Investing in cardiovascular research benefits economy

Main Category: Cardiovascular / Cardiology
Also Included In: Public Health
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
Investing in cardiovascular research benefits economy

Investing in cardiovascular disease research in Canada provides economic and societal benefits to Canadians, according to new research published in CMAJ Open.

"Our main goal was to understand how much "bang" we were getting from our research "buck" and whether investing in cardiovascular disease research is worthwhile from a population health perspective," writes Dr. Claire de Oliveira, scientist and health economist with the Centre for Addiction and Mental Health (CAMH), Toronto, with coauthors.

Cardiovascular disease is the number one cause of hospitalization and death in Canada. For every $69 spent on cardiovascular health care in the country, $1 was spent on research through public and charitable sector funding.

"We found an internal rate of return of 20.6% for investment in cardiovascular disease research by the public and charitable sectors," the authors write. "Thus, for every $1 spent on public or charitable sources, Canadians receive an income stream of about $0.21 per year in perpetuity. Considering a minimum acceptable rate of return of 12%, this investment is quite attractive."

The internal rate of return is "the annual monetary benefit to the economy for each dollar invested in cardiovascular disease research."

Spending on cardiovascular disease research in Canada has increased from roughly $13 million in 1975 to $41 million in 1990 and $96 million in 2005.

The authors hope this study will help funders determine the return on investment and whether they are spending appropriately.

"Our estimates provide evidence that investing in cardiovascular disease research is valuable and that investments in medical research are returned many times over in societal benefits," conclude the authors.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Estimating the payoffs from cardiovascular disease research in Canada: an economic analysis

CMAJ Open - doi: 10.9778/cmajo.20130003

Authors: Claire de Oliveira, MA, PhD, Hai V. Nguyen, PhD, Harindra C. Wijeysundera, MD, PhD, William W.L. Wong, PhD, Gloria Woo, PhD, Paul Grootendorst, PhD, Peter P. Liu, MD, MSc, Murray D. Krahn, MD, MSc

CMAJ Open

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Research shows that people are remaining healthier later in life

Main Category: Seniors / Aging
Also Included In: Public Health
Article Date: 30 Jul 2013 - 1:00 PDT Current ratings for:
Research shows that people are remaining healthier later in life

A new study, conducted by David Cutler, the Otto Eckstein Professor of Applied Economics, shows that, even as life expectancy has increased over the past two decades, people have become increasingly healthier later in life.

"With the exception of the year or two just before death, people are healthier than they used to be," Cutler said. "Effectively, the period of time in which we're in poor health is being compressed until just before the end of life. So where we used to see people who are very, very sick for the final six or seven years of their life, that's now far less common. People are living to older ages and we are adding healthy years, not debilitated ones."

The study results are based on data collected between 1991 and 2009 from nearly 90,000 individuals who responded to the Medicare Current Beneficiary Survey (MCBS). Cutler reported these findings in work with Mary Beth Landrum of Harvard Medical School and Kaushik Ghosh of the National Bureau of Economic Research.

To understand whether people are becoming healthier, Cutler first had to answer a question that, at least initially, seemed impossible to solve: How far are people from death?

"There are two basic scenarios that people have proposed about the end of life," he said. "The first argues that what medical science is doing is turning us into light bulbs - that is, we work well until suddenly we die. This is also called the rectangularization of the life curve, and what it says is that we're going to have a fairly high quality of life until the very end.

"The other idea says life is a series of strokes, and medical care has simply gotten better at saving us," he continued. "So we can live longer because we've prevented death, but those years are not in very good health, and they are very expensive - we're going to be in wheelchairs, in and out of hospitals and in nursing homes."

While researchers have tried to tackle the question of which model is more accurate, different studies have produced competing results. One reason for the confusion, Cutler suggested, is that such efforts are simply looking at the wrong end of someone's life.

"Most of our surveys measure health at different ages, and then use a model to estimate how long people have to live," he said. "But the right way to do this is to measure health backwards from death, not forwards. We should start when someone dies, then go back a year and measure their health, then go back two years, three years, and so on."

The MCBS allows researchers to do just that, Cutler said, by linking survey responses to participants' Medicare records for the rest of their life, meaning researchers can calculate - in some cases to the day - exactly how far participants were from death when they answered the survey.

By comparing that data with survey responses on how well people were able to care for themselves - whether they were able to cook, clean, bathe themselves, dress themselves, walk and manage money - Cutler was able to determine how healthy people were relative to how close or far away they were from dying.

