate trials, one in which the subjects received flavanol-rich cocoa and another during which they consumed processed cocoa with very low levels of flavanols. Neither the participants nor researchers knew which type of cocoa was consumed in each of the trials. This double-blind study design prevents researchers' or participants' expectations from affecting the results.

About two hours after consuming the cocoa, participants breathed air with 5% carbon dioxide -- about 100 times the normal concentration in air. This is a standard method for challenging brain vasculature to determine how well it responds, Gratton said.

The body typically reacts by increasing blood flow to the brain, he said.

"This brings in more oxygen and also allows the brain to eliminate more carbon dioxide," he said.

With functional near-infrared spectroscopy, a technique that uses light to capture changes in blood flow to the brain, the team measured oxygenation in the frontal cortex, a brain region that plays a key role in planning, regulating behavior and decision-making.

"This allows you to measure how well the brain defends itself from the excess carbon dioxide," Fabiani said.

Researchers also challenged participants with complex tasks that required them to manage sometimes contradictory or competing demands.

Most of the participants had a stronger and faster brain oxygenation response after exposure to cocoa flavanols than they did at baseline or after consuming cocoa lacking flavanols, the researchers found.

"The levels of maximal oxygenation were more than three times higher in the high-flavanol cocoa versus the low-flavanol cocoa, and the oxygenation response was about one minute faster," Rendeiro said.

After ingesting the cocoa flavanols, participants also performed better on the most challenging cognitive tests, correctly solving problems 11% faster than they did at baseline or when they consumed cocoa with reduced flavanols. There was no measurable difference in performance on the easier tasks, however.

"This suggests that flavanols might only be beneficial during cognitive tasks that are more challenging," Rendeiro said.

Participants varied in their responses to cocoa flavanols, the researchers found.

"Although most people benefited from flavanol intake, there was a small group that did not," Rendeiro said. Four of the 18 study subjects had no meaningful differences in brain oxygenation response after consuming flavanols, nor did their performance on the tests improve.

"Because these four participants already had the highest oxygenation responses at baseline, this may indicate that those who are already quite fit have little room for improvement," Rendeiro said. "Overall, the findings suggest that the improvements in vascular activity after exposure to flavanols are connected to the improvement in cognitive function."

https://www.sciencedaily.com/releases/2020/11/201124092154.htm

The long road to dementia

November 17, 2020

Science Daily/DZNE - German Center for Neurodegenerative Diseases

Alzheimer's disease develops over decades. It begins with a fatal chain reaction in which masses of misfolded beta-amyloid proteins are produced that in the end literally flood the brain. Researchers including Mathias Jucker from the Hertie Institute for Clinical Brain Research (HIH) in Tübingen and the German Center for Neurodegenerative Diseases (DZNE) show in the journal Nature Neuroscience that this chain reaction starts much earlier in mice than commonly assumed. This means that in addition to the well-known early phase of the disease with protein deposits but without symptoms of dementia, there is an even earlier phase in which the chain reaction is triggered by invisible tiny seeds of aggregation. If this is confirmed to occur also in humans, a treatment addressing the causes of disease would have to prevent this process. The scientists have already identified an antibody that might accomplish this.

To this end, they searched among the already known antibodies directed against misfolded beta-amyloid proteins for antibodies that can recognize and possibly also eliminate these early seeds of aggregation that currently escape biochemical detection. Of the six antibodies investigated, only aducanumab had an effect: Transgenic mice that were treated for only 5 days before the first protein deposits manifested, later on in life showed only half of the usual amount of deposits in their brains. "This acute antibody treatment obviously removes seeds of aggregation, and the generation of new seeds takes quite some time, so that much less deposits are formed in the weeks and months after the treatment." Mathias Jucker commented on the findings. "Indeed, the mice had only half the brain damage six months after this acute treatment."

