Category Archives: Dementia: International Policies

The onset of Alzheimer’s disease: the importance of family history

News Release
February 26, 2018 | QUEBEC – The onset of Alzheimer’s disease: the importance of family history

You’re about to turn 60, and you’re fretting. Your mother has had Alzheimer’s disease since the age of 65. At what age will the disease strike you? A Canadian study published in JAMA Neurology shows that the closer a person gets to the age at which their parent exhibited the first signs of Alzheimer’s, the more likely they are to have amyloid plaques, the cause of the cognitive decline associated with the disease, in their brain.

In this study involving a cohort of 101 individuals, researcher Sylvia Villeneuve (Douglas Mental Health University Institute; CIUSSS de l’Ouest-de-l’Île-de-Montréal) shows that the difference between a person’s age and the age of their parent at the onset of the disease is a more important risk factor than their actual age.

A 60-year-old whose mother developed Alzheimer’s at age 63 would be more likely to have amyloid plaques in their brain than a 70-year-old whose mother developed the disease at age 85,” explains Villeneuve, an assistant professor at McGill University and a core faculty member at The Neuro’s McConnell Brain Imaging Centre.

Her team of scientists also found that the genetic impact of Alzheimer’s disease is much greater than previously thought.

“Upon examining changes in the amyloid biomarker in the cerebrospinal fluid samples from our subjects, we noticed that this link between parental age and amyloid deposits is stronger in women than in men. The link is also stronger in carriers of the ApoE4 gene, the so-called ‘Alzheimer’s gene’,” says Villeneuve.

Towards earlier detection of the disease

The researcher and her team successfully duplicated their results in two independent groups, one, consisting of 128 individuals from a University of Washington-St. Louis cohort, the other consisting of 135 individuals from a University of Wisconsin-Madison cohort. They also reproduced their results using an imaging technique that enables one to see amyloid plaques directly in the brains of living persons.

Their study is paving the way for the development of inexpensive methods for the early identification of people at risk for Alzheimer’s disease. According to the Alzheimer Society of Canada, 564,000 Canadians currently have Alzheimer’s disease or another form of dementia. The figure will be 937,000 within 15 years. Presently, there is no truly effective treatment for this disease.

This research was funded by grants from a Canadian research chair, the Canadian Institutes of Health Research, the Canadian Foundation for Innovation, the Canadian Brain Research Fund, the Alzheimer Society of Canada, and the Fonds de recherche du Québec — Santé.

The article entitled “Proximity to parental symptom onset and amyloid burden in sporadic Alzheimer’s disease” was published in JAMA Neurology on February 26, 2018. DOI:10.1001/jamaneurol.2017.5135

Source: http://www.douglas.qc.ca/?locale=en

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Bilingualism could offset brain changes in Alzheimer’s

A Concordia study sheds light on how language history relates to brain plasticity

News Release
February 6, 2018 | QUEBEC – Bilingualism could offset brain changes in Alzheimer’s

After more than a decade of research, this much we know: it’s good for your brain to know another language.

A new Concordia study goes further, however, focusing specifically on the effects of knowing a second language for patients with Alzheimer’s disease (AD) and mild cognitive impairment (MCI; a risk state for AD).

“Most of the previous research on brain structure was conducted with healthy younger or older adults,” says Natalie Phillips, a professor in the Department of Psychology.

“Our new study contributes to the hypothesis that having two languages exercises specific brain regions and can increase cortical thickness and grey matter density. And it extends these findings by demonstrating that these structural differences can be seen in the brains of multilingual AD and MCI patients.”

Phillips’s study, led by recent Concordia psychology grad Hilary D. Duncan (PhD 17), is soon to be published in Neuropsychologia(Jan, 2018).

New methods: Enter the MRI

Phillips and her team are the first to use high-resolution, whole-brain MRI data and sophisticated analysis techniques to measure cortical thickness and tissue density within specific brain areas.

Namely, they investigated language and cognition control areas in the frontal regions of the brain, and medial temporal lobe structures that are important for memory and are brain areas known to atrophy in MCI and AD patients.

“Previous studies used CT scans, which are a much less sensitive measure,” says Phillips, founding director of Concordia’s Cognition, Aging and Psychophysiology (CAP) Lab.

