Adults Sought for Study on Aging and Mobility

                                                               Walking stickman
The Biomechanics Laboratory in the kinesiology department is recruiting volunteers for a study about the effects of age and exercise on walking and muscle function. The researchers hope to learn about how changes in muscle function with age are related to the onset of disability.

The lab is looking for individuals who meet the following criteria: ages 55-70 with healthy body weight who participate in fewer than five 30-minute bouts of exercise per week (or less than a total of 150 minutes of planned exercise per week), no history of reconstructive surgery of the legs, no major health issues (heart disease, diabetes, neurological disease), able to walk for 30 minutes and no contraindications to MRI (metal implant, claustrophobia).

The study consists of two visits: a 1-hour visit to an MRI facility in Amherst and one 3-hour visit to the Biomechanics Lab on campus. During the lab visit researchers will collect data on how participants’ joints move as they walk over the ground and on a treadmill. The study will also collect data on the strength of the muscles in participants’ thighs. All procedures are non-invasive.

Source: UMass

ALS progression linked to increased protein instability

The new study provides evidence that proteins linked to more severe forms of ALS are less stable structurally and more prone to form clusters or aggregates. Mutants of the superoxide dismutase (SOD) protein formed long, rod-shaped aggregates (shown here as red lattice), compared to the compact folded structure of wild-type SOD (purple ribbons). Credit: Image courtesy of the Getzoff and Tainer labs, The Scripps Research Institute.

A new study by scientists from The Scripps Research Institute (TSRI), Lawrence Berkeley National Laboratory (Berkeley Lab) and other institutions suggests a cause of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.

"Our work supports a common theme whereby loss of protein stability leads to disease," said John A. Tainer, professor of structural biology at TSRI and senior scientist at Berkeley Lab, who shared senior authorship of the new research with TSRI Professor Elizabeth Getzoff.

Getzoff, Tainer and their colleagues, who focused on the effects of mutations to a gene coding for a protein called superoxide dismutase (SOD), report their findings this week in the online Early Edition of the Proceedings of the National Academy of Sciences. The study provides evidence that those proteins linked to more severe forms of the disease are less stable structurally and more prone to form clusters or aggregates.

"The suggestion here is that strategies for stabilizing SOD proteins could be useful in treating or preventing SOD-linked ALS," said Getzoff.

Striking in the Prime of Life

ALS is notorious for its ability to strike down people in the prime of life. It first leapt into public consciousness when it afflicted baseball star Lou Gehrig, who succumbed to the disease in 1941 at the age of only 38. Recently, the ALS Association's Ice Bucket Challenge has enhanced public awareness of the disease.

ALS kills by destroying muscle-controlling neurons, ultimately including those that control breathing. At any one time, about 10,000 Americans are living with the disease, according to new data from the Centers for Disease Control and Prevention, but it is almost always lethal within several years of the onset of symptoms.

SOD1 mutations, the most studied factors in ALS, are found in about a quarter of hereditary ALS cases and seven percent of ordinary "sporadic" ALS cases. SOD-linked ALS has nearly 200 variants, each associated with a distinct SOD1 mutation. Scientists still don't agree, though, on just how the dozens of different SOD1 mutations all lead to the same disease.

One feature that SOD1-linked forms of ALS do have in common is the appearance of SOD clusters or aggregates in affected motor neurons and their support cells. Aggregates of SOD with other proteins are also found in affected cells, even in ALS cases that are not linked to SOD1 mutations.

In 2003, based on their and others' studies of mutant SOD proteins, Tainer, Getzoff and their colleagues proposed the "framework destabilization" hypothesis. In this view, ALS-linked mutant SOD1 genes all code for structurally unstable forms of the SOD protein. 
Inevitably some of these unstable SOD proteins lose their normal folding enough to expose sticky elements that are normally kept hidden, and they begin to aggregate with one another, faster than neuronal cleanup systems can keep up -- and that accumulating SOD aggregation somehow triggers disease.

Faster Clumping, Worse Disease

In the new study, the Tainer and Getzoff laboratories and their collaborators used advanced biophysical methods to probe how different SOD1 gene mutations in a particular genetic ALS "hotspot" affect SOD protein stability.

To start, they examined how the aggregation dynamics of the best-studied mutant form of SOD, known as SOD G93A, differed from that of non-mutant, "wild-type" SOD. To do this, they developed a method for gradually inducing SOD aggregation, which was measured with an innovative structural imaging system called SAXS (small-angle X-ray scattering) at Berkeley Lab's SIBYLS beamline.

"We could detect differences between the two proteins even before we accelerated the aggregation process," said David S. Shin, a research scientist in Tainer's laboratories at Berkeley Lab and TSRI who continues structural work on SOD at Berkeley.

The G93A SOD aggregated more quickly than wild-type SOD, but more slowly than an SOD mutant called A4V that is associated with a more rapidly progressing form of ALS.