Although research on Alzheimer's has been dealing with seeds of aggregation for quite some time, nobody really knows what they look like. They are currently only defined by their role as triggers for this fatal chain reaction. In this respect, they are similar to so-called prions that cause BSE in cattle, scrapie in sheep and Creutzfeldt-Jakob disease in humans. Pathogenic prions force their correctly folded peers into their abnormal shape. Jucker and coworkers therefore used the antibody aducanumab to learn more about the structure of the seeds of aggregation. They were able to show that aducanumab recognizes protein aggregates, but not individual beta-amyloid chains. The scientists now hope to use the antibody as a fishhook to isolate and better describe these seeds of aggregation.

"Our results suggest that we need to focus more on this very early phase of Alzheimer's and look for biomarkers for it. We also need more antibodies that recognize different types of the seeds of aggregation and help us to understand how they trigger the chain reaction and how they can be used for therapy," Jucker said.

There is currently consensus that treatment of Alzheimer's disease must begin earlier, not when memory decline has already begun. However, the results of the Tübingen scientists are now redefining the term "earliness" in mice. Until now, the phase with protein deposits but without symptoms of dementia has been considered to be "early." The new studies suggest that a treatment of Alzheimer's that addresses the causes should start much earlier.

https://www.sciencedaily.com/releases/2020/11/201117113056.htm

Link between Alzheimer's disease and gut microbiota is confirmed

November 13, 2020

Science Daily/Université de Genève

In recent years, the scientific community has suspected that the gut microbiota plays a role in the development of the disease. A team now confirms the correlation, in humans, between an imbalance in the gut microbiota and the development of amyloid plaques in the brain, which are at the origin of Alzheimer's disease.

Alzheimer's disease is the most common cause of dementia. Still incurable, it directly affects nearly one million people in Europe, and indirectly millions of family members as well as society as a whole. In recent years, the scientific community has suspected that the gut microbiota plays a role in the development of the disease. A team from the University of Geneva (UNIGE) and the University Hospitals of Geneva (HUG) in Switzerland, together with Italian colleagues from the National Research and Care Center for Alzheimer's and Psychiatric Diseases Fatebenefratelli in Brescia, University of Naples and the IRCCS SDN Research Center in Naples, confirm the correlation, in humans, between an imbalance in the gut microbiota and the development of amyloid plaques in the brain, which are at the origin of the neurodegenerative disorders characteristic of Alzheimer's disease. Proteins produced by certain intestinal bacteria, identified in the blood of patients, could indeed modify the interaction between the immune and the nervous systems and trigger the disease. These results, to be discovered in the Journal of Alzheimer's Disease, make it possible to envisage new preventive strategies based on the modulation of the microbiota of people at risk.

The research laboratory of neurologist Giovanni Frisoni, director of the HUG Memory Centre and professor at the Department of Rehabilitation and Geriatrics of the UNIGE Faculty of Medicine, has been working for several years now on the potential influence of the gut microbiota on the brain, and more particularly on neurodegenerative diseases. "We have already shown that the gut microbiota composition in patients with Alzheimer's disease was altered, compared to people who do not suffer from such disorders," he explains. "Their microbiota has indeed a reduced microbial diversity, with an over-representation of certain bacteria and a strong decrease in other microbes. Furthermore, we have also discovered an association between an inflammatory phenomenon detected in the blood, certain intestinal bacteria and Alzheimer's disease; hence the hypothesis that we wanted to test here: could inflammation in the blood be a mediator between the microbiota and the brain? "

The brain under influence

Intestinal bacteria can influence the functioning of the brain and promote neurodegeneration through several pathways: they can indeed influence the regulation of the immune system and, consequently, can modify the interaction between the immune system and the nervous system. Lipopolysaccharides, a protein located on the membrane of bacteria with pro-inflammatory properties, have been found in amyloid plaques and around vessels in the brains of people with Alzheimer's disease. In addition, the intestinal microbiota produces metabolites -- in particular some short-chain fatty acids -- which, having neuroprotective and anti-inflammatory properties, directly or indirectly affect brain function.