The study looked at MRIs from participating patients from the Jewish General Hospital Memory Clinic in Montreal.

Their sample included 34 monolingual MCI patients, 34 multilingual MCI patients, 13 monolingual AD patients and 13 multilingual AD patients.

Phillips believes their study is the first to assess the structure of MCI and AD patients’ language and cognition control regions. It is also the first to demonstrate an association between those regions of the brain and memory function in these groups, and the first to control for immigration status in these groups.

“Our results contribute to research that indicates that speaking more than one language is one of a number of lifestyle factors that contributes to cognitive reserve,” Phillips says.

“They support the notion that multilingualism and its associated cognitive and sociocultural benefits are associated with brain plasticity.”

What’s next?

Phillips and her team are already building on their findings.

“Our study seems to suggest that multilingual people are able to compensate for AD-related tissue loss by accessing alternative networks or other brain regions for memory processing. We’re actively investigating that hypothesis now.”

Read the cited study, “Structural brain differences between monolingual and multilingual patients with mild cognitive impairment and Alzheimer disease: Evidence for cognitive reserve.

Source: NEW RESEARCH: Bilingualism could offset brain changes in Alzheimer’s

“Pop Drop” Study finds more ER visits & higher costs for older disabled patients with stressed caregivers

News release

“Pop Drop” Study finds more ER visits & higher costs for older disabled patients with stressed caregivers

Fatigue, sadness and poor health among the spouses who take care of disabled elders can mean higher Medicare bills for the patients.

Emergency room staff call it a “pop drop” – when a disabled older person comes in for medical attention, but it seems like the person who takes care of them at home is also seeking a break from the demands of caregiving.

It’s been hard to actually study the phenomenon. A new University of Michigan study suggests that tired family caregivers are associated with greater ER visits and higher overall health care costs for the person they care for.

In a paper in the new issue of the Journal of the American Geriatrics Society, the team reports their findings from a study of 3,101 couples over the age of 65, each with one spouse acting as caregiver for their disabled partner.

The researchers looked at the Medicare payments and emergency department visits for the disabled spouses in the six months after the caregiver spouses took standard tests to measure their fatigue, mood, sleep habits, health and happiness.

Even after they took into account many factors, the researchers found that in just those six months, emergency department visits were 23 percent higher among patients whose caregivers had scored high for fatigue or low on their own health status.

Patients with fatigued or sad caregivers also had higher Medicare costs in that same time period: $1,900 more if the caregiver scored high for fatigue, and $1,300 more if the caregiver scored high for sadness, even after all other factors were taken into account.

The cost of unpaid help

“Many of us who work in clinical settings feel that patients with high home caregiving needs, such as dementia, often rely on the medical system as a source of respite for their spouses or other caregivers, because other respite isn’t paid for,” says lead author Claire Ankuda, M.D., M.P.H. “But there hasn’t been a lot of data about it, and only recently has our society been talking about caregivers and potential ways to incentivize and support them as a way of keeping patients living at home.”

“Informal caregivers, including spouses, enable older adults with functional disability to stay out of the nursing home and live at home where they’d prefer to be,” says senior author Deborah Levine, M.D., M.P.H., an assistant professor of internal medicine and neurology at U-M. “Our findings suggest that we need to do a better job of identifying and supporting caregivers experiencing distress, in order to help caregivers feel better and hopefully improve outcomes in older adults with disability.”

Long-term data gives key insights

The couples in the study were all taking part in the long-term Health and Retirement Study, conducted by the U-M Institute for Social Research on behalf of the National Institutes of Health. Ankuda, Levine and their colleagues probed HRS data because it allowed them to correct for factors that other, short-term studies can’t – such as the baseline level of Medicare costs, demographic differences including income and education, and even whether the couples have adult children living nearby.

The findings add hard new data about the link between caregivers’ own experiences and the amount the Medicare system pays to take care of those the caregivers take care of at home.

Nearly 15 million older adults get help with everyday activities from spouses and other family or friend caregivers. In the new study, the researchers included couples where one spouse got help from the other with activities such as bathing, dressing, walking, getting into or out of bed, shopping, cooking, and taking medications.

