Older people who have “mental lapses,” or times when their thinking seems disorganized or illogical or when they stare into space, may be more likely to have Alzheimer’s disease than people who do not have these lapses, according to a study published in the January 19, 2010, print issue of Neurology®, the medical journal of the American Academy of Neurology.

These mental lapses, also called cognitive fluctuations, are common in a type of dementia called dementia with Lewy bodies, but researchers previously did not know how frequently they occurred in people with Alzheimer’s disease and, equally important, what effect fluctuations might have on their thinking abilities or assessment scores.

The study involved 511 people with an average age of 78. Researchers interviewed the participant and a family member, evaluated the participants for dementia and tested their memory and thinking skills.

People with three or four of the following symptoms met the criteria for having mental lapses:

– Feeling drowsy or lethargic all the time or several times per day despite getting enough sleep the night before

– Sleeping two or more hours before 7 p.m.

– Having times when the person’s flow of ideas seems disorganized, unclear, or not logical — Staring into space for long periods

A total of 12 percent of the people with dementia in the study had mental lapses. Of 216 people with very mild or mild dementia, 25 had mental lapses. Of the 295 people with no dementia, only two had mental lapses.

Those with mental lapses were 4.6 times more likely to have dementia than those without mental lapses. People with mental lapses also tended to have more severe Alzheimer’s symptoms and perform worse on tests of memory and thinking skills than people who did not have lapses.

“When older people are evaluated for problems with their thinking and memory, doctors should consider also assessing them for these mental lapses,” said senior study author James E. Galvin.

Cognitive fluctuations, or episodes when train of thought temporarily is lost, are more likely to occur in older persons who are developing Alzheimer’s disease than in their healthy peers, according to scientists at Washington University School of Medicine in St. Louis.

Cognitive fluctuations include excessive daytime sleepiness, staring into space and disorganized or illogical thinking.

“If you have these lapses, they don’t by themselves mean that you have Alzheimer’s,” says senior author James Galvin, M.D., a Washington University neurologist at Barnes-Jewish Hospital. “Such lapses do occur in healthy older adults. But our results suggest that they are something your doctor needs to consider if he or she is evaluating you for problems with thinking and memory.”

The study appears in the Jan. 19 issue of Neurology.

Earlier research had associated cognitive fluctuations with another form of dementia called dementia with Lewy bodies, but little information existed on the potential for links between Alzheimer’s and such lapses.

Data for the new study came from Alzheimer’s disease evaluations of 511 older adults with memory problems. Average age of the participants was 78. Researchers gave participants standard tests of thinking and memory skills. They also interviewed participants and a family member, checking for prolonged daytime sleepiness, drowsiness or lethargy in spite of sufficient sleep the night before, periods of disorganized or illogical thinking, or instances of staring into space for long periods of time.

A total of 12 percent of the participants had at least three of these symptoms, meeting the criteria for cognitive fluctuations. Those with mental lapses were 4.6 times more likely to be diagnosed with Alzheimer’s. Of 216 diagnosed with very mild or mild dementia, 25 had mental lapses; of the 295 with no dementia, only two had mental lapses. In addition, participants with mental lapses did worse on tests of memory and thinking than people without mental lapses.

“We have some ideas about why the biology of dementia with Lewy bodies causes these mental lapses, but nothing comparable for Alzheimer’s,” Galvin says. “It’s possible that some of the patients who were diagnosed with Alzheimer’s disease in this study will go on to develop dementia with Lewy bodies, but at the time of the study, they weren’t showing any of the Lewy body dementia’s core features.”

Lewy body dementia, which causes clumps of proteins known as Lewy bodies to form in neurons, is thought to be the second most common form of dementia after Alzheimer’s. Clinically, it can overlap with Parkinson’s disease and Alzheimer’s disease. Pronounced cognitive fluctuations are a hallmark of Lewy body dementia, as are visual hallucinations and rapid eye movement behavior sleep disorder.

