Monday, September 30, 2013

Global study: World not ready for aging population

Global study: World not ready for aging population
In this Sept. 26, 2013 photo, 80-year-old Marianne Blomberg works out at a gym in Stockholm. Much of the world is not prepared to support the ballooning population of elderly people, including many of the fastest-aging countries, according to a global study scheduled to be released Tuesday, Oct. 1, by the United Nations and an elder rights group. The Swedish government has suggested people continue working beyond 65, a prospect Blomberg cautiously welcomes but warns should not be a requirement. (AP Photo/TT News Agency, Jonas Ekstromer)
The world is aging so fast that most countries are not prepared to support their swelling numbers of elderly people, according to a global study going out Tuesday by the United Nations and an elder rights group.
30 sept 2013--The report ranks the social and economic well-being of elders in 91 countries, with Sweden coming out on top and Afghanistan at the bottom. It reflects what advocates for the old have been warning, with increasing urgency, for years: Nations are simply not working quickly enough to cope with a population graying faster than ever before. By the year 2050, for the first time in history, seniors over the age of 60 will outnumber children under the age of 15.
Truong Tien Thao, who runs a small tea shop on the sidewalk near his home in Hanoi, Vietnam, is 65 and acutely aware that he, like millions of others, is plunging into old age without a safety net. He wishes he could retire, but he and his 61-year-old wife depend on the $50 a month they earn from the tea shop. And so every day, Thao rises early to open the stall at 6 a.m. and works until 2 p.m., when his wife takes over until closing.
"People at my age should have a rest, but I still have to work to make our ends meet," he says, while waiting for customers at the shop, which sells green tea, cigarettes and chewing gum. "My wife and I have no pension, no health insurance. I'm scared of thinking of being sick—I don't know how I can pay for the medical care."
Thao's story reflects a key point in the report, which was released early to The Associated Press: Aging is an issue across the world. Perhaps surprisingly, the report shows that the fastest aging countries are developing ones, such as Jordan, Laos, Mongolia, Nicaragua and Vietnam, where the number of older people will more than triple by 2050. All ranked in the bottom half of the index.
The Global AgeWatch Index (www.globalagewatch.org) was created by elder advocacy group HelpAge International and the U.N. Population Fund in part to address a lack of international data on the extent and impact of global aging. The index, released on the U.N.'s International Day of Older Persons, compiles data from the U.N., World Health Organization, World Bank and other global agencies, and analyzes income, health, education, employment and age-friendly environment in each country.
The index was welcomed by elder rights advocates, who have long complained that a lack of data has thwarted their attempts to raise the issue on government agendas.
"Unless you measure something, it doesn't really exist in the minds of decision-makers," said John Beard, Director of Ageing and Life Course for the World Health Organization. "One of the challenges for population aging is that we don't even collect the data, let alone start to analyze it. ... For example, we've been talking about how people are living longer, but I can't tell you people are living longer and sicker, or longer in good health."
The report fits into an increasingly complex picture of aging and what it means to the world. On the one hand, the fact that people are living longer is a testament to advances in health careand nutrition, and advocates emphasize that the elderly should be seen not as a burden but as a resource. On the other, many countries still lack a basic social protection floor that provides income, health care and housing for their senior citizens.
Global study: World not ready for aging population
In this Sunday, Sept. 29, 2013 photo, an elderly man listens to a speaker at a political rally in New Delhi. Much of the world is not prepared to support the ballooning population of elderly people, including many of the fastest-aging countries, according to a global study scheduled to be released Tuesday, Oct. 1, by the United Nations and an elder rights group. (AP Photo/Altaf Qadri)
Afghanistan, for example, offers no pension to those not in the government. Life expectancy is 59 years for men and 61 for women, compared to a global average of 68 for men and 72 for women, according to U.N. data.
That leaves Abdul Wasay struggling to survive. At 75, the former cook and blacksmith spends most of his day trying to sell toothbrushes and toothpaste on a busy street corner in Kabul's main market. The job nets him just $6 a day—barely enough to support his wife. He can only afford to buy meat twice a month; the family relies mainly on potatoes and curried vegetables.
"It's difficult because my knees are weak and I can't really stand for a long time," he says. "But what can I do? It's even harder in winter, but I can't afford treatment."
Although government hospitals are free, Wasay complains that they provide little treatment and hardly any medicine. He wants to stop working in three years, but is not sure his children can support him. He says many older people cannot find work because they are not strong enough to do day labor, and some resort to begging.
"You have to keep working no matter how old you are—no one is rich enough to stop," he says. "Life is very difficult."
Many governments have resisted tackling the issue partly because it is viewed as hugely complicated, negative and costly—which is not necessarily true, says Silvia Stefanoni, chief executive of HelpAge International. Japan and Germany, she says, have among the highest proportions of elders in the world, but also boast steady economies.
"There's no evidence that an aging population is a population that is economically damaged," she says.
Prosperity in itself does not guarantee protection for the old. The world's rising economic powers—the so-called BRICS nations of Brazil, Russia, India, China and South Africa—rank lower in the index than some poorer countries such as Uruguay and Panama.
Global study: World not ready for aging population
In this Thursday, Sept, 26, 2013 photo, Abdul Wasay, 75, sells toothbrushes and toothpaste on a busy street market In Kabul, Afghanistan, where he says he usually spends most of his days. In a country with no pension system for people not in government service, it's a hard life for the former blacksmith and cook. He makes just $6 a day and it's barely enough to help support his wife. (AP Photo/Ahmad Jamshid)
However, the report found, wealthy nations are in general better prepared for aging than poorer ones. Sweden, where the pension system is now 100 years old, makes the top of the list because of its social support, education and health coverage, followed by Norway, Germany, the Netherlands and Canada. The United States comes in eighth.
Sweden's health system earns praise from Marianne Blomberg, an 80-year-old Stockholm resident.
"The health care system, for me, has worked extraordinarily well," she says. "I suffer from atrial fibrillation and from the minute I call emergency until I am discharged, it is absolutely amazing. I can't complain about anything—even the food is good."
Still, even in an elder-friendly country like Sweden, aging is not without its challenges. The Swedish government has suggested people continue working beyond 65, a prospect Blomberg cautiously welcomes but warns should not be a requirement. Blomberg also criticized the nation's finance minister, Anders Borg, for cutting taxes sharply for working Swedes but only marginally for retirees.
"I go to lectures and museums and the theater and those kinds of things, but I probably have to stop that soon because it gets terribly expensive," she says. "If you want to be active like me, it is hard. But to sit home and stare at the walls doesn't cost anything."
© 2013 The Associated Press. All rights reserved.

