Category Archives: Dementia & Carers

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.

Advertisements

Building a better world: can architecture shape behaviour?

Wgb9htgw 1387429359.jpg?ixlib=rb 1.1
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.

MIND Diet May Slow Cognitive Decline in Stroke Survivors 

Study results presented at the American Stroke Association International Conference

News Releases – Rush University Medical Center

January 25, 2018

A diet created by researchers at Rush University Medical Center may help substantially slow cognitive decline in stroke survivors, according to preliminary research presented on Jan. 25 at the American Stroke Association’s International Stroke Conference 2018 in Los Angeles. The findings are significant because stroke survivors are twice as likely to develop dementia compared to the general population.

The diet, known as the MIND diet, is short for Mediterranean-DASH Diet Intervention for Neurodegenerative Delay. The diet is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets. Both have been found to reduce the risk of cardiovascular conditions such as hypertensionheart attack and stroke.

“The foods that promote brain health, including vegetables, berries, fish and olive oil, are included in the MIND diet,” said Dr. Laurel J. Cherian, a vascular neurologist and assistant professor in Rush’s Department of Neurological Sciences. “We found that it has the potential to help slow cognitive decline in stroke survivors.”

Cherian is the lead author of the study, which was funded by the National Institute of Aging (grant numbers R01AG054476 and R01AG17917).

Study assessed survivors’ cognitive function, monitored their diets

Study co-author Martha Clare Morris, ScD, a Rush nutritional epidemiologist, and her colleagues developed the MIND diet based on information from years of research about what foods and nutrients have good, and bad, effects on the functioning of the brain. The diet has been associated with reduced Alzheimer’s risk in seniors who adhered to its recommendations. Even people who moderately adhered had reduced risk of AD and cognitive decline.

Rush is currently seeking volunteers to participate in the study, which aims to show whether a specific diet can prevent cognitive decline and brain changes with age. Those interested in participating in the study can call (708) 660-MIND (6463) or email mindstudychicago@rush.edu.

The MIND diet has 15 dietary components, including 10 “brain-healthy food groups” and five unhealthy groups — red meat, butter, cheese, pastries and sweets, and fried or fast food.

To adhere to and benefit from the MIND diet, a person would need to eat at least three servings of whole grains, a green leafy vegetable and one other vegetable every day — along with a glass of wine — snack most days on nuts, have beans every other day or so, eat poultry and berries at least twice a week and fish at least once a week. The diet also specifies limiting intake of the designated unhealthy foods, limiting butter to less than 1 1/2 teaspoons a day and eating less than five servings a week of sweets and pastries, and less than one serving per week of whole fat cheese, and fried or fast food.

“I was really intrigued by the results of a previous MIND study, which showed that the people who were most highly adherent to the MIND diet cognitively functioned as if they were 7.5 years younger than the least adherent group,” Cherian said. “It made me wonder if those findings would hold true for stroke survivors, who are twice as likely to develop dementia compared to the general population.”

From 2004 to 2017, Cherian and colleagues studied 106 participants of the Rush Memory and Aging Project who had a history of stroke for cognitive decline, including decline in one’s ability to think, reason and remember. They assessed people in the study every year until their deaths or the study’s conclusion, for an average of 5.9 years, and monitored patients’ eating habits using food journals.

The researchers grouped participants into those who were highly adherent to the MIND diet, moderately adherent and least adherent. They also looked at additional factors that are known to affect cognitive performance, including age, gender, education level, participation in cognitively stimulating activities, physical activity, smoking and genetics.

Related diets not associated with slower cognitive decline

The study participants whose diets scored highest on the MIND diet score had substantially slower rate of cognitive decline than those who scored lowest. The estimated effect of the diet remained strong even after taking into account participants’ level of education and participation in cognitive and physical activities. In contrast to the results of slower decline with higher MIND diet score, stroke survivors who scored high on the Mediterranean and DASH diets, did not have significant slowing in their cognitive abilities.

“The Mediterranean and DASH diets have been shown to be protective against coronary artery disease and stroke, but it seems the nutrients emphasized in the MIND diet may be better suited to overall brain health and preserving cognition,” Cherian said.

According to Cherian, studies have found that folate, vitamin E, omega-3 fatty acids, carotenoids and flavonoids are associated with slower rates of cognitive decline, while substances such as saturated and hydrogenated fats have been associated with dementia.

The right foods may protect stroke survivors’ cognition

“I like to think of the MIND diet as a way to supercharge the nutritional content of what we eat. The goal is to emphasize foods that will not only lower our risk of heart attacks and stroke, but make our brains as resilient as possible to cognitive decline,” she said.

“Our study suggests that if we choose the right foods, we may be able to protect stroke survivors from cognitive decline.” Cherian cautions, however, that the study was observational, with a relatively small number of participants, and its findings cannot be interpreted in a cause-and-effect relationship.