First it was exercise on prescription, then it was arts on prescription, soon it could be singing on prescription, as the clinical evidence builds up, and as more and more projects promote the benefits of singing to health and wellbeing, both for those in generally good health and those with physical and mental health problems, or who find themselves socially excluded or isolated.

Consider this scenario: you go to your doctor and instead of coming away clutching a prescription for a bottle of pills or a referral to a counsellor, you have a leaflet about a local singing group. This is the vision of Grenville Hancox MBE, Director of the Sidney De Haan Research Centre for Arts and Health based at Canterbury Christ Church University in the UK.

Imagine the day, says Hancox, when your GP says: “Go and have a sing with that lot down the road” instead of “take these pills three times a day!”

Exercise on prescription schemes have been gaining ground all across the UK over the last decade, to the point where there are now national standards for GP exercise referral schemes. And more recently, Arts on prescription appeas to be growing too, as exemplified with projects by Healing Arts on the Isle of Wight (Time Being) and East Kent Health Promotion Department.

But the idea that involvement in group singing can benefit health and wellbeing is also growing; the Sidney De Haan Research Centre lists several established projects:

* Singing for the Brain, East Berkshire Alzheimer’s Society.
* Sing Your Heart Out, Hellesdon Hospital, Norwich
* Serendipity Singing for Health Choir, Midlothian
* Singing is Good for You, Voices Foundation
* Singing Medicine, Birmingham Children’s Hospital
* Sounds Lively Choir, Isle of Wight

And at Sidney De Haan they are also working on “providing a convincing rationale” for a practical scheme for Singing on Prescription that “can be tested for its effectiveness through controlled evaluation”, according to a statement on their website.

Chreanne Montgomery-Smith, a support and development officer with the West Berkshire branch of the Alzheimer’s Society founded Singing for the Brain in 2002.

She wrote in 2006 in the Journal of Dementia Care she believed there were seven therapeutic outcomes from singing in a group that were of particular benefit to people with Alzheimer’s, although one can see how these might apply to people in many other situations too:

* Communication: the singing warm up (exercises involving whole body, neck, shoulders, jaw, face, lips, tongue, diaphragm) strengthen neural connections to the voice and breath, and doing them in a group is fun and non-threatening compared to doing it one-to-one.

* Cognition: singing challenges concentration and attention, especially when techniques such as singing from memory, combining rhythm with action, and mental substitution are used.

* Engagement: for example making eye contact across the group and expressing to the audience the emtional message of a song.

* Confidence: joining a singing group can build confidence from the gradual gaining of skills, vocal strength and the thrill of being able to remember so much. Fear of failure is lessened when everyone is in the same situation and group members laugh together when they make mistakes.

* Relationships: in a group with a shared purpose and a leader that treats everyone equally, there is a chance to get away from those situations where you are a person with a condition, and relate to people in a different way. You make friends, find and give support, and express frustrations and emotions about relationship problems in many songs that cover those areas of life (Montgomery-Smith gives the example of “A Fine Romance” as a “safe” way to express one’s frustration with a life partner).

* Empowerment: by leading singing rounds, taking responsibility for setting out chairs, getting scores ready, writing lyrics, greeting new members, there is a wide range of roles that help people feel more in charge of themselves and their lives and what they contribute to a group. Former carers also benefit: giving them a new role when they have lost a major one.

* Exercise and stress reduction: an excellent way to reduce stress is learning to exhale; it increases circulation as the diaphragm massages internal organs. It releases endorphins and improves the immune response, according to research that showed immune system changes in salivary Immunoglobulin A and Cortisol.
Dr Nicholas Hopkinson, who is leading the study at the Royal Brompton, said the study was trialling a novel approach with teaching breathing techniques. Often, when you try to teach a patient directly, they become even more conscious of the need to breath correctly, and this can make things worse, he said.