Sunday, September 29, 2013

Link between antidepressants and diabetes risk is real

Clinicians should be extra vigilant when prescribing antidepressants as they could pose a risk of type 2 diabetes, researchers at the University of Southampton have warned.
29 sept 2013--A systematic review, carried out by the University, showed that people taking antidepressants are at a higher risk of type 2 diabetes; however it is not certain whether the medication is responsible.
The use of antidepressant medication has risen sharply over recent years reaching 46.7 million prescriptions issued in the UK in 2011.
A number of studies have been carried out to establish whether antidepressants are linked with diabetes but results have varied depending on the methods used, type of medication and the number of participants.
University of Southampton researchers assessed 22 studies and three previous systematic reviews that looked into the effects of antidepressants on diabetes risk. Overall, people taking antidepressants were more likely to have diabetes. However, the researchers warned that different types of antidepressants may carry different risks and long-term prospective randomized control trials are needed to look at the effects of individual tablets.
Published in Diabetes Care, the team said that there are "several plausible" reasons why antidepressants are associated with an increased risk of diabetes. For example, several antidepressants are associated with significant weight gain which increases the risk of type 2 diabetes. However, they also say that several studies which explored this association still observed an increased risk of diabetes after adjustment for changes in body weight, implying other factors could be involved.
Dr Katharine Barnard, Health Psychologist from the University of Southampton comments: "Antidepressants are used widely in the UK, with a significant increase in their use recently. Our research shows that when you take away all the classic risk factors of type 2 diabetes; weight gain, lifestyle etc, there is something about antidepressants that appears to be an independent risk factor. With 46 million prescriptions a year, this potential increased risk is worrying. Heightened alertness to the possibility of diabetes in people taking antidepressants is necessary until further research is conducted."
Richard Holt, Professor in Diabetes and Endocrinology at the University of Southampton, adds: "While depression is an important clinical problem and antidepressants are effective treatments for this debilitating condition, clinicians need to be aware of the potential risk of diabetes, particularly when using antidepressants in higher doses or for longer duration. When prescribing antidepressants, doctors should be aware of this risk and take steps to monitor for diabetes and reduce that risk of diabetes through lifestyle modification."
More information: Antidepressant Medication as a Risk Factor for Type 2 Diabetes and Impaired Glucose Regulation: Systematic Review, Diabetes Care, 2013.
Provided by University of Southampton

Saturday, September 28, 2013

Study suggests walnuts in diet can improve endothelial functions for overweight adults

Medical researchers from the Yale-Griffin Prevention Research Center in Connecticut have found evidence suggestive that adding walnuts to one's diet can protect against diabetes and heart disease in at-risk individuals. Their original research article, "Effects of Walnuts on Endothelial Function in Overweight Adults with Visceral Obesity: A Randomized, Controlled, Crossover Trial," is now available in the Journal of the American College of Nutrition, the Official Publication of the American College of Nutrition, and a publication from Routledge.
28 sept 2013--For the study, a sample of 46 adults aged 30-75 were selected. Participants had a Body Mass Index larger than 25, and a waist circumference exceeding 40 inches for men and 35 inches for women. They were also required to be non-smokers, and all exhibited one or more additional risk factors for metabolic syndrome, a precursor of diabetes and cardiovascular disease. The group was randomly assigned to two 8-week sequences of either a walnut-enriched ad libitum diet or an ad libitum diet without walnuts. Those chosen for the walnut diet were instructed to consume 56g of shelled, unroasted English walnuts per day as a snack or with a meal.
"We know that improving diets tends to be hard, but adding a single food is easy," explained Dr. David Katz, Director of the Yale-Griffin Prevention Research Center and lead author of the research team. "Our theory is that if a highly nutritious, satiating food like walnuts is added to the diet, there are dual benefits: the benefits of that nutrient rich addition and removal of the less nutritious foods."
The research found that daily intake of 56g of walnuts improves endothelial function in overweight adults with visceral adiposity. The addition of walnuts to the diet does not lead to weight gain. Further study on the topic is still suggested. "The primary outcome measure was the change in flow-mediated vasodilatation (FMD) of the brachial artery," wrote the research group. "Secondary measures included serum lipid panel, fasting glucose and insulin, Homeostasis Model Assessment–Insulin Resistance values, blood pressure, and anthropometric measures. FMD improved significantly from baseline when subjects consumed a walnut-enriched diet as compared with the control diet. Beneficial trends in systolic blood pressure reduction were seen, and maintenance of the baseline anthropometric values was also observed. Other measures were unaltered."
Provided by Taylor & Francis

Friday, September 27, 2013

New early detection test for prostate cancer: Mi-Prostate Score test improves on PSA for predicting cancer

New early detection test for prostate cancer: Mi-Prostate Score test improves on PSA for predicting cancer
Arul Chinnaiyan, M.D., Ph.D., and Scott Tomlins, M.D., Ph.D.

More than 1 million men will undergo a prostate biopsy this year, but only about one-fifth of those biopsies will result in a cancer diagnosis.
27 sept 2013--The reason is that the traditional prostate cancer screening test – a blood test to measure prostate specific antigen, or PSA – does not give doctors a complete picture.
Now, the University of Michigan Health System has begun offering a new urine test called Mi-Prostate Score to improve on PSA screening for prostate cancer. The test incorporates three specific markers that could indicate cancer and studies have shown that the combination is far more accurate than PSA alone.
"Many more men have elevated PSA than actually have cancer but it can be difficult to determine this without biopsy. We need new tools to help patients and doctors make better decisions about what to do if serum PSA is elevated. Mi-Prostate Score helps with this," says Scott Tomlins, M.D., Ph.D., assistant professor of pathology and urology at the University of Michigan.
Researchers validated the new test on nearly 2,000 urine samples. Mi-Prostate Score, or MiPS, was significantly more accurate than PSA alone for predicting cancer as well as predicting aggressive prostate cancer that is likely to grow and spread quickly.
Mi-Prostate Score developed from a discovery in the lab of Arul Chinnaiyan, M.D., Ph.D., in 2005 of a genetic anomaly that occurs in about half of all prostate cancers, an instance of two genes changing places and fusing together.
This gene fusion, T2:ERG, is believed to cause prostate cancer. Studies in prostate tissues show that the gene fusion almost always indicates cancer.
The new urine test looks for the T2:ERG fusion as well as another marker, PCA3. This is combined with serum PSA measure to produce a risk assessment for prostate cancer. The test also predicts risk for having an aggressive tumor, helping doctors and patients make decisions about whether to wait and monitor test levels or pursue immediate biopsy.
"This combination test is not designed to say definitively at diagnosis whether a man has aggressive prostate cancer, but it can provide a more accurate estimate of the likelihood of having cancer and the likelihood of that cancer being aggressive," Tomlins says.
Provided by University of Michigan