“This is a preliminary study that will hopefully be confirmed by other studies, including a randomized diet intervention study instroke survivors,” she says. “For now, I think there is enough information to encourage stroke patients to view food as an important tool to optimize their brain health.”

Source: MIND Diet May Slow Cognitive Decline in Stroke Survivors – News Releases – Rush University Medical Center

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

child-887058_1280

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.

child-2933293_1280

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.

Older Adults Are Still Likely Underestimating Cognitive Impairment in Their Families

grandma-515530_960_720

News release

 Study Finds Racial Differences in Reporting and Overall Trend of Underreporting Cognitive Impairment

An increasing number of older adults are reporting cognitive impairment in their families over the past two decades, according to a new study led by researchers at NYU Rory Meyers College of Nursing and East Carolina University’s Brody School of Medicine.

The study, which also finds ethnic and racial differences in reporting cognitive impairment, is published in Preventing Chronic Disease, a journal of the Centers for Disease Control and Prevention.

The aging population in the U.S. is growing rapidly, with the number of people age 65 and over in 2010 (40.2 million) projected to more than double by 2050. With the rapid increase in the aging population, the size of the population with cognitive impairment and dementia will continue to accelerate, highlighting the importance of identifying cognitive changes.

“Cognitive impairment may serve as a precursor to future dementia. Early detection of cognitive impairment can facilitate timely medical treatments, appropriate care planning, and prevention efforts,” said Bei Wu, PhD, Dean’s Professor in Global Health and director of Global Health & Aging Research at NYU Meyers, co-director of NYU Aging Incubator, and the study’s senior author.

The study sought to examine the trends of self-reported cognitive impairment among five major racial/ethnic groups from 1997 to 2015 in the United States. The researchers used data from the National Health Interview Survey, including 155,682 individuals age 60 and above in their sample. The large sample included people of a variety of races and ethnicities, including Asian Americans,  Blacks, Hispanics, Native Americans, non-Hispanic Blacks, and non-Hispanic Whites.

Rather than using a screening test or clinical examination to evaluate cognitive impairment, respondents were asked to report if any family member was “limited in anyway because of difficulty remembering or because of experiencing periods of confusion.”

The researchers found an increasing trend in self-reported cognitive impairment: the overall rate increased from 5.7 percent in 1997 to 6.7 percent in 2015 among older adults in the U.S. This finding may suggest that awareness of cognitive impairment, perhaps from heightened public attention to and interest in Alzheimer’s disease, has improved to some extent.

grandma-748254_960_720

When looking at each racial/ethnic group, however, the increasing trend was significant only among White respondents. In Whites, the rate of self-reported cognitive impairment increased from 5.2 percent in 1997 to 6.1 percent in 2015. Asian American, Black, Hispanic, and Native American respondents had higher rates of self-reported cognitive impairment than Whites, but these rates did not significantly increase from 1997 to 2015.

Regardless of the overall increasing trend, the rates of self-reported cognitive impairment were still low, which may suggest underreporting. The researchers note that the rates of self-reported cognitive impairment are much lower than the estimated prevalence of cognitive impairment. For adults 65 years and older, the rate of self-reported cognitive impairment was 6.3 percent in 2000 and 7.5 percent in 2012, while the estimated prevalence of cognitive impairment in the same age group was 21.2 percent in 2000 and 18.8 percent in 2012.

These findings underscore the need to further promote awareness of cognitive impairment, especially in minority populations. Different cultures hold different beliefs and perceptions of disease and aging. For instance, research has found that compared to Whites, minorities are less likely to seek treatment for psychiatric symptoms because of lack of access to care or due to stigma.

“Culturally specific health education is needed in individuals, family members, and healthcare providers to improve awareness and knowledge of signs and early symptoms of Alzheimer’s and other dementia,” said Huabin Luo, PhD, of East Carolina University.

In addition to Wu and Luo, Gary Yu of NYU Meyers coauthored the study.

The language of dementia is slowly changing

There has been, for many years, discussions, requests, even what could be seen as begging from may of us diagnosed with dementia to use respectful language. That means, respectful from our point of view, not those who are not diagnosed with dementia.

Of course, people with dementia do suffer some of the time, but we did before dementia too, but were not then termed as sufferers all the time. Some individuals with dementia may wish to refer to themselves as sufferers, and of course, that is totally their right, but I believe it is not ok to do so publicly, as it infers that we are all ok with that negative label.

The following is my guest blog published by Dementia Australia after attending the Alzheimer’s Disease International (ADI) Conference in Puerto Rico in 2014

I repeat: “Please don’t call us sufferers”

During the recent ADI2014 conference, it was apparent…

View original post 745 more words

Why a drug treatment for dementia has eluded us

 

File 20180109 83553 1tp4671.jpg?ixlib=rb 1.1

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.