"To determine whether inflammation mediators and bacterial metabolites constitute a link between the gut microbiota and amyloid pathology in Alzheimer's disease, we studied a cohort of 89 people between 65 and 85 years of age. Some suffered from Alzheimer's disease or other neurodegenerative diseases causing similar memory problems, while others did not have any memory problems," reports Moira Marizzoni, a researcher at the Fatebenefratelli Center in Brescia and first author of this work. "Using PET imaging, we measured their amyloid deposition and then quantified the presence in their blood of various inflammation markers and proteins produced by intestinal bacteria, such as lipopolysaccharides and short-chain fatty acids."

A very clear correlation 

"Our results are indisputable: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain," explains Moira Marizzoni. "Indeed, high blood levels of lipopolysaccharides and certain short-chain fatty acids (acetate and valerate) were associated with both large amyloid deposits in the brain. Conversely, high levels of another short-chain fatty acid, butyrate, were associated with less amyloid pathology."

This work thus provides proof of an association between certain proteins of the gut microbiota and cerebral amyloidosis through a blood inflammatory phenomenon. Scientists will now work to identify specific bacteria, or a group of bacteria, involved in this phenomenon.

A strategy based on prevention 

This discovery paves the way for potentially highly innovative protective strategies -- through the administration of a bacterial cocktail, for example, or of pre-biotics to feed the "good" bacteria in our intestine. "However, we shouldn't be too quick to rejoice," says Frisoni. "Indeed, we must first identify the strains of the cocktail. Then, a neuroprotective effect could only be effective at a very early stage of the disease, with a view to prevention rather than therapy. However, early diagnosis is still one of the main challenges in the management of neurodegenerative diseases, as protocols must be developed to identify high-risk individuals and treat them well before the appearance of detectable symptoms." This study is also part of a broader prevention effort led by the UNIGE Faculty of Medicine and the HUG Memory Centre.

https://www.sciencedaily.com/releases/2020/11/201113124042.htm

Positive outlook predicts less memory decline

October 29, 2020

Science Daily/Association for Psychological Science

We may wish some memories could last a lifetime, but many physical and emotional factors can negatively impact our ability to retain information throughout life.

A new study published in the journal Psychological Science found that people who feel enthusiastic and cheerful -- what psychologists call "positive affect" -- are less likely to experience memory decline as they age. This result adds to a growing body of research on positive affect's role in healthy aging.

A team of researchers analyzed data from 991 middle-aged and older U.S. adults who participated in a national study conducted at three time periods: between 1995 and 1996, 2004 and 2006, and 2013 and 2014.

In each assessment, participants reported on a range of positive emotions they had experienced during the past 30 days. In the final two assessments, participants also completed tests of memory performance. These tests consisted of recalling words immediately after their presentation and again 15 minutes later.

The researchers examined the association between positive affect and memory decline, accounting for age, gender, education, depression, negative affect, and extraversion.

"Our findings showed that memory declined with age," said Claudia Haase, an associate professor at Northwestern University and senior author on the paper. "However, individuals with higher levels of positive affect had a less steep memory decline over the course of almost a decade," added Emily Hittner, a PhD graduate of Northwestern University and the paper's lead author.

Areas of future research might address the pathways that could connect positive affect and memory, such as physical health or social relationships.

https://www.sciencedaily.com/releases/2020/10/201029135501.htm

Link between sleep apnea and increased risk of dementia

November 11, 2020

Science Daily/Monash University

A new study by Monash University has found that obstructive sleep apnea (OSA) has been linked to an increased risk of dementia.

The study, published in the Journal of Alzheimer's Disease, and led by Dr Melinda Jackson from the Turner Institute for Brain and Mental Health, found that severe OSA is linked to an increase in a protein, called beta-amyloid, that builds up on the walls of the arteries in the brain and increases the risk of dementia.

The study involved 34 individuals with recently diagnosed untreated OSA and 12 individuals who were asymptomatic for sleep disorders. It explored associations between brain amyloid burden using a PET brain scan, and measures of sleep, demographics and mood.

The OSA group recorded a higher amyloid burden, poorer sleep efficiency and less time spent in stage N3 sleep (a regenerative period where your body heals and repairs itself).