Thursday, September 26, 2013

Vitamin D alone does little to protect bone health in postmenopausal women

While calcium supplements noticeably improved bone health in postmenopausal women, vitamin D supplements did not reduce bone turnover, according to a recent study accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).
26 sept 2013--Bone turnover is the body's natural process for breaking down old bone. In young people, the body forms enough new bone to replace what is lost. After age 30, however, bone mass in women begins to decline and the process speeds up after menopause. Osteoporosis develops when the body cannot replace bone as fast as it is broken down.
"Vitamin D and calcium interact to suppress bone turnover by decreasing parathyroid hormone levels," said the study's lead author, John Aloia, MD, of Winthrop University Hospital in Mineola, NY. "This can be beneficial in women who are vitamin D deficient. In women who already are receiving the recommended daily allowance of vitamin D, however, the study found there was no advantage to adding a vitamin D supplement."
The double-blind, placebo-controlled, parallel group, longitudinal factorial design study divided 159 postmenopausal women into four groups. One group received a combination of vitamin D and calcium, one was given 1,200 milligrams of calcium daily, one took 4,000 IU of vitamin D daily and the last group received placebos. To measure the effect supplements had on bone health, researchers measured bone turnover markers, such as parathyroid hormone levels in the blood, over the course of six months. In all, 120 women completed the study.
Researchers found a significant decline in bone turnover markers among women who were given daily calcium supplements. The vitamin D supplements did not have any effect on bone turnover markers, although the supplements did decrease parathyroid hormone levels.
"These findings suggest that vitamin D supplements over the recommended dietary allowance (RDA) do not protect bone health, whereas calcium supplements do have an effect," Aloia said. "Women do need to be cautious about the possibility of vascular side effects from too much calcium and should consult their physicians about whether their diet is adequate or whether they should take supplements at all."
More information: The article, "Calcium and Vitamin D Supplementation in Postmenopausal Women," was published online, ahead of print.
Provided by The Endocrine Society

Wednesday, September 25, 2013

Blood pressure cuff may save lives in patients with acute heart attack

Blood pressure cuff may save lives in patients with acute heart attack
A simple blood pressure cuff can reduce the damage to the cardiac muscle caused by a heart attack Credit: Aarhus University Hospital, Communication Unit
25sept 2013--In patients with an acute heart attack, remote ischemic conditioning – intermittent inflation of a blood pressure cuff to cut off blood flow to the arm during transportation to hospital for acute balloon dilatation – reduces subsequent cardiac symptoms and mortality after acute heart attack. The results are presented by researchers from Aarhus University Hospital and Aarhus University in European Heart Journal online 12 September 2013.
Activating the body's defense mechanism
Lack of oxygen for short periods of time in a distant organ by intermittently stopping blood flow to a limb, can protect another organ (i.e., the heart), during a prolonged period of lack of oxygen as it is the case during a heart attack. Professor Hans Erik Bøtker and his research team have previously demonstrated that remote ischemic conditioning reduces cardiac tissue damage on average 30% in patients undergoing acute balloon treatment for a heart attack. In patients treated with conditioning, a blood pressure cuff was placed around the upper arm and inflated to 200 mmHg for 5 minutes to cut off blood flow, and then released. The arm then rested for 5 minutes, and then the blood pressure cuff was re-applied. This procedure was repeated 4 times.
The rate of complications is halved
The researchers have now followed 251 patients assigned to receive conditioning or no conditioning in addition to usual care during transportation to the heart centre for up to 4 years. During the follow-up period the initial salvage of heart tissue by conditioning was translated into a clinical benefit for the patients. The occurrence of new heart symptoms was reduced by 51% in the conditioning group compared to the control group. The total number of deaths was low and death caused by heart disease was reduced by 61%.
The underlying mechanisms are thought to involve activation of endogenous protective systems that induces resistance towards tissue damage in the heart during a heart attack and in particular when re-opening the occluded heart vessel by balloon dilatation. Ph.D student Astrid Drivsholm Sloth, who conducted the present study, characterizes the treatment as promising and predicts that it will have widespread potential in the treatment of heart attacks. However, larger studies are required confirm the clinical implications of this smaller pilot trial such that it can be clarified whether the new intervention can reduce mortality and the development of heart failure after a heart attack.
Provided by Aarhus University