Subsequent experiments with G93A and five other G93 mutants (in which the amino acid glycine at position 93 on the protein is replaced with a different amino acid) revealed that the mutants formed long, rod-shaped aggregates, compared to the compact folded structure of wild-type SOD. The mutant SOD proteins that more quickly formed longer aggregates were again those that corresponded to more rapidly progressing forms of ALS.

What could explain these SOD mutants' diminished stability? Further tests focused on the role of a copper ion that is normally incorporated within the SOD structure and helps stabilize the protein. Using two other techniques, electron-spin resonance (ESR) spectroscopy and inductively coupled plasma mass spectrometry (ICP-MS), the researchers found that the G93-mutant SODs seemed normal in their ability to take up copper ions, but had a reduced ability to retain copper under mildly stressing conditions -- and this ability was lower for the SOD mutants associated with more severe ALS.

"There were indications that the mutant SODs are more flexible than wild-type SOD, and we think that explains their relative inability to retain the copper ions," said Ashley J. Pratt, the first author of the study, who was a student in the Getzoff laboratory and postdoctoral fellow with Tainer at Berkeley Lab.

Toward New Therapies

In short, the G93-mutant SODs appear to have looser, floppier structures that are more likely to drop their copper ions -- and thus are more likely to misfold and stick together in aggregates.

Along with other researchers in the field, Getzoff and Tainer suspect that deviant interactions of mutant SOD trigger inflammation and disrupt ordinary protein trafficking and disposal systems, stressing and ultimately killing affected neurons.

"Because mutant SODs get bent out of shape more easily," said Getzoff, "they don't hold and release their protein partners properly. By defining these defective partnerships, we can provide new targets for the development of drugs to treat ALS."

The researchers also plan to confirm the relationship between structural stability and ALS severity in other SOD mutants.

"If our hypothesis is correct," said Shin, "future therapies to treat SOD-linked ALS need not be tailored to each individual mutation -- they should be applicable to all of them."

Source: The Scripps Research Institute

Existing drug, riluzole, may prevent foggy 'old age' brain, research shows

Better memory makers: When researchers looked at certain neurons (similar to the one shown on top) in rats treated with riluzole, they found an important change in one brain region, the hippocampus: more clusters of so-called spines, receiving connections that extend from the branches of a neuron (bottom). Credit: Image courtesy of Rockefeller University

Forgetfulness, it turns out, is all in the head. Scientists have shown that fading memory and clouding judgment, the type that comes with advancing age, show up as lost and altered connections between neurons in the brain. But new experiments suggest an existing drug, known as riluzole and already on the market as a treatment for ALS, may help prevent these changes.

Researchers at The Rockefeller University and The Icahn School of Medicine at Mount Sinai found they could stop normal, age-related memory loss in rats by treating them with riluzole. This treatment, they found, prompted changes known to improve connections, and as a result, communication, between certain neurons within the brain's hippocampus.

"By examining the neurological changes that occurred after riluzole treatment, we discovered one way in which the brain's ability to reorganize itself -- its neuroplasticity -- can be marshaled to protect it against some of the deterioration that can accompany old age, at least in rodents," says co-senior study author Alfred E. Mirsky Professor Bruce McEwen, head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. The research is published this week in Proceedings of the National Academy of Sciences.

Neurons connect to one another to form circuits connecting certain parts of the brain, and they communicate using a chemical signal known as glutamate. But too much glutamate can cause damage; excess can spill out and excite connecting neurons in the wrong spot. In the case of age-related cognitive decline, this process damages neurons at the points where they connect -- their synapses. In neurodegenerative disorders, such as Alzheimer's disease, this contributes to the death of neurons.

Used to slow the progress of another neurodegenerative condition, ALS (also known as Lou Gehrig's disease), riluzole was an obvious choice as a potential treatment, because it works by helping to control glutamate release and uptake, preventing harmful spillover. The researchers began giving riluzole to rats once they reached 10 months old, the rat equivalent of middle age, when their cognitive decline typically begins.

After 17 weeks of treatment, the researchers tested the rats' spatial memory -- the type of memory most readily studied in animals -- and found they performed better than their untreated peers, and almost as well as young rats. For instance, when placed in a maze they had already explored, the treated rats recognized an unfamiliar arm as such and spent more time investigating it.

When the researchers looked inside the brains of riluzole-treated rats, they found telling changes to the vulnerable glutamate sensing circuitry within the hippocampus, a brain region implicated in memory and emotion.

"We have found that in many cases, aging involves synaptic changes that decrease synaptic strength, the plasticity of synapses, or both," said John Morrison, professor of neuroscience and the Friedman Brain Institute and dean of basic sciences and the Graduate School of Biomedical Sciences at Mount Sinai. "The fact that riluzole increased the clustering of only the thin, most plastic spines, suggests that its enhancement of memory results from both an increase in synaptic strength and synaptic plasticity, which might explain its therapeutic effectiveness."