By learning to sing, the patients are being approached more “from the side”, said Hopkinson, they are learning to “use their voice and their breathing for a different purpose, for singing, hoping that the skills that they gain through that in terms of controlling their breathing will actually be helpful in day-to-day life,” he told the BBC.

Voice trainer Phoene Cave said she saw improvements in breathing control after just one session.

“I’m helping them to become aware of their bodies in a way that they’re not used to,” she told the BBC.

The class always starts with vocal exercises, including collective sighing, buzzing noises, and making “ha-ha” sounds up and down the scales.

Research suggests that regular singing practice also helps people with dyspnea, improves mood and reduces depression.

John Townsend, a patient in the Royal Brompton and member of the singing group, said that the evidence was plain to see. He explained how when they start their lessons, people from the wards just come along and join in:

“You can hear it all the way along the wards. And people are cheerful.”

“They become cheerful and they’re not even singing. So of course it’s a great thing,” said Townsend.

We all have at one time or another experienced the typical signs of an infection: the fever, the listlessness, the lack of appetite. They are orchestrated by the brain in response to circulating cytokines, the signaling molecules of the immune system. But just how cytokines’ reach extends beyond the almost impenetrable blood-brain barrier has been the topic of much dispute.

In their latest study, researchers at the Salk Institute for Biological Studies describe how, depending on the nature of the stimulus, resident macrophages lined up along the blood-brain barrier play opposing roles in the transmission of immune signals into the brain.

“These macrophages act as accelerators to enlist the brain’s participation in dealing with immune insults, but when necessary slam on the brakes to prevent the central inflammatory response from going overboard,” explains postdoctoral researcher Jordi Serrats, Ph.D., who co-led the study with Jennifer C. Schiltz, Ph.D., formerly a postdoctoral researcher in the Salk’s Neuronal Structure and Function Laboratory and now an assistant professor at the Uniformed Services University in Bethesda, Maryland.

The Salk researchers’ findings, which are published in the Jan. 14, 2010 edition of the journal Neuron, may pave the way for novel therapies for sufferers of chronic neurodegenerative diseases, such as Amyotrophic Lateral Sclerosis (ALS), Parkinson’s, Alzheimer’s and prion diseases, in which central inflammatory mechanisms play an important role.

“The fact that we have identified a potent anti-inflammatory mechanism in the brain presents a new target to intervene in the wide range of central nervous system diseases that possess an inflammatory component,” says the study’s senior author, Paul E. Sawchenko, Ph.D., a professor in the Neuronal Structure and Function Laboratory.

In response to an infection, inflammatory cytokines such as interleukin-1 are generated at the site of infection. These cytokines circulate in the blood and communicate with neurons in the brain to engage the hypothalamo-pituitary-adrenal (HPA) axis, an integral part of the brain’s stress response machinery. The HPA axis involves the interaction of the hypothalamus, the pituitary gland, which sits just below the hypothalamus and the adrenal glands at the top of the kidneys.

Like a central command center, the hypothalamus sends out corticotropin-releasing factor, which stimulates the pituitary gland to secrete adrenocorticotropic hormone. The latter signals the adrenal glands to ramp up the production of glucocorticoids, which mobilize energy reserves to cope with inflammatory insults. But they also act as very powerful immunosuppressants preventing excessive cytokine production and immune cell proliferation.

“Cytokines are big molecules that don’t cross the blood-brain barrier freely,” says Sawchenko. “The question of how these molecules access the brain to trigger this whole array of adaptive responses such as fever, inactivity, sleepiness, and activation of the brain’s stress response machinery has been a nagging problem in the side of neuroimmunology for many years.”

Earlier research by Sawchenko and others suggested a vascular route whereby cytokines interact with vessel walls to generate secondary messengers, which then engage the relevant circuitry in the brain. Tightly packed endothelial cells, which line almost 400 miles of narrow capillaries throughout the brain, are perfectly positioned to record circulating immune signals but they require a very strong signal to become activated. Perivascular macrophages, on the other hand, are more sensitive but don’t have direct access to the bloodstream.