Tuesday, September 24, 2013

Simple, two-question survery accurately screens cancer patients for depression

Cancer patients can be accurately screened for major depression with a simple two-question survey, according to a study presented Sept. 23 at the American Society for Radiation Oncology's 55th Annual Meeting.
24 sept 2013--The two-question screening test proved to be as accurate as a longer nine-question screening test.
The study was presented at plenary session by William Small, Jr., MD, FASTRO, chair of the Department of Radiation Oncology of Loyola University Medical Center.
"We found that a two-question survey can effectively screen for depression," Small said. "We hope this will prompt more centers to screen for depression, and to refer patients for treatment when necessary."
The two-question survey asks whether, over the last two weeks, a patient has experienced:
  • Little interest or pleasure in doing things
  • Feeling down, depressed or hopeless
For each question, the patient can answer not at all (worth zero points); several days (1 point); more than half the days (two points); or nearly every day (3 points). A patient who scores a total of three or more points on both questions is considered to be at risk for being depressed.
The study included 455 cancer patients receiving radiation therapy at 37 centers in the United States. Patients were surveyed before or within two weeks of receiving their first radiation treatment. Sixteen percent screened positive for depression.
For comparison purposes, patients who screened positive were administered an in-depth telephone interview known as SCID, which is considered the gold standard for diagnosing depression. A random sample of patients who screened negative for depression also underwent the SCID interview. (SCID stands for Structured Clinical Interview for DSM IV Disorders.)
The two-question survey consists of the first two questions of the nine-question Patient Health Questionnaire. The study found that the abbreviated two-question survey was just as accurate as the full nine-question survey. In statistical terms, both surveys had an "area under the curve" of 0.83. (A 100 percent accurate test would have an area under the curve of 1.0.)
The two-question screening test was more accurate than two other screening tests researchers administered. These less-accurate screening tests are the Hopkins Symptom Checklist (0.79 area under the curve) and the National Comprehensive Cancer Network Distress Thermometer (0.60 area under the curve).
The study found that 78 percent of centers routinely screen patients for depression at the radiation therapy facility, with 51 percent screening at the initial visit. Mental health services were available at 68 percent of radiation therapy facilities. However, 67 percent of sites offered only social workers; 17 percent offered psychologists and 22 percent offered psychiatrists.
"We think the results of this large, nationwide trial will have a major impact on how cancer patients are screened for depression," Small said.
More information: The study is titled "Two Item Questionnaire Effectively Screens for Depression in Cancer Patients Receiving Radiotherapy."
Provided by Loyola University Health System

Monday, September 23, 2013

Metformin may increase risk of cognitive impairment

Metformin may increase risk of cognitive impairment
Metformin may increase the risk of cognitive impairment in patients with diabetes; however, calcium supplementation may attenuate this risk, according to research published online Sept. 5 in Diabetes Care.
23 sept 2013—Metformin may increase the risk of cognitive impairment in patients with diabetes; however, calcium supplementation may attenuate this risk, according to research published online Sept. 5 in Diabetes Care.
Eileen M. Moore, Ph.D., of the University of Melbourne in Australia, and colleagues conducted a subgroup analysis involving 104 patients with type 2 diabetes and 22 patients with impaired glucose tolerance who participated in the Australian Imaging, Biomarkers and Lifestyle study of aging. The authors sought to determine whether metformin, serum vitamin B12, or calcium supplements are associated with cognitive impairment in patients with diabetes.
The researchers found that, overall, patients with diabetes were 51 percent more likely to exhibit cognitive impairment than those without diabetes, and those taking metformin were more than twice as likely (2.23-fold) to exhibit cognitive impairment. After adjusting for age, sex, level of education, history of depression, serum vitamin B12, and metformin use, cognitive performance was improved for those patients who were also taking calcium supplements.
"Adequately powered, prospective, controlled trials are warranted to investigate further the association between diabetes, cognitive decline, and the effect of metformin therapy, as well as the possible amelioration using vitamin B12 and/or calcium supplementation," the authors write.
Several authors disclosed financial ties the biotechnology industry.
More information: Abstract 

Sunday, September 22, 2013

Digoxin use associated with higher risk of death for patients diagnosed with heart failure

Digoxin, a drug commonly used to treat heart conditions, was associated with a 72 percent higher rate of death among adults with newly diagnosed systolic heart failure, according to a Kaiser Permanente study that appears in the current online issue of Circulation: Cardiovascular Quality and Outcomes.
22 sept 2013--Digoxin is a drug derived from digitalis, a plant that has been used for more than 200 years to treat heart failure.
"These findings suggest that the use of digoxin should be reevaluated for the treatment of systolic heart failure in contemporary clinical practice" said Alan S. Go, MD, senior author of the study and research scientist at the Kaiser Permanente Division of Research.
The results of this study contrast with the findings of a randomized trial by the Digitalis Investigation Group conducted between 1991 and 1993, which showed that digoxin did not lower mortality among therapy patients with systolic heart failure, or, a malfunction in the way the left ventricle of the heart pumps blood. Following the group's study, professional societies issued clinical guidelines endorsing the use of digoxin for patients with systolic dysfunction.
The current study was conducted among 2,891 adults within Kaiser Permanente in Northern California who had newly diagnosed systolic heart failure between 2006 and 2008 and no prior digoxin use. Eighteen percent of the participants initiated digoxin during the study period.
Researchers followed the patients through December 31, 2010, to evaluate the effectiveness and safety of digoxin therapy. They found that digoxin use was associated with higher mortality but no significant difference in the risk of heart failure hospitalization.
There were a total of 801 deaths (737 off digoxin and 64 on digoxin). After adjustment for potential confounders, digoxin use was associated with a 72 percent higher relative rate of death.
There were 1,723 hospitalizations for heart failure overall (1,596 off digoxin, 127 on digoxin). However, after adjustment for potential confounders, digoxin use was not significantly associated with hospitalization for heart failure.
"Our community-based study population is more likely to represent patients with systolic heart failure in the modern era with regard to pathogenesis and treatment patterns," Dr. Go said. "Therefore, our results may more accurately represent the outcomes expected with digoxin for patients with systolic heart failure in typical present-day practices. As with all medication, treatment, or therapy plans, care decisions should always be made by physicians and their patients working together, with the patient's particular care needs and goals in mind."
Provided by Kaiser Permanente