OSA is a common sleep disorder, affecting about 1 billion people worldwide and is caused by the collapse of the airway during sleep, resulting in intermittent dips in oxygen levels and arousals from sleep.

"The significance of finding the association between increased brain amyloid in patients with OSA will allow for further research to explore in more detail the implications of treating OSA for reducing dementia risk," Dr Jackson said.

https://www.sciencedaily.com/releases/2020/11/201111104918.htm

Why protecting the brain against infection takes guts

November 4, 2020

Science Daily/University of Cambridge

The brain is uniquely protected against invading bacteria and viruses, but its defence mechanism has long remained a mystery. Now, a study in mice, confirmed in human samples, has shown that the brain has a surprising ally in its protection: the gut.

The brain is arguably the most important organ in the body, as it controls most other body systems and enables reasoning, intelligence, and emotion. Humans have evolved a variety of protective measures to prevent physical damage to the brain: it sits in a solid, bony case -- the skull -- and is wrapped in three layers of watertight tissue known as the meninges.

What has been less clear is how the body defends the brain from infection. Elsewhere in the body, if bacteria or viruses enter the bloodstream, our immune system kicks in, with immune cells and antibodies that target and eliminate the invader. However, the meninges form an impermeable barrier preventing these immune cells from entering the brain.

In research published today in Nature, a team led by scientists at the University of Cambridge, UK, and the National Institute of Health, USA, have found that the meninges are home to immune cells known as plasma cells, which secrete antibodies. These cells are specifically positioned next to large blood vessels running within the meninges allowing them to secrete their antibody 'guards' to defend the perimeter of the brain. When the researchers looked at the specific type of antibody produced by these cells, they got a surprise -- the antibody they observed is normally the type found in the intestine.

Plasma cells are derived from a particular type of immune cell known as a B cell. Every B cell has an antibody on its surface that is unique to that cell. If an antigen (the part of a bacterium or virus that triggers an immune response) binds to that surface antibody, the B cell becomes activated: it will divide to make new offspring that also recognise that same antigen.

During division, the B cell introduces a mutation into the antibody gene so that one amino acid is changed and its binding characteristics are slightly different. Some of these B cells will now produce antibodies that enable better binding to the pathogen -- these go on to expand and multiply; B cells whose antibodies are less good at binding die off. This helps ensure the body produces the best antibodies for targeting and destroying particular antigens.

Normally, the antibodies found in the blood are a type known as Immunoglobulin G (IgG), which are produced in the spleen and bone marrow -- these antibodies protect the inside of the body. However, the antibodies found in the meninges were Immunoglobulin A (IgA), which are usually made in the gut lining or in the lining of the nose or lungs -- these protect mucosal surfaces, the surfaces that interface with the outside environment.

The team were able to sequence the antibody genes in B cells and plasma cells in the gut and meninges and show that they were related. In other words, the cells that end up in the meninges are those that have been selectively expanded in the gut, where they have recognised particular pathogens.

"The exact way in which the brain protects itself from infection, beyond the physical barrier of the meninges, has been something of a mystery, but to find that an important line of defence starts in the gut was quite a surprise," said lead scientist Professor Menna Clatworthy from the Department of Medicine and CITIID at the University of Cambridge and the Wellcome Sanger Institute.

"But actually, it makes perfect sense: even a minor breach of the intestinal barrier will allow bugs to enter the blood stream, with devastating consequences if they're able to spread into the brain. Seeding the meninges with antibody-producing cells that are selected to recognise gut microbes ensures defence against the most likely invaders."

The team made the discovery using mice, which are commonly used to study physiology as they share many characteristics similar to those found in the human body. They showed that when the mice had no bacteria in their gut, the IgA-producing cells in the meninges were absent, showing that these cells actually originate in the intestine where they are selected to recognise gut microbes before taking up residence in the meninges. When the researchers removed the plasma cells in the meninges -- and hence no IgA was present to trap bugs -- microbes were able to spread from the bloodstream into the brain.