To disentangle the exact role of these two cell types, Serrats took advantage of the macrophages’ ability to engulf and ingest solid particles. He injected liposomes containing clodronate, a drug that can cause cell death, into the lateral cerebral ventricle. The liposomes were taken up by the macrophages, which were selectively killed off.

Without perivascular macrophages, the animals were unable to respond to blood-borne interleukin-1 and initiate the brain’s so-called acute phase responses, which help the body deal with the challenge at hand but also cause the familiar feeling of “being sick.” But to their surprise, the Salk researchers found that the same cells put a damper on the pro-inflammatory activities of endothelial cells, which form the lining of blood vessels and are only stirred to action-but very powerfully once they are-when they encounter lipopolysaccharide, a key component of the cell wall of certain bacteria.

“Many neurodegenerative diseases are worsened by systemic inflammation or infections,” says Sawchenko. “Once we identify the molecules that mediate the two-way communication between perivascular macrophages and endothelial cells we can develop strategies for managing the adverse health consequences of central inflammatory responses.”

An international team of researchers studying the long term effects of electromagnetic waves like those emitted by cell phones on mice were surprised to find they protected their brains against Alzheimer’s and even reversed the memory damage caused by the disease.

The study was the work of neuroscientists, electrical engineers, and neurologists from universities in the US, Japan and China, and is being published online on 7 January in the Journal of Alzheimer’s Disease. The study was led by University of South Florida (USF) researchers at Florida’s Alzheimer’s Disease Research Center (ADRC), a statewide project sponsored by the National Institute on Aging.

One of the hallmarks of Alzheimer’s disease is the accumulation of sticky deposits or plaques of beta-amyloid protein in the brain.

While it is not clear what role plaques play in Alzheimer’s, many experts believe they stop brain cells communicating with each other and also disrupt other processes that cells rely on to survive. Most treatments for Alzheimer’s try to target beta-amyloid protein.

In this study, researchers took mice genetically engineered to develop symptoms of Alzheimer’s disease, exposed them to cell phone waves and discovered the electromagnetic radiation prevented build up of amyloid protein in the brains of young mice, erased deposits of the protein in the brains of old Alzheimer’s mice, and also reversed memory damage.

Lead author of the study, USF research professor Dr Gary Arendash told the press that:

“It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer’s symptoms.”

“It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer’s mice.”

A USF statement describes the study as “highly-controlled”: the researchers were able to isolate the effects of cell phone exposure from other lifestyle factors like diet and exercise.

For the study the researchers used 96 mice, most of which where genetically altered to develop beta-amyloid plaques and memory problems mimicking Alzheimer’s disease as they got older (the “Alzheimer’s mice). The others were not genetically engineered in this way and acted as controls (the “normal” mice).

The researchers exposed both groups of mice: the ones genetically predisposed to develop Alzheimer’s and the normal controls, to an electromagnetic field like that generated by standard cell phones for two periods lasting one hour each every day for between seven and nine months.

To achieve this effect the researchers arranged the animals’s cages in a circle around an antenna generating the cell phone signal. All the animals were kept at the the same distance from the antenna and exposed to electromagnetic waves typically emitted by a cell phone pressed up against a human head, said the USF researchers in a statement.

The results showed that:

* Exposure started when they were young adults, ie before showing signs of memory impairment, appeared to protect the Alzheimer’s mice from becoming cognitively impaired.

* Exposed older Alzheimer’s mice performed as well on tests measuring memory and thinking skills as normal older mice without dementia.

* When older, previously unexposed Alzheimer’s mice already showing memory problems were exposed to the electromagnetic field, their memory impairment vanished.

* Normal mice exposed to the electromagnetic waves for several months showed above normal memory performance.