Saturday, September 21, 2013

ALZHEIMER DAY SPECIALS NEWS

Alzheimer's 'epidemic' straining caregiver, community resources: report

Alzheimer's 'Epidemic' straining caregiver, community resources: report
Worldwide situation calls for comprehensive changes, authors say.
21 sept 2013—The so-called global Alzheimer's epidemic is leading to a shortage of caregivers for seniors and a lack of support for family members who look after elderly relatives, according to a new report.
Released Thursday, the report said the number of dependent older adults will increase to 277 million by 2050, and half of seniors who require personal care have dementia.
As the world's population ages, the traditional system of informal care provided by family, friends and the community will require much greater support from governments. This means leaders worldwide need to make dementia a priority by implementing national plans and having discussions about future strategies for long-term care, according to the World Alzheimer's 2013 report.
Worldwide, 13 percent of people 60 and older require long-term care, the report said. Between 2010 and 2050, the number of older adults with care needs will nearly triple, from 101 million to 277 million.
Long-term care is mainly about care for people with dementia, according to the report. About half of all older people who need personal care have dementia, and 80 percent of seniors in nursing homes have dementia. The worldwide cost of dementia is currently more than $600 billion.
More attention needs to be paid to helping dementia patients and their families "live well with dementia," the report said. It also called for a 10-fold increase in research funding to "re-energize" the work on dementia prevention, treatment and care.
Among specific recommendations are the following:
  • Having systems in place to monitor the quality of dementia care in all settings, whether in the community or care homes
  • Promoting autonomy and choice for patients at all stages of dementia and for their caregivers
  • Better integration and coordination between health and social care systems to meet patients' and caregivers' needs.
  • Adequately training frontline caregivers, with systems in place to ensure that paid and unpaid caregivers receive appropriate financial rewards—both to sustain the informal care system and improve recruitment and retention of paid caregivers
  • Properly valuing unpaid work of family caregivers. Although care in care homes is a preferred option for a significant minority, quality of life at home can be just as good and costs are comparable.
  • Monitoring quality of care in care homes through the quality of life and satisfaction of their residents, in addition to routine inspections.
"People with dementia have special needs. Compared with other long-term-care users they need more personal care, more hours of care and more supervision, all of which is associated with greater strain on caregivers, and higher costs," report author Martin Prince, a professor at the Institute of Psychiatry at King's College London, said in a college news release. "Their needs for care start early in the disease course, and evolve constantly over time, requiring advanced planning, monitoring and coordination."
"We need to value the unpaid contribution of family caregivers more, and reward paid caregivers better," Prince said. "We can build quality into our care systems, but to do so while containing costs and achieving equity of access for all will be a challenge."
More information: The U.S. National Institute on Aging has more about Alzheimer's disease.

Scientists reveal how beta-amyloid may cause Alzheimer's

Scientists reveal how beta-amyloid may cause Alzheimer's
Artist rendering of β-amyloid oligomers (red) and receptor LilrB2 or PirB (green) in neuronal synapses of Alzheimer’s brains. Inhibitory immune receptors LilrB2 in human brain and its murine ortholog PirB were discovered to act as neuronal receptors for β-amyloid oligomers, which contribute to synaptic dysfunction and memory defects in Alzheimer’s disease. Credit: Eric Smith, Carla Shatz, and Taeho Kim

Scientists at the Stanford University School of Medicine have shown how a protein fragment known as beta-amyloid, strongly implicated in Alzheimer's disease, begins destroying synapses before it clumps into plaques that lead to nerve cell death.
21 sept 2013--Key features of Alzheimer's, which affects about 5 million Americans, are wholesale loss of synapses—contact points via which nerve cells relay signals to one another—and a parallel deterioration in brain function, notably in the ability to remember.
"Our discovery suggests that Alzheimer's disease starts to manifest long before plaque formation becomes evident," said Carla Shatz, PhD, professor of neurobiology and of biology and senior author of a study that will be published Sept. 20 in Science.
Investigators at Harvard University also contributed to the study. The research, conducted in mice and in human brain tissue, may help to explain the failures in recent years of large-scale clinical trials attempting to slow the progression of Alzheimer's by pharmacologically ridding the brain of amyloid plaques. It may also point the way to better treatments at earlier stages of the disease.
Beta-amyloid begins life as a solitary molecule but tends to bunch up—initially into small clusters that are still soluble and can travel freely in the brain, and finally into the plaques that are hallmarks of Alzheimer's. The study showed for the first time that in this clustered form, beta-amyloid can bind strongly to a receptor on nerve cells, setting in motion an intercellular process that erodes their synapses with other nerve cells.
Synapses are the connections between nerve cells. They are essential to storing memories, processing thoughts and emotions, and planning and ordering how we move our bodies. The relative strength of these connections, moreover, can change in response to new experiences.
Using an experimental mouse strain that is highly susceptible to the synaptic and cognitive impairments of Alzheimer's disease, Shatz and her colleagues showed that if these mice lacked a surface protein ordinarily situated very close to synapses, they were resistant to the memory breakdown and synapse loss associated with the disorder. The study demonstrated for the first time that this protein, called PirB, is a high-affinity receptor for beta-amyloid in its "soluble cluster" form, meaning that soluble beta-amyloid clusters stick to PirB quite powerfully. That trips off a cascade of biochemical activities culminating in the destruction of synapses.
Shatz is the Sapp Family Provostial Professor, as well as the director of Bio-X, a large Stanford interdisciplinary consortium drawing on medical, engineering and biology faculty. She has been studying PirB for many years, but in a different context. In earlier work, Shatz explored the role of PirB in the brain using genetically engineered mice that lacked it. She discovered that PirB, previously thought to be used only by cells in the immune system, is also found on nerve cells in the brain, where it slows the ability of synapses to strengthen in proportion to the extent to which they are engaged, and actually promotes their weakening. Such brakes are desirable in the brain because too-easy synaptic strength-shifting could trigger untoward consequences like epilepsy.
In the new study, Shatz's team employed a different genetically engineered mouse strain whose genome contained mutant copies of two separate human genes. Each of these mutations is known to predispose individuals to Alzheimer's disease. When both mutations are present in mice, which ordinarily never develop amyloid plaques, the result is abundant amyloid plaque deposition with advancing age, as well as an eventual decline in performance on various tests of memory.
Versatile proteins could be new target for Alzheimer's drugs
PirB (red) is heavily concentrated on the surface of growing nerve cells. Credit: Dr. Carla Shatz, Stanford University.
"I've always found it strange that these mice—and, in fact, all the mouse models for Alzheimer's disease that we and other people study—seem not to have any problems with memory until they get old," Shatz said. "These mice's brains have high levels of beta-amyloid at a very early age."
Shatz found herself wondering if there might be a more sensitive measure of beta-amyloid's early effects on young brains. A study she co-authored in 2012 demonstrated that a particular mouse brain region, whose constituent synapses are normally quite nimble at shifting their relative strengths in response to early-life experiences, showed no such flexibility in young Alzheimer's-prone mice. This suggested that subtle Alzheimer's-related effects might appear far earlier than plaques or memory loss do.
Now, Shatz wondered whether eliminating PirB from the Alzheimer's mouse strain could restore that flexibility. So her team bred the Alzheimer's-genes-carrying strain with the PirB-lacking strain to create hybrids. Experimentation showed that the brains of young "Alzheimer's mice" in which PirB was absent retained as much synaptic-strength-shifting flexibility as those of normal mice. PirB-lacking Alzheimer's mice also performed as well in adulthood as normal mice did on well-established tests of memory, while their otherwise identical PirB-expressing peers suffered substantial synapse and memory loss.
"The PirB-lacking Alzheimer's mice were protected from the beta-amyloid-generating consequences of their mutations," Shatz said. The question now was, why?
Taeho Kim, PhD, a postdoctoral scholar in Shatz's lab and the lead author of the new study, advanced a hypothesis he had cooked up in 2011 while describing his research to a captive audience of one—his then-4-year-old son, whom he was driving to the Monterey Bay Aquarium: Maybe PirB and beta-amyloid were binding. This might cause PirB to stomp on the brakes even more than it usually does, weakening synapses so much they could disappear altogether, taking memories with them.
Further experiments showed that, indeed, beta-amyloid binds strongly to PirB. While PirB is specifically a mouse protein, Kim also identified for the first time an analogous beta-amyloid receptor in the human brain: a protein called LilrB2.
In another experiment, Kim compared proteins in the brains of PirB-lacking Alzheimer's mice to those in the brains of PirB-expressing Alzheimer's mice. The latter showed significantly increased activity on the part of a few workhorse proteins, notably an enzyme called cofilin. Subsequent studies also found that cofilin activity in the brains of autopsied Alzheimer's patients is substantially higher than in the brains of people without the disorder.
Here the plot thickens: Cofilin works by breaking down actin, a building-block protein essential to maintaining synaptic structure. And, as the new study also showed, beta-amyloid's binding to PirB results in biochemical changes to cofilin that revs up its actin-busting, synapse-disassembling activity.
"No actin, no synapse," Shatz said.
Kim's hypothesis appears to have been correct. Beta-amyloid binds to PirB (and, the researchers proved, to its human analog, LilrB2), boosting cofilin activity and busting synapses' structural integrity.
Although there may be other avenues of destruction along which synapses are forced to walk, Shatz doubts there are very many. She said she thinks the direct participation of beta-amyloid—as well as cofilin, so clearly implicated in synaptic breakdown—suggests that this pathway is important. "We looked at human brains in this study, too, and we found that a similar derangement of cofilin activity is present in Alzheimer's brains but not healthy brains," she said.
Shatz suggested that drugs that block beta-amyloid's binding to PirB on nerve-cell surfaces—for example, soluble PirB fragments containing portions of the molecule that could act as decoy—might be able to exert a therapeutic effect. "I hope this finding will be enticing enough to pharmaceutical and biotechnology companies that someone will try pushing this idea forward," she said.
More information: Human LilrB2 Is a beta-Amyloid Receptor and Its Murine Homolog PirB Regulates Synaptic Plasticity in an Alzheimer's Model," by T. Kim et al. Science, 2013. DOI: 10.1126/science.1242077
Provided by Stanford University Medical Center