The team confirmed the presence of IgA cells in the human meninges by analysing samples that were removed during surgery, showing that this defence system is likely to play an important role in defending humans from infections of the central nervous system -- meningitis and encephalitis.

https://www.sciencedaily.com/releases/2020/11/201104121444.htm

Western diet impairs odor-related learning and olfactory memory in mice

November 4, 2020

Science Daily/American Chemical Society

Problems with the sense of smell appear to be an early indicator of cognitive decline in people with type 2 diabetes. However, it's unknown whether factors such as diet and obesity play a role in who develops these symptoms. Now, researchers reporting in ACS Chemical Neuroscience found that mice fed a moderate-fat, high-sugar chow (simulating a Western diet) showed a faster decline in their ability to learn and remember new odors.

Some people with type 2 diabetes (T2D) show signs of olfactory dysfunction, including problems with detecting, discriminating or recalling odors, or even a complete loss of smell. These symptoms are strongly associated with cognitive impairment, and evidence suggests they could be an early indicator of the condition in people with T2D. Obesity, which is the main risk factor for T2D, has also been associated with olfactory dysfunction, but the impact of obesity on the sense of smell specifically in these patients is unclear, as studies have produced conflicting results. Also, it's unknown whether certain nutrients in the diet, such as fat and sugar, affect the sense of smell. To find out, Grazyna Lietzau, Cesare Patrone and colleagues wanted to compare the effects of two diets on different olfactory functions in mice: a high-fat, moderate-sugar diet (HFD); and a moderate-fat, high-sugar diet (similar to a Western diet, WD). In mice, both diets cause obesity and T2D-like features.

At one, three and eight months, the team performed tests to assess different olfactory functions in the mice. By eight months, both the HFD- and WD-fed mice had impaired odor detection, odor-related learning and olfactory memory compared with the control mice. However, the WD-fed mice had a faster decline in the latter two abilities, showing olfactory dysfunction as early as 3 months after beginning the diet. These findings indicate that a high dietary sugar content, rather than hyperglycemia or weight gain, is linked with early deterioration of olfactory functions related to learning and memory, the researchers say. How sugar causes these effects, and whether they are also seen in humans, the researchers acknowledge, remains to be determined.

https://www.sciencedaily.com/releases/2020/11/201104103713.htm

New method shows great potential for the treatment of Alzheimer's disease

November 3, 2020

Science Daily/Uppsala University

In Alzheimer's disease, a protein (peptide) forms clumps in the brain and causes sufferers to lose their memory. In a recently published article, a research group at Uppsala University described a new treatment method that increases the body's own degradation of the building blocks that lead to these protein clumps.

In Alzheimer's disease, the peptide amyloid-beta begins to form clumps in the brain. This process is called aggregation and the clumps so created are called aggregates. The treatment methods for Alzheimer's disease that are currently in clinical trials are attempts to bind to these disease-causing aggregates. But they are unable to bind to the smallest aggregates, which many now believe are the most toxic to neurons.

The treatment method developed in the new Uppsala research study using mice degrades the building blocks from which these aggregates form before they have a chance to aggregate. This treatment method therefore reduces the formation of all types of aggregates.

It has long been known that the peptide somatostatin, which was used by the researchers in the Uppsala group, can activate the body's own degradation of amyloid-beta, which is the peptide that forms the aggregates. However, it has not been possible to use somatostatin as a drug in the past because it has a very short half-life in the blood of only a few minutes, and does not cross the blood-brain barrier into the brain where the aggregates are formed.

"So to be able to use somatostatin as a treatment, we fused it to a brain transport protein which allows the somatostatin to enter the brain. This has proved very effective. When we used the transport protein, we also saw that the time that the somatostatin remained in the brain increased to several days, which is fantastic," says Fadi Rofo, doctoral student at the Department of Pharmaceutical Biosciences and the study's first author.

In the study, the researchers saw the greatest effect in hippocampus, the part of the brain that forms memories and the first part to be affected by Alzheimer's disease.

"The fact that we have seen that the effect is most evident in the hippocampus in particular is very good. Our hope is that this method will be able to act in a very targeted way and have few side effects, which have been a problem in other studies," says Greta Hultqvist, assistant professor at the Department of Pharmaceutical Biosciences, who led the research study.