Helping with these tasks on a daily basis, without pay or respite, can take a toll on the caregiver’s own health, wellness and mental state – which can lead to burnout. Medicare does not offer payment or formal respite coverage for family or friends who take regular care of older adults – and only covers home care by certified agencies under certain circumstances.

More research & services needed

Ankuda notes that studies on the impact of supporting family caregivers more formally are just beginning to produce results.

Meanwhile, health policy researchers are beginning to suggest that it may make fiscal sense to incentivize home caregiving, to keep seniors from needing more expensive nursing home care.

“I definitely think there are specific services that could help caregivers, if we can identify those people who are highest risk and provide a basic level of support such as an around-the-clock geriatric care call line that could help caregivers feel less isolated and talk to a nurse about whether, for example, to go to the emergency department,” Ankuda says. “This is a high-cost, vulnerable population.”

Formal respite care, peer support groups and other options could also help stave off fatigue and sadness – and the hospital staff who notice “pop drop” practices could help steer caregivers to such options. So could the primary care clinicians who take care of both the disabled spouse and the caregiver.

Because the new study takes into account the level of Medicare spending for the disabled spouse in the six months before their caregiver was interviewed, it may actually underestimate the impact of caregiver fatigue, she notes.

Indeed, before the authors corrected for the full range of factors, they documented that Medicare costs were lower for patients whose spouse-caregivers who reported being happy or rested. They also saw higher costs among patients whose caregivers had higher depression scores on a standard mood questionnaire.

One factor that wasn’t associated with higher costs in the new study was the caregiver’s score on a standard measure of sleep habits. Sleep disruption is harder to quantify in older people, Ankuda notes. But the measurement of fatigue, which can result from both the strain of caregiving and poor sleep, was clearly associated with both higher rates of emergency department visits and higher overall costs.

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Claire
Ankuda

M.D., M.P.H.

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Deborah
Levine

M.D., M.P.H.

Oversedation in Nursing Homes

Source: Human Rights Watch
Published: 5th Feb 2018

The human rights watch has produced a report on the use of sedation in nursing homes. The report titled “they want docile” highlights the plight of people with dementia being chemically restraint through overmedication of antipsychotic drugs.

 

Read the full report here https://www.hrw.org/report/2018/02/05/they-want-docile/how-nursing-homes-united-states-overmedicate-people-dementia 

Too many times I’m given too many pills…. [Until they wear off], I can’t even talk. I have a thick tongue when they do that. I ask them not to [give me the antipsychotic drugs]. When I say that, they threaten to remove me from the [nursing] home. They get me so I can’t think. I don’t want anything to make me change the person I am.
—Walter L., an 81-year-old man given antipsychotic drugs in a Texas nursing facility, December 2016.

It used to be like a death prison here. We cut our antipsychotics in half in six months. Half our residents were on antipsychotics. Only 10 percent of our residents have a mental illness.
—A director of nursing at a facility in Kansas that succeeded in reducing its rate of antipsychotic drug use, January 2017.

Building a better world: can architecture shape behaviour?

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US architect Frank Lloyd Wright, who designed Fallingwater, believed that appropriate architecture would save the US from corruption.
Via Tsuji

Jan Golembiewski, University of Sydney

In 1966, a British planner called Maurice Broady came up with a new term for the architectural lexicon: architectural determinism.

This was to describe the practice of groundlessly asserting that design solutions would change behaviour in a predictable and positive way.

It was a new phrase but the belief system behind it – that buildings shape behaviour – had allowed the heroes of architecture to make all kinds of outlandish claims.

A hopeful history

Leon Battista Alberti, an Italian Renaissance-era architect, claimed in the 1400s that balanced classical forms would compel aggressive invaders to put down their arms and become civilians.

Frank Lloyd Wright, the US architect who designed one of the most famous buildings in America, Fallingwater, similarly believed appropriate architecture would save the US from corruption and turn people back to wholesome endeavours.

British author and thinker Ebenezer Howard believed companies would be more efficient if their employees lived in village-like garden communities.

Swiss-born French architect Le Corbusier made claims about how his Villa Savoye building in France would heal the sick – and when it did just the opposite, he only avoided court because of the commencement of the second world war.