Study finds brain training enhances brain health of adults over 50

Study finds brain training enhances brain health of adults over 50
The structural connection (in green) between the temporal and frontal lobe (in blue), improved after 12 hours of directed brain training. Credit: Cerebral Cortex, Oxford University Press publication

Strategy-based cognitive training has the potential to reverse age-related brain decline, according to the results of a study conducted by researchers at the Center for BrainHealth at The University of Texas at Dallas.
21 sept 2013--The findings were published online by Cerebral Cortex. The study has found that complex cognitive training significantly improves cognitive brain health.
"The world's aging population is growing disproportionately. Our expected lifespan has reached an all-time high of more than 78 years, yet previous research shows cognitive decline may begin in the early 40s," said Dr. Sandra Bond Chapman, founder and chief director of the Center for BrainHealth and Dee Wyly Distinguished University Chair at UT Dallas. "Until recently, cognitive decline in healthy adults was viewed as an inevitable consequence of aging. This research shows that neuroplasticity can be harnessed to enhance brain performance and provides hope for individuals to improve their own mental capacity and cognitive brain health by habitually exercising higher-order thinking strategies no matter their age."
The study found that one-hour sessions of directed brain training per week for 12 weeks can alter brain function, inducing increased blood flow, enhanced information communication across key brain regions, and expansion of the structural connections between brain regions related to new learning.
Using three MRI-based measurements, researchers examined brain changes across three time points in a randomized sample of individuals ages 56 to 71. The study found three significant training-related brain changes at rest: increases in global and regional cerebral blood flow (CBF), greater synchrony in important brain networks, and increased white matter integrity, which is the wiring of the brain that allows information to travel betweenbrain cells.
"Advances in imaging are allowing us to measure brain change in a short time period," said Dr. Sina Aslan, founder and president of Advance MRI and collaborator on the study. "Through this research we are able to see that cognitive training increases brain blood flow, which is a sensitive physiological marker of brain health. Previous research shows brain blood flow decreases in people beginning in their 20s. The finding that global brain blood flow can be increased with complex mental activity, as this study demonstrates, suggests that staying mentally active helps reverse and potentially prevent brain losses and cognitive decline with aging."
The capacity to increase whole brain blood flow after complex mental training may have clinical implications in both healthy aging populations and those diagnosed with brain disease such as Alzheimer's, Aslan said.
"Greater levels of brain blood flow are associated with higher cognitive performance," Chapman said. "With upwards of 8 percent increase in brain blood flow, this research shows that participants are regaining measurablebrain health. The brain and cognitive gains may help achieve a younger working brain with all the benefits of rich experience, knowledge base and wisdom as manifested in an older brain."
Chapman also suggested that the findings are important for younger adults and encourages adoption of healthy brain habits in early adulthood to stave off cognitive decline.
Also noteworthy was that researchers found significant improvement in cognitive performance, as well as a significant relationship between brain changes and improved cognitive performance. Among the participants who were randomized into the brain training group, researchers saw improvement in two cognitive domains: strategic reasoning, which is the ability to synthesize generalized meanings or extract larger ideas from lengthy input, and a measure of executive function that demonstrates the ability to abstract concepts. As a follow up to the study, researchers have investigated how long the improvements have been maintained and have found that the brain gains measured have been maintained at one year post-training and longer.
Both the brain and cognitive plasticity changes in response to strategy-based mental training demonstrate the neurogenerative potential in the cognitively healthy aging brain.
"We are increasingly interested in examining cognitive change with age," said Dr. Molly Wagster of the National Institute on Aging, part of the National Institutes of Health, which co-funded the study.
"Most older Americans likely will experience subtle changes in their ability to learn and remember, and studies such as this – examining one way to possibly affect cognitive change – are important," Wagster said. "It advances our understanding of how cognitive training might affect brain changes associated with cognitive decline. While further study is needed, this research suggests that it may never be too late to participate in activities to maintain or even improve our cognitive health."
Provided by University of Texas at Dallas

Memory-related brain network shrinks with aging

Memory-related brain network shrinks with aging
Network of brain regions, highlighted in red and yellow, show atrophy in both healthy aging and neurodegenerative disease. The regions highlighted are susceptible to normal aging and dementia.