Going forward, Cutler hopes to unravel the reasons why some conditions are today less debilitating than in the past. Part of the change, he said, will certainly be chalked up to increased access and improvements to care, but there are a host of other factors that make answering the question "very very difficult."

"There seems to be a clear relationship between some conditions that are no longer as debilitating as they once were and areas of improvement in medicine," he said. "The most obvious is cardiovascular disease - there are many fewer heart attacks today than there used to be, because people are now taking cholesterol-lowering drugs, and recovery is much better from heart attacks and strokes than it used to be. A person who suffered a stroke used to be totally disabled, but now many will survive and live reasonable lives. People also rebound quite well from heart attacks."

What's more, he said, as standards of care have improved, so too has the public's knowledge of how to live healthier lives.

"People are much better educated about their health now," Cutler said. "People are taking steps to help prevent long-term cognitive decline. We don't have any way yet to slow down something like Alzheimer's or Parkinson's, but there is a lot we can do for other health problems."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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The research reported here was sponsored by the National Institute on Aging.

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Research approach highlights potential therapeutic targets for Alzheimer's disease

Main Category: Alzheimer's / Dementia
Article Date: 26 Jul 2013 - 1:00 PDT Current ratings for:
Research approach highlights potential therapeutic targets for Alzheimer's disease

Key molecular pathways that ultimately lead to late-onset Alzheimer's disease, the most common form of the disorder, have been identified by researchers at Columbia University Medical Center (CUMC). The study, which used a combination of systems biology and cell biology tools, presents a new approach to Alzheimer's disease research and highlights several new potential drug targets. The paper was published in the journal Nature.

Much of what is known about Alzheimer's comes from laboratory studies of rare, early-onset, familial (inherited) forms of the disease. "Such studies have provided important clues as to the underlying disease process, but it's unclear how these rare familial forms of Alzheimer's relate to the common form of the disease," said study leader Asa Abeliovich, MD, PhD, associate professor of pathology and cell biology and of neurology in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at CUMC. "Most important, dozens of drugs that 'work' in mouse models of familial disease have ultimately failed when tested in patients with late-onset Alzheimer's. This has driven us, and other laboratories, to pursue mechanisms of the common form of the disease."

Non-familial Alzheimer's is complex; it is thought to be caused by a combination of genetic and environmental risk factors, each having a modest effect individually. Using so-called genome-wide association studies (GWAS), prior reports have identified a handful of common genetic variants that increase the likelihood of Alzheimer's. A key goal has been to understand how such common genetic variants function to impact the likelihood of Alzheimer's.

In the current study, the CUMC researchers identified key molecular pathways that link such genetic risk factors to Alzheimer's disease. The work combined cell biology studies with systems biology tools, which are based on computational analysis of the complex network of changes in the expression of genes in the at-risk human brain.

More specifically, the researchers first focused on the single most significant genetic factor that puts people at high risk for Alzheimer's, called APOE4 (found in about a third of all individuals). People with one copy of this genetic variant have a three-fold increased risk of developing late-onset Alzheimer's, while those with two copies have a ten-fold increased risk. "In this study," said Dr. Abeliovich, "we initially asked: If we look at autopsy brain tissue from individuals at high risk for Alzheimer's, is there a consistent pattern?"

Surprisingly, even in the absence of Alzheimer's disease, brain tissue from individuals at high risk (who carried APOE4 in their genes) harbored certain changes reminiscent of those seen in full-blown Alzheimer's disease," said Dr. Abeliovich. "We therefore focused on trying to understand these changes, which seem to put people at risk. The brain changes we considered were based on 'transcriptomics' - a broad molecular survey of the expression levels of the thousands of genes expressed in brain."

Using the network analysis tools mentioned above, the researchers then identified a dozen candidate "master regulator" factors that link APOE4 to the cascade of destructive events that culminates in Alzheimer's dementia. Subsequent cell biology studies revealed that a number of these master regulators are involved in the processing and trafficking of amyloid precursor protein (APP) within brain neurons. APP gives rise to amyloid beta, the protein that accumulates in the brain cells of patients with Alzheimer's. In sum, the work ultimately connected the dots between a common genetic factor that puts individuals at high risk for Alzheimer's, APOE4, and the disease pathology.

Among the candidate "master regulators" identified, the team further analyzed two genes, SV2A and RFN219. "We were particularly interested in SV2A, as it is the target of a commonly used anti-epileptic drug, levetiracetam. This suggested a therapeutic strategy. But more research is needed before we can develop clinical trials of levetiracetam for patients with signs of late-onset Alzheimer's disease."