To assess the mice’s memory skills, the researchers adapted a test designed to assess mild cognitive impairment in humans.

“Since we selected electromagnetic parameters that were identical to human cell phone use and tested mice in a task closely analogous to a human memory test, we believe our findings could have considerable relevance to humans, said Arendash.

It took several months for the effects of the electromagnetic wave exposure to show in the mice: this suggests it would take years in humans.

Arendash and colleagues concluded that electromagnetic field exposure could be an effective, drug-free, non-invasive way to prevent and treat Alzheimer’s disease in humans.

They are now investigating the effect of different frequencies and strengths of electromagnetic radiation: eg will it be more or less rapid, and will the cognitive benefits be greater or less, than they found in this study.

Co-author of the study and major member of the USF team, Dr Chuanhai Cao, said:

“If we can determine the best set of electromagnetic parameters to effectively prevent beta-amyloid aggregation and remove pre-existing beta amyloid deposits from the brain, this technology could be quickly translated to human benefit against AD [Alzheimer's disease]“.

“Since production and aggregation of beta-amyloid occurs in traumatic brain injury, particularly in soldiers during war, the therapeutic impact of our findings may extend beyond Alzheimer’s disease,” said Cao.

When they monitored the mice during their one-hour exposures when the electromagnetic field was turned on, the researchers noticed that after several months, the brain temperature of the Alzheimer’s mice rose slightly; this did not happen in the normal mice.

Speculating on this observation in the light of the other results, the researchers suggest perhaps the temperature increase helped brain cells to release the newly-formed beta-amyloid plaques.

As an explanation for the improved memory function in the normal mice after months of exposure, they suggested perhaps the electromagnetic waves increased brain activity by boosting blood flow and energy metabolism in the brain.

“Our study provides evidence that long-term cell phone use is not harmful to brain,” said Cao, adding that:

“To the contrary, the electromagnetic waves emitted by cell phones could actually improve normal memory and be an effective therapy against memory impairment.”

Arendash said it will be a while yet before we know exactly what is going on: how the waves produce these beneficial effects on memory. But one thing is clear he said:

“The cognitive benefits of long-term electromagnetic exposure are real, because we saw them in both protection- and treatment-based experiments involving Alzheimer’s mice, as well as in normal mice.”

A diet rich in methionine, an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds, can possibly increase the risk of developing Alzheimer’s disease, according to a study by Temple researchers.

The researchers published their findings, titled “Diet-induced hyperhomocysteinemia increases Amyloid-β formation and deposition in a mouse model of Alzheimer’s disease,” in the journal Current Alzheimer Research

“When methionine reaches too high a level, our body tries to protect itself by transforming it into a particular amino acid called homocysteine,” said lead researcher Domenico Pratico, an associate professor of pharmacology in the School of Medicine. “The data from previous studies show even in humans

when the level of homocysteine in the blood is high, there is a higher risk of developing dementia. We hypothesized that high levels of homocysteine in an animal model of Alzheimer’s would accelerate the disease.”

Using a seven-month old mouse model of the disease, they fed one group an eight-month diet of regular food and another group a diet high in methionine. The mice were then tested at 15 months of age the equivalent of a 70-year-old human.

“We found that the mice with the normal diet had normal homocysteine levels, but the mice with the high methionine diet had significantly increased levels of homocysteine, very similar to human subjects with hyperhomocysteinemia,” said Praticò. “The group with the high methionine diet also had up to 40 percent more amyloid plaque in their brains, which is a measurement of how much Alzheimer’s disease has developed.

The researchers also examined capacity to learn a new task and found it diminished in the group with the diet high in methionine.

Still, Praticò emphasized, methionine is an essential amino acid for the human body and “stopping one’s intake of methionine won’t prevent Alzheimer’s. But people who have a diet high in red meat, for instance, could be more at risk because they are more likely to develop this high level of circulating homocysteine,” he said.