Brain regions associated with memory shrink as adults age, and this size decrease is more pronounced in those who go on to develop neurodegenerative disease, reports a new study published Sept. 18 in the Journal of Neuroscience (Vol. 33:38). The volume reduction is linked with an overall decline in cognitive ability and with increased genetic risk for Alzheimer's disease, the authors say.
21 sept 2013--"Our results identify a specific pattern of structural brain changes that may provide a possible brain marker for the onset of Alzheimer's disease," said Nathan Spreng, assistant professor of human development and the Rebecca Q. and James C. Morgan Sesquicentennial Faculty Fellow in Cornell's College of Human Ecology.
The study is one of the first to measure structural changes in a collection of brain regions – not just one single area – over the adult life course and from normal aging to neurodegenerative disease, said Spreng, who co-authored the study with Gary R. Turner of York University in Toronto.
Overall, they studied brain data from 848 individuals spanning the adult lifespan, using data from the Open Access Series of Imaging Studies and the Alzheimer's Disease Neuroimaging Initiative (ADNI). About half of the ADNI sample was assessed multiple times over several years, allowing the researchers to measure brain changes over time and determine who did and did not progress to dementia.
The researchers found that brain volume in the default network (a set of brain regions associated with internally generated thoughts such as memory) declined in both healthy and pathological aging. The researchers noted the greatest decline in Alzheimer's patients and in those who progressed from mild cognitive impairment to Alzheimer's disease. Reduced brain volumes in these regions were associated with declines in cognitive ability, the presence of known biological markers of Alzheimer's disease and with carrying the APOE4 variant of APOE gene, a known risk factor for Alzheimer's.
"While elements of the default network have previously been implicated in aging and neurodegenerative disease, few studies have examined broad network changes over the full adult life course with such large participant samples and including both behavioral and genetic data," said Spreng. "Our findings provide evidence for a network-based model of neurodegenerative disease, in which progressive brain changes spread through networks of connected brain regions."
The study, "Structural Covariance of the Default Network in Healthy and Pathological Aging," was supported in part by the Canadian Institutes of Health Research.
Provided by Cornell University

Trial to test prevention of Alzheimer's has begun

More than a century ago, Alois Alzheimer, a Bavarian physician, first identified the neurodegenerative brain condition that came to be known as Alzheimer's disease. Finding ways to diagnose and treat this disease has frustrated scientists and clinicians ever since.
21 sept 2013--Now the long and hard-fought campaign against Alzheimer's has reached a potentially significant milestone: the launch of the first clinical trials to test whether giving new drug treatments before dementia can prevent Alzheimer's.
Brent Whitney, 34, who has an inherited form of Alzheimer's but does not yet have symptoms of the disease, hopes to participate in the study. The lives of his grandmother and 10 of her 13 siblings were cut short by the Alzheimer's gene mutation, and the mutation continues to affect succeeding generations of the family.
"The start of this trial is a very exciting moment in Alzheimer's disease research, and it gives me renewed hope for a future without Alzheimer's," Whitney said. "I hope my grandchildren someday learn of this condition in history books, like I learned about polio."
The trial is testing two new drug treatments and is led by principal investigator Randall Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor in Neurology at Washington University School of Medicine in St. Louis and director of the Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU).
"We believe that the diverse portfolio of drugs and approaches of the DIAN-TU trial will accelerate the discovery of an effective treatment for Alzheimer's," Bateman said. "This trial is possible because of the outstanding support of multiple stakeholders, including patients and family members, pharma partners, the Alzheimer's Association, the National Institutes of Health, academic researchers and highly dedicated trial operations groups."
The new trial is funded by a unique mix of private and public resources, including:
  • A grant from the National Institutes of Health (NIH) for fiscal year 2013 in the amount of $1.5 million, awarded on Sept. 18, with the total amount of as much as $6 million over the four years of the project;
  • The largest Alzheimer's Association grant given to date, nearly $4.2 million;
  • Donation of the treatments used in the trials from the drugs' manufacturers, Roche and Eli Lilly and Company, which also provided major financial support for the trial;
  • Donation of a new agent for imaging brain plaques, Amyvid, by Avid Radiopharmaceuticals, Inc., a wholly owned subsidiary of Lilly; and
  • Donation by CogState of a computerized set of cognitive skills tests to help assess cognitive function in participants.
John C. Morris, MD, is director of the Charles F. and Joanne Knight Alzheimer's Disease Research Center and principal investigator of the Dominantly Inherited Alzheimer Network, which laid much of the scientific groundwork that made a DIAN-TU trial of preventive treatments possible.
"Trying to prevent Alzheimer's symptoms from occurring is a new strategy, but much of what we've learned in recent years about Alzheimer's and the brain has suggested that prevention has a significantly better chance of succeeding than treatment after cognitive impairment," said Morris, the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology. "We are most appreciative of the support we have received to test this new approach."
For more information on the trial, see http://www.DIANXR.org.
One of the treatments under study in the new trial is gantenerumab, an antibody made by Roche that binds to all forms of aggregated amyloid beta and helps remove them from the brain.
Another treatment that will be evaluated is a monoclonal antibody known as solanezumab that binds to soluble monomeric forms of amyloid-beta after they are produced, allowing them to be cleared before they clump together to form beta-amyloid plaques.
David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of neurology, is listed on the patent related to the antibody that is co-owned by Washington University in St. Louis and Lilly. Washington University has licensed its patent rights to Lilly. The financial interests of the university and Holtzman in this patent are managed in accordance with applicable conflict-of-interest policies and regulations.
Provided by Washington University School of Medicine