It took a long list of failures over the millennia before postmodern theorists took to critiquing architectural fantasy with malevolent vengeance. The high-point of this trend was the delight shared over the demolition of the famously dangerous and dysfunctional Pruitt-Igoe urban housing complex in St Louis in the US.

It was designed by architects George Hellmuth, Minoru Yamasaki and Joseph Leinweber to provide “community gathering spaces and safe, enclosed play yards.” By the 1960s, however, it was seen as a hotspot for crime and poverty and demolished in the 1970s.

The demolition of Pruitt-Igoe in 1972 fuelled resistance to deterministic thinking.
Wikimedia

The loss of faith in architecture’s power has been regrettable. Architects’ well-meant fantasies once routinely provided clients with hope and sometimes even with results.

Without this promise, the profession was left inept before the better structural knowledge of engineers, the cumulative restrictions imposed by generations of planners, the calculations of project-managers and the expediency of a draughtsman’s CAD (computer-aided design) skills in turning a client’s every whim into reality.

Without fiction, architecture has become a soulless thing. But was determinism dismissed too soon? Is there a role for imagined futures without rationalist restrictions?

Restoring the faith

Just think of some of the ways architecture can manipulate your own experience. In his book, Happy City: Transforming Our Lives Through Urban Design, US author Charles Montgomery points out that some environments predictably affect our moods.

The fact is that environments do affect us, regardless of whether by design or by accident. In 2008, researchers in the UK found that a ten-minute walk down a South London main street increased psychotic symptoms significantly.

In my own research, I find that the healthier a person is, the more a good environment will affect them positively and the less a bad one will affect them negatively. Mentally ill patients show about 65 times more negative reactivity to bad environments than controls and all these reactions translate directly into symptoms.

The same patients have about half the positive responsiveness. That’s fewer smiles, less laughter and a reported drop in feeling the “fun of life”.

But that’s not all. The potential for architecture is richer still. The ease with which architecture can embrace sublime aesthetics makes it great for generating awe.

Psychiatrists have found that awe reduces the prevalence and severity of mood disorders. Could sublime architecture even potentially save lives?

The psychological effects of architecture are difficult to prove, but difficulty doesn’t dilute the value of a building that hits the right notes and creates a sense of awe. Each building type has different functions, and for each there’s an imperative to use the building to help create an optimal mood, desire or sense of coherence, security or meaning.

Awe reduces mood disorders: Gaudi’s Sacrada Familia church in Spain.
Wikimedia

Fortunately, there’s a resurgence of belief that buildings can change behaviour, led by a few architectural journals: World Health Design, Environment Behavior and HERD.

Most of these focus on health care design, because that’s where behavioural changes have life and death consequences.

But nobody dares make any promises. As such, research rarely opens the black box of environmental psychology, leaving findings unexplained and prone to failure.

To give architecture back its mojo, a new interest in how architecture changes us must be fostered. Clients have to learn to trust architects again and research funding bodies have to re-gear to encourage research into how buildings affect our mood, health and behaviours.

Finally, architecture schools have to teach students how they might predict psychological, emotional, healing and functional effects.

The ConversationAll innovation, ultimately, is led by the imagination – even if that means taking risks and sometimes getting it wrong.

Jan Golembiewski, Researcher in Environmental Determinants of Mental Health, University of Sydney

This article was originally published on The Conversation. Read the original article.

If you develop Alzheimer’s, will your children get it too?

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Rebecca Sims, Cardiff University

The most common question I get asked is “Will my child get Alzheimer’s disease?” In my experience, this concern is one of the biggest worries for sufferers, and given the devastating effects of the disease, it is not hard to see why it is a difficult thought to contemplate.

For those people with a familial form of Alzheimer’s disease, the answer is quite straightforward. This type of disease is caused by one or more mutation(s) in one of three genes: the amyloid precursor protein (APP), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2). All of these genes are involved in the production of the amyloid protein. This protein accumulates to form sticky buildups known as plaques, which are found between the cells of the Alzheimer brain and are characteristic of disease.