More than half of HIV patients experience memory problems and other cognitive impairments as they age, and doctors know little about the underlying causes. New research from Washington University School of Medicine in St. Louis suggests HIV-related cognitive deficits share a common link with Alzheimer’s-related dementia: low levels of the protein amyloid beta in the spinal fluid.

However, by analyzing biomarkers in the fluid surrounding the brain and spinal cord, the researchers report Dec. 8 in the journal Neurology, they could distinguish patients with HIV-related cognitive impairments from patients with mild Alzheimer’s disease. This is important because as patients with HIV age, some will develop cognitive deficits related to HIV and others to Alzheimer’s. New treatments in the pipeline to improve memory and thinking may not work for both conditions.

“HIV patients with cognitive dysfunction don’t have early Alzheimer’s – although some of the symptoms may be similar,” says lead author David Clifford, M.D., an authority on the neurological complications of HIV and director of Washington University’s AIDS Clinical Trials Unit. “The underlying biology of both conditions may be related to amyloid, and we think this clue can help us find the cause of cognitive impairment in HIV patients.

Cognitive dysfunction is a major problem among the estimated 1 million Americans living with HIV. The impairments are often mild but can affect a person’s daily life, relationships and ability to hold a job. They include difficulties with memory, processing complex information and making decisions. These problems are expected to worsen as HIV patients live longer, due to potent drug cocktails that keep the virus in check.

In the new research, the scientists looked at the spinal fluid of 49 HIV patients with cognitive impairments, 21 HIV patients with normal cognitive function, 68 patients with mild Alzheimer’s and 50 normal, healthy “controls.” The Alzheimer’s patients were older (average age 74) than the controls (average age 50), impaired HIV patients (average age 48) and cognitively normal HIV patients (average age 43).

They tested the spinal fluid for the presence of amyloid beta – the protein that folds and accumulates in the brains of Alzheimer’s patients and is thought to play a key role in driving the brain damage that characterizes the disease. They also looked at other biomarkers associated with Alzheimer’s, including tau, a protein found in tangled nerve fibers in Alzheimer’s patients.

When amyloid beta accumulates in the brains of Alzheimer’s patients, levels decrease in the spinal fluid, and Clifford and his colleagues expected to find low levels of the protein in samples of the Alzheimer’s patients they studied.

But they were surprised to find the same low levels in the spinal fluid of HIV patients with cognitive dysfunction. Both groups of patients had significantly lower amyloid beta levels than HIV patients without cognitive impairments and the normal controls. The lower levels are an indicator that amyloid beta in the brain alters the normal turnover of the protein in the body.

Although Australian and European researchers had uncovered a link between HIV-related cognitive deficits and amyloid beta in 2005 in a smaller study, Clifford thought that finding was an artifact and embarked on the current study largely to disprove it.

“I really did not expect the biology of HIV cognitive dysfunction to be related to Alzheimer’s,” Clifford says. “If you look at the brains of HIV patients with cognitive impairments, they don’t look like Alzheimer’s brains – they don’t have the same atrophy or a plethora of plaques and tangles characteristic of Alzheimer’s.”

But low amyloid beta is where the similarity to Alzheimer’s disease ends. The researchers found that patients with mild Alzheimer’s had significantly higher levels of tau than either group of HIV patients or normal controls – a finding that strongly suggests Alzheimer’s and HIV cognitive dysfunction are not one and the same, Clifford says.

He suspects the HIV-related cognitive impairment may be due to low levels of the virus that hide out in the brain, beyond the reach of drugs that can’t easily cross the blood-brain barrier. Another cause may be low-grade inflammation in the brain that is driven by the virus.

Almost all HIV patients in the study were taking anti-retroviral therapy. “I am almost certain the dementia in AIDS patients is linked to HIV and not to anti-retroviral drugs – we see it even in patients who haven’t received HIV therapy,” Clifford says. “However, the more subtle impairment may be in some way associated with a change in the way the body processes amyloid beta. This will certainly be an important area of future research.”