The study was conducted in mice, but the researchers believe that somatostatin would have the same effect in humans and that this type of treatment could be more effective than those trialled so far.

https://www.sciencedaily.com/releases/2020/11/201103104719.htm

Hard physical work may significantly increase the risk of dementia

October 26, 2020

Science Daily/University of Copenhagen The Faculty of Health and Medical Sciences

Men in jobs with hard physical work have a higher risk of developing dementia compared to men doing sedentary work, new research reveals. The researchers therefore urge the health authorities to make their recommendations concerning physical activity more specific.

The muscles and joints are not the only parts of the body to be worn down by physical work. The brain and heart suffer too. A new study from the University of Copenhagen shows that people doing hard physical work have a 55-per cent higher risk of developing dementia than those doing sedentary work. The figures have been adjusted for lifestyle factors and lifetime, among other things.

The general view has been that physical activity normally reduces the risk of dementia, just as another study from the University of Copenhagen recently showed that a healthy lifestyle can reduce the risk of developing dementia conditions by half.

Here the form of physical activity is vital, though, says associate professor Kirsten Nabe-Nielsen from the Department of Public Health at the University of Copenhagen.

"Before the study we assumed that hard physical work was associated with a higher risk of dementia. It is something other studies have tried to prove, but ours is the first to connect the two things convincingly," says Kirsten Nabe-Nielsen, who has headed the study together with the National Research Centre for the Working Environment with help from Bispebjerg-Frederiksberg Hospital.

"For example, the WHO guide to preventing dementia and disease on the whole mentions physical activity as an important factor. But our study suggests that it must be a 'good' form of physical activity, which hard physical work is not. Guides from the health authorities should therefore differentiate between physical activity in your spare time and physical activity at work, as there is reason to believe that the two forms of physical activity have opposite effects," Kirsten Nabe-Nielsen says and explains that even when you take smoking, blood pressure, overweight, alcohol intake and physical activity in one's spare time into account, hard physical work is associated with an increased occurrence of dementia.

One of the study's co-authors is Professor MSO Andreas Holtermann from the National Research Centre for the Working Environment. He hopes the dementia study from the University of Copenhagen will contribute to shine a spotlight on the importance of prevention, as changes in the brain begin long before the person leaves the labour market.

"A lot of workplaces have already taken steps to improve the health of their staff. The problem is that it is the most well-educated and resourceful part of the population that uses these initiatives. Those with a shorter education often struggle with overweight, pain and poor physical fitness, even though they take more steps during the day and to a larger extent use their body as a tool. For workmen, it is not enough for example to avoid heavy lifts if they wish to remain in the profession until age 70. People with a shorter education doing manual labour also need to take preventive steps by strengthening the body's capacity via for example exercise and strength training," he says.

The study is based on data from the Copenhagen Male Study (CMS), which included 4,721 Danish men, who back in the 1970s reported data on the type of work they did on a daily basis. The study included 14 large Copenhagen-based companies, the largest being DSB, the Danish Defence, KTAS, the Postal Services and the City of Copenhagen.

Through the years, the researchers have compiled health data on these men, including data on the development of dementia conditions.

According to Kirsten Nabe-Nielsen, previous studies have suggested that hard physical work may have a negative effect on the heart blood circulation and thus also on the blood supply to the brain. This may for example lead to the development of cardiovascular diseases like high blood pressure, blood clots in the heart, heart cramps and heart failure.

The National Research Centre for the Working Environment continues to work on the results with a view to identifying healthier ways of doing hard physical work. They have therefore begun to collect data from social and healthcare assistants, child care workers and packing operatives, among others, in order to produce interventions meant to organise hard physical work in such a way that it has an 'exercise effect'.

They thus hope to see companies successfully change work procedures, ensuring for example that heavy lifts will have a positive effect rather than wear down the workers. The results will be published on an ongoing basis.

https://www.sciencedaily.com/releases/2020/10/201026114240.htm