Those of us who are concerned that they may be at risk from familial Alzheimer’s disease can get a definitive answer through one of the many genetic tests available. A single copy of the mutated gene inherited from an affected parent will ultimately cause disease, with symptoms likely to be noticed before the age of 65 and typically between 30 and 60 years of age. Anyone concerned that they may suffer from this form of Alzheimer’s should seek a referral to a genetic counsellor.

Fortunately, families with a familial form of disease represent less than 1% of all families afflicted by this debilitating disease. For the remaining Alzheimer’s disease families, the answer as to the inheritance of disease is much less clear, and disease onset is certainly not inevitable.

Influencing disease

A combination of both genetic and environmental factors, such as age and gender, contribute to non-familial (also known as sporadic) disease risk, but how these risk factors interact and how many risk factors are required to cause disease is still unknown.

The genetics of non-familial Alzheimer’s is complex: we know that nearly thirty genes, common in the general population, influence disease risk, with potentially hundreds more involved. Additionally, two genes of low frequency have consistently been identified, with an imminent publication by the International Genomics of Alzheimer’s Project, showing another two rare genes have a relatively large effect on disease risk.

Perhaps most excitingly for researchers, genetics scientists have shown that four biological processes in Alzheimer’s disease – that were not previously thought to play a casual role in disease onset – are actually involved. The first process is the immune response, in particular the actions of immune cells and how these potentially dysfunction, attacking the brain, which results in brain cell death.

The second is the transport of molecules into the cell, suggesting that there is a mechanism for the movement of damaging proteins into the brain. The third process that has a role in the onset of Alzheimer’s is the synthesis and breakdown of fatty molecules. And the fourth is the processing of proteins that alters protein breakdown, movement, activity and interactions – all of which are essential for normal protein function.

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Lifestyle risk

Age is the greatest risk factor for disease, with the likelihood of developing Alzheimer’s roughly doubling every five years over the age of 65. Women also have more chance of developing the disease than men, potentially due to a reduction in female hormones after menopause.

Medical conditions that increase risk for dementia include cardiovascular factors (type 2 diabetes, high blood pressure, cholesterol levels, and obesity), and depression. While lifestyle factors such as physical inactivity, a diet that increases cholesterol, smoking and excessive alcohol intake, have all been shown to influence disease risk.

Even for those with a high number of genetic, environmental and lifestyle risk factors, Alzheimer’s disease is not inevitable. Likewise, individuals with a low number of risk factors for disease are not precluded from developing Alzheimer’s.

Given this lack of certainty and the lack of effective treatments for Alzheimer’s, most experts don’t recommend genetic testing for non-familial disease. This thinking may well evolve in the future, however, when research identifies new risk genes and improves our understanding of the dysfunctional processes in Alzheimer’s disease.

The Conversation

Answering the burning question, whether you will pass Alzheimer’s disease on to your children, is therefore still a near impossibility. But, as early diagnostic techniques improve, and with the prospect of a number of vaccines and therapeutics currently in clinical trials, risk prediction for Alzheimer’s disease may become mainstream and part of a developing precision medicine culture.

Rebecca Sims, Research Fellow, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University

This article was originally published on The Conversation. Read the original article.

Why a drug treatment for dementia has eluded us

 

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Have our hopes of a drug treatment for dementia been dashed by drug company Pfizer giving up on research efforts?
from http://www.shutterstock.com

Jürgen Götz, The University of Queensland

Finding a cure for neurodegenerative diseases such as Alzheimer’s is challenging. They’re difficult to diagnose, and drugs struggle to get into the brain as the brain’s blood supply is largely separate to the rest of the body. Not surprisingly, several companies have left this territory in recent years. This week, pharmaceutical giant Pfizer announced it will stop research into developing drugs to treat Alzheimer’s disease, after costly failed attempts over the past decade.

In recent years some clinical trials involving potential dementia drugs have had disappointing setbacks. In 2012, Pfizer and Johnson & Johnson halted development of the antibody drug bapineuzumab, after it failed in late-stage trials to treat patients with mild to moderate Alzheimer’s.