The researchers evaluated the role of SV2A, using human-induced neurons that carry the APOE4 genetic variant. (The neurons were generated by directed conversion of skin fibroblasts from individuals at high risk for Alzheimer's, using a technology developed in the Abeliovich laboratory.) Treating neurons that harbor the APOE4 at-risk genetic variant with levetiracetam (which inhibits SV2A) led to reduced production of amyloid beta. The study also showed that RFN219 appears to play a role in APP-processing in cells with the APOE4 variant.

"Our findings suggest that both SV2A and RFN219 are candidate drug targets," said Dr. Abeliovich. "What's exciting to us is that these approaches may play a role in the development of drugs for the common non-familial form of Alzheimer's disease. This has been an enormous challenge."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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The paper is titled, "Integrative genomics identifies APOE ?4 effectors in Alzheimer's disease." The other contributors are all members of CUMC's Taub Institute for Research on Alzheimer's Disease and the Aging Brain: Herve Rhinn, Ryousuke Fujita, Liang Qiang, Rong Chen, and Joseph H. Lee. Dr. Lee is also a member of CUMC's Gertrude H. Sergievsky Center.

The authors declare no financial or other conflicts of interest. Subsequent to the acceptance of this paper, Dr. Abeliovich received a grant from UCB, Inc. for an unrelated study.

The study was supported by grants from the National Institutes of Health (R01AG042317 and RO1NS064433).

Columbia University Medical Center

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Research Into Special Degradable Particles To Reduce Tooth Decay Wins Venture Prize Award - Could Bring Toothache Relief To Millions

Main Category: Dentistry
Article Date: 12 Jul 2013 - 2:00 PDT Current ratings for:
Research Into Special Degradable Particles To Reduce Tooth Decay Wins Venture Prize Award - Could Bring Toothache Relief To Millions

Researchers have developed new degradable particles, about the same size as small holes in teeth, which are designed to enter these holes and physically block and repair decayed teeth.

These particles are special glasses and can be incorporated into toothpaste and will dissolve in the mouth releasing calcium and phosphate that form tooth mineral. This reduces tooth pain, cuts back on the incidences of tooth decay and repairs teeth.

This could bring relief to the estimated 20 million adults in UK (40 per cent of the UK adult population) who are prone to tooth sensitivity. Indeed, untreated tooth decay or cavities in permanent teeth is the most common of all 291 major diseases and injuries assessed in the latest Global Burden of Diseases study. It affects 35 per cent of the world's population.

The team behind this development, led by Professor Robert Hill from Queen Mary, University of London have won the £25,000 materials science Venture Prize, awarded by the Worshipful Company of Armourers and Brasiers.

"These new particles dissolve faster than existing ones and are also softer than tooth enamel," said Professor Hill. "They have a more expanded open structure and this allows water to go into the glass structure faster and the calcium and phosphate ions to come out faster. Also, while existing particles are significantly harder and abrade away the enamel during brushing, our new particles will be softer."

Tooth pain is associated with hot, cold or mechanical stimulation and is caused by fluid flow within small tubes located within the tooth. These tubes can become exposed as a result of the gums receding, hence the expression "long in the tooth" or through the loss of the outer enamel coating as a result of tooth decay, acid erosion or mechanical wear associated with tooth brushing. These new bioactive particles can also re-mineralise the holes via the release of calcium and phosphate ions.

"This is a hugely exciting development which could benefit millions of people not only throughout the UK and Europe but right across the world," said Professor Bill Bonfield, chairman of the Armourers & Brasiers Venture Prize judging panel. "It meets our aim to encourage innovative scientific entrepreneurship in the UK and provide funding, which is often difficult to source, to bring new materials science research like this to market."

In addition to Professor Hill, who is head of dental physical sciences at Barts and the London School of Medicine and Dentistry, Queen Mary. The team comprises: Dr David Gillam clinical lecturer and dentist, Dr Natalia Karpukhina an expert on bioactive glasses and Dr Pushkar Wadke from Queen Mary Innovations.

"This award will enable us to get our research from the laboratory into a prototype toothpaste, said Professor Hill. "The difficult step is getting money to enable the translation of research in the laboratory into commercial products. This is what the Venture Prize Award will enable us to do."

This development has come at an appropriate time. The latest Global Industry Analysts report outlined that the total world market for toothpaste is forecast to reach US$12.6 billion (£8.1billion) by the year 2015. This increase it outlines will be led by product innovations, rising population levels and greater awareness about oral hygiene.

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Alongside Professor Bonfield on the judging panel were Cambridge based materials scientist Professor Sir Colin Humphreys, representatives from First Ventures which invests and advises high potential technology companies and Members of the Armourers & Brasiers Company.

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