Cognitive enhancers don't improve cognition, function in people with mild cognitive impairment

Cognitive enhancers—drugs taken to enhance concentration, memory, alertness and moods—do not improve cognition or function in people with mild cognitive impairment in the long term, according to a new study by researchers at St. Michael's Hospital.
21 sept 2013--In fact, patients on these medications experienced significantly more nausea, diarrhea, vomiting and headaches, according to the study published today in the Canadian Medical Association Journal.
"Our findings do not support the use of cognitive enhancers for mild cognitive impairment," wrote Dr. Andrea Tricco and Dr. Sharon Straus, who are both scientists in the hospital's Li Ka Shing Knowledge Institute. Dr. Straus is also a geriatrician at the hospital.
Mild cognitive impairment is a condition characterized by memory complaints without significant limitations in everyday activity. Between 3 and 42 per cent of people are diagnosed with the condition each year, about 4.6 million people worldwide. Each year about 3 to 17 per cent of people with mild cognitive impairment will develop dementia, such as Alzheimer's disease. Given the aging population, it's estimated the number of Canadians with dementia will double to more than 1 million in the next 25 years.
It has been hypothesized that cognitive enhancers may delay the onset of dementia. Families and patients are increasingly requesting these drugs even though their efficacy for patients with mild cognitive impairment has not been established. In Canada, cognitive enhancers can be obtained only with special authorization.
Drs. Tricco and Straus conducted a review of existing evidence to understand the efficacy and safety of cognitive enhancers. They looked at eight randomized trials that compared one of four cognitive enhancers (donepezil,rivastigmine, galantamine or memantine) to a placebo among patients diagnosed with mild cognitive impairment.
While they found short-term benefits to using these drugs on one cognition scale, there were no long-term effects after about a year and a half. No other benefits were observed on the second cognition scale or on function, behaviour, and mortality. As well, patients on these medications experienced significantly more nausea, diarrhea, vomiting and headaches. One study also found a higher risk of a heart condition known as bradycardia (slow heartbeat) among patients who received galantamine.
"Our results do not support the use of cognitive enhancers for patients with mild cognitive impairment," the authors wrote. "These agents were not associated with any benefit and led to an increase in harms. Patients and their families should consider this information when requesting these medications. Similarly, health care decision-makers may not wish to approve the use of these medications for mild cognitive impairment, because these drugs might not be effective and are likely associated with harm."
This study was funded by the Drug Safety and Effectiveness Network/Canadian Institutes of Health Research.
Another St. Michael's study published in the CMAJ in April found no evidence that drugs, herbal products or vitamin supplements help prevent cognitive decline in healthy older adults. That review, led by Dr. Raza Naqvi, a University of Toronto resident, found some evidence that mental exercises, such as computerized memory training programs, might help.
Provided by St. Michael's Hospital

Friday, September 20, 2013

More diseases responsible for dementia than previously thought, research finds

More diseases responsible for dementia than previously thought, research finds
A recent study by the Clinical Institute of Neurology at the MedUni Vienna has shown that neurodegenerative diseases other than Alzheimer's disease are more common among older people than previously thought. Researchers believe that more personalised treatment may offer considerable opportunities to address this.
20sept 2013--The Vienna Trans-Danube Aging (VITA) study has just been published in the September edition of the highly respected journal Acta Neuropathologica and has been created by researchers at the Medical University of Vienna, the SMZ-Ost Donauspital and the Ludwig Boltzmann Institute of Gerontology. The study's primary author, Gabor G. Kovacs from the Clinical Institute of Neurology, sums up the key findings of the study as follows: "The VITA study shows that, in addition to the classic Alzheimer's-associated changes in the ageing brain, there are other neurodegenerative conditions that are characterised by protein deposits in the brain."
VITA study as the starting point for more personalised treatment concepts for patients with dementia
The scientists also discovered that combinations of these "proteinopathies" with each other and with diseases of the blood vessels are more common than previously assumed. According to Dr. Kovacs, some of thesepathological changes can lead to dementia progressing more quickly. However there also appear to be variations that are less "harmful" and which therefore progress less quickly.
Says Kovacs: "Further studies are therefore required in which patients will be monitored in order to determine which of the combinations are associated with more favourable or more deleterious prognoses for the patients." The authors also outline new conditions that are associated with dementia in the ageing brain. Kovacs believes that the factors identified in this context represent the starting point from which patients with dementia will in future be able to be offered more personalised and therefore more effective treatment.
Pan-European long-term study led by the MedUni Vienna
As part of the long-term VITA study which has been ongoing since 2000, a group of residents of Vienna's districts 21 and 22 who were born between May 1925 and June 1926 was investigated. Regular medical examinations were performed at Vienna's SMZ-Ost Donauspital. A total of 233 people who died at the Donauspital also underwent general pathological and specifically neuropathological examinations.
The VITA study is an important part of the ongoing EU project DEVELAGE. Under the supervision of the Institute of Neurology at the MedUni Vienna, eight partner centres from six European countries (Austria, France, Germany, Italy, the Netherlands and Spain) are collaborating on the DEVELAGE project (www.develage.eu). The VITA study was initiated by a research group established by the MedUni Vienna and the Donauspital and led by Peter Fischer, Director of the Psychiatry Department at Vienna's SMZ-Ost Donauspital.
World Congress of Neurology in Vienna from 21st to 26th September 2013
At the end of September (21 to 26 September 2013), the international research elite will be converging on Vienna for the 21st World Congress of Neurology. The world's largest specialist conference on the subject of neurology will this year be inspired by the motto of "Neurology in the age of globalisation", and is being organised jointly by the WFN (World Federation of Neurology) and the ÖGN (Austrian Neurology Society) with the collaboration of the EFNS (European Federation of Neurological Societies). President of the congress is Eduard Auff, Head of the University Department of Neurology at the MedUni Vienna. More information on the World Congress of Neurology can be found at: www.wcn-neurology.org
More information: Kovacs, G. et al. Non-Alzheimer neurodegenerative pathologies and their combinations are more frequent than commonly believed in the elderly brain: a community-based autopsy series, Acta Neuropathol, 2013 Sep;126(3):365-84. www.ncbi.nlm.nih.gov/pubmed/23900711
Provided by Medical University of Vienna