Despite this week’s announcement, Pfizer’s support of the UK’s Dementia Discovery Fund, an initiative involving the government, major pharmaceutical companies, and Alzheimer’s Research UK, may be where their money can make the most impact in this space. The fund aims to boost dementia research investment by financing early-stage drug development projects. And other pharma companies, such as Eli Lilly, Biogen and Novartis have continued to pursue dementia drug development with modest but promising success to date.

So what makes dementia such a difficult condition to treat with drugs, and is progress being made towards a treatment?


Read more: Alzheimer’s breakthrough? Have we nearly cured dementia? Not just yet…


Why dementia is so hard to treat

Despite the vast number of people affected globally, with an estimated 46.8 million people currently living with dementia, there is currently no cure. While current treatments manage symptoms (the latest drug to gain FDA approval was memantine, in 2003) they offer no prospect of recovery.

Part of the difficulty in finding treatments for dementia stems from the fact it’s not a single disease, but a complex health problem with more than 50 underlying causes. Dementia can be better thought of as an umbrella term describing a range of conditions that cause parts of the brain to deteriorate progressively.


Read more: What causes Alzheimer’s disease? What we know, don’t know and suspect


Most drug treatments currently in development have targeted the pathology of Alzheimer’s disease, the most common form of dementia, which accounts for about 60 to 70% of all cases.

Finding a successful treatment for Alzheimer’s faces two major hurdles: the first being we still don’t know enough about the disease’s underlying biology. For example, we don’t know what exactly regulates the toxic build-up of amyloid-β plaques and tau tangles in the brain that are found in Alzheimer’s patients, which specific types of these are toxic, or why the disease progresses at different rates in different people.

It doesn’t help that symptoms of Alzheimer’s develop gradually and slowly and a diagnosis might only be made years after the brain has started to undergo neurodegenerative changes. To boot, it’s not uncommon for Alzheimer’s to be present as well as other forms of dementia.

The second major hurdle to finding a treatment is that drugs need to first cross the blood-brain barrier. The blood–brain barrier provides a defence against disease-causing pathogens and toxins that may be present in our blood, and by design exists to keep out foreign substances from the brain. The downside is that it also keeps the vast majority of potential drug treatments from reaching the brain.


Read more – Explainer: what is the blood-brain barrier and how can we overcome it?


The brain has a blood barrier that protects it from pathogens that invade the rest of our body, which also means drugs can’t get in there.
from http://www.shutterstock.com

Promising steps in the right direction

Currently available medications such as those which block the actions of an enzyme that destroys an important chemical messenger in the brain for memory (acetylcholinesterase inhibitors) or blocks the toxic effects of another messenger, glutamate (memantine) temporarily manage symptoms. But new treatments are focused on slowing or reversing the disease process itself, by targeting the underlying biology.

One approach, called immunotherapy, involves creating antibodies that bind to abnormal developments in the brain (such as amyloid-β or tau), and mark them for destruction by a range of mechanisms. Immunotherapy is experiencing a surge of interest and a number of clinical trials – targeting both amyloid-β and tau – are currently underway.

Aducanumab, an antibody targeting amyloid-β, has shown promise in clinical trials and phase 3 trials are currently ongoing, as are several tau-based strategies. If any are successful, we would have a vaccine for Alzheimer’s.


Read more – How Australians Die: cause #3 – dementia (Alzheimer’s)


It’s estimated only 0.1% of antibodies circulating in the bloodstream enter the brain – this also includes the therapeutic antibodies currently used in clinical trials. An approach my team is taking is to use ultrasound to temporarily open the blood-brain barrier, which increases the uptake of Alzheimer’s drugs or antibody fragments.

We’ve had success in mice, finding ultrasound can clear toxic tau protein clumps, and that combining ultrasound with an antibody fragment treatment is more effective than either treatment alone in removing tau and reducing Alzheimer’s symptoms. The next challenge will be translating this success into human clinical trials.

The task of dementia drug development is no easy feat, and requires collaboration across government, industry and academia. In Australia, the National Dementia Network serves this purpose well. It’s only through perseverance and continued investment in research that we’ll one day have a treatment for dementia.


The ConversationWith thanks to Queensland Brain Institute Science Writer Donna Lu.

Jürgen Götz, Director, Clem Jones Centre for Ageing Dementia Research, The University of Queensland

This article was originally published on The Conversation. Read the original article.