Dementia patients with a certain type of changes in their brain’s white matter are more likely to be apathetic than those who do not have these changes, reveals a patient study carried out by the Sahlgrenska Academy and Sahlgrenska University Hospital.

Changes in the brain’s white matter are common among the elderly and dementia patients, and often appear as blurred patches on CT and MRI images.

“A likely explanation for the changes is that the small blood vessels that supply the white matter are not working as they should,” says Michael Jonsson, PhD-student at the Sahlgrenska Academy and consultant psychiatrist at Sahlgrenska University Hospital’s memory clinic. “This results in that the long nerve fibres and their fatty sheaths degenerate.”

Apathy is one of the most common psychological problems associated with dementia. Just over half of all dementia patents are emotionally blunted and lack motivation and initiative. This new study shows that this apathy is far more common in patients who have the characteristic changes in the brain. This discovery suggests that there is a common biological reason behind this apathy, irrespective of which type of dementia a patient has. The changes are located deep in the brain and primarily affect the neural pathways that run from this part of the brain to the frontal lobes, which are important for taking the initiative and the ability to plan.

“Even though we think we know a bit about which pathways are affected in cases of apathy, we still need to find out more about the anatomy and chemistry behind the development of these symptoms,” says Jonsson. “This is vital if we are to develop medication to treat apathy.”

The study involved 176 patients with Alzheimer’s, vascular dementia or mixed dementia. 82 per cent of the patients with changes in their white matter were apathetic, while 58 per cent of all of the dementia patients were apathetic.

Given that apathy reduces quality of life for patients with dementia and increases the risk of institutionalisation, a great deal of research is under way to find a treatment. Treatments that do not involve medication, such as increased physical exercise, cognitive stimulation and massage, do not seem to work.

“Some studies have shown that the medicines currently used for Alzheimer’s can have a positive impact on apathy in other types of dementia too,” says Jonsson. “Other medicines may also be of interest, but we need to carry out more research in this area.”

Dementia

The most common symptoms of dementia are forgetfulness, impaired speech and problems with recognition and orientation. It is a condition that can affect all our mental faculties and is more common as we get older. Around seven per cent of the Swedish population over the age of 65 and just over 20 per cent of the over-80s have severe dementia.

Women who store fat on their waist in middle age are more than twice as likely to develop dementia when they get older, reveals a new study from the Sahlgrenska Academy.

The study has just been published in the scientific journal Neurology.

“Anyone carrying a lot of fat around the middle is at greater risk of dying prematurely due to a heart attack or stroke,” says Deborah Gustafson, senior lecturer at the Sahlgrenska Academy. “If they nevertheless manage to live beyond 70, they run a greater risk of dementia.”

The research is based on the Prospective Population Study of Women in Gothenburg, which was started at the end of the 1960s when almost 1,500 women between the ages of 38 and 60 underwent comprehensive examinations and answered questions about their health and lifestyle.

A follow-up 32 years later showed that 161 women had developed dementia, with the average age of diagnosis being 75. This study shows that women who were broader around the waist than the hips in middle age ran slightly more than twice the risk of developing dementia when they got old. However, the researchers could find no link to a high body mass index (BMI).

“Other studies have shown that a high BMI is also linked to dementia, but this was not the case in ours,” says Gustafson. “This may be because obesity and overweight were relatively unusual among the women who took part in the Prospective Population Study.”

The study was carried out at the Neuropsychiatric Epidemiology Research Unit as part of the Sahlgrenska Academy’s major research project EpiLife.

Dementia

The most common symptoms of dementia are forgetfulness, impaired speech and problems with recognition and orientation. It is a condition that can affect all our mental faculties and which is more common as we get older. Around seven per cent of the Swedish population over the age of 65 and just over 20 per cent of the over-80s have severe dementia.