In this case, the clusters involved thin spines, a rapidly adaptable type of spine. The riluzole-treated animals had more clustering than the young animals and their untreated peers, who had the least. This discovery led the researchers to speculate that, in general, the aged brain may compensate by increasing clustering. Riluzole appears to enhance this mechanism.

"In our study, this phenomenon of clustering proved to be the core underlying mechanism that prevented age-related cognitive decline. By compensating the deleterious changes in glutamate levels with aging and Alzheimer's disease and promoting important neuroplastic changes in the brain, such as clustering of spines, riluzole may prevent cognitive decline," says first author Ana Pereira, an instructor in clinical investigation in McEwen's laboratory.

Taking advantage of the overlap of neural circuits vulnerable to age-related cognitive decline and Alzheimer's disease, Pereira is currently conducting a clinical trial to test the effectiveness of riluzole for patients with mild Alzheimer's.

Source: Rockefeller University

Scientist finds genetic wrinkle to block sun-induced skin aging

UBC researchers created a device to act as a tanning bed for mice. Credit: Image courtesy of University of British Columbia

A scientific team at UBC and Providence Health Care have genetically engineered mice with less wrinkled skin, despite repeated exposure to wrinkle-inducing ultraviolet (UV) light.

The findings, published last week in Aging Cell, raises hope for a drug that would block the activity of Granzyme B in certain places, and thus prevent the aging and deterioration of tissues that depend on collagen -- not just skin, but blood vessels and lung passages.

viDA Therapeutics, a company co-founded by David Granville, a professor in the Department of Pathology and Laboratory Medicine and a principal investigator in the Centre for Heart Lung Innovation of UBC and St. Paul's Hospital, is currently developing a Granzyme-B inhibitor based on technology licensed from UBC. The company plans to test a topically applied drug within two years on people with discoid lupus erythematosus, an autoimmune disease worsened by sunlight that can lead to disfiguring facial scarring. (The musician Seal has such a condition.)

If the drug proves effective in preventing lupus-related skin lesions, there is potential for a cosmetic product to prevent the normal, gradual aging of the skin, which is mostly caused by sun exposure. But the drug might also be used for life-threatening conditions, such as aneurysms and chronic obstructive pulmonary disease, caused by the breakdown of collagen and other proteins that provide structure to blood vessels and lung passages.

Background

A serendipitous discovery: Granville was investigating the role of Granzyme B in atherosclerosis and heart attacks. He and his team wanted to see if the blood vessels of mice lacking Granzyme B were more resistant to hardening and narrowing, which is a major cause of heart attacks in human. In the process, they discovered that such mice retained youthful-looking skin compared to the aged skin on normal mice.

The Canadian Institutes of Health Research (CIHR), Genome BC, and Mitacs financially support this research.

An experimental tanning bed: Granville's team constructed a device to simulate sun exposure on mice. Each mouse was put in a carousel that slowly turned under UV lamps, exposing them for three to four minutes, three times a week -- enough to cause redness, but not to burn. After 20 weeks of repetitive exposure, it became clear that the skin of mice lacking Granzyme B had aged much less -- and their collagen was more intact -- compared to the control groups.

Source: University of British Columbia

Simple textiles can be used with catalysts to enable complex chemical reactions

To attach the "chemical tools" to the nylon fibers the chemist simply irradiate the soaked textile with UV light.

In future, it will be much easier to produce some active pharmaceutical substances and chemical compounds than was the case to date. An international team working with chemists from the Max-Planck-Institut für Kohlenforschung in Mülheim an der Ruhr have immobilised various catalysts on nylon in a very simple way. Catalysts mediate between the reagents in a chemical reaction and control the process leading to the desired end product. When textile material is used as a support for the chemical auxiliaries, the reaction can proceed on a large surface thereby increasing its efficiency.

One of the catalysts that the researchers used in this way plays an important role in the synthesis of a pharmaceutical agent which could only be used previously in dissolved form, making the production process very complicated and expensive. Immobilising this catalyst on fabric simplifies production considerably. This process may be expected to yield similar advantages for other chemical processes.

Functional textiles are usually understood as the textiles used to make windproof jackets, breathable footwear and particularly effective thermal underwear. However, the term could soon refer to something else -- textiles which are "functionalised" with the help of organic catalysts. Working in collaboration with scientists from the Deutsches 

Textilforschungszentrum in Krefeld and Sungkyunkwan University in Suwon, Korea, researchers at the Max-Planck-Institut für Kohlenforschung in Mülheim an der Ruhr have developed a process for immobilising different organic catalysts on textiles with the help of ultraviolet light. The fabric thereby acts as a support for the substances on which a chemical reaction occurs.

Up to now, science has focused more on the macroscopic functionality of textiles, for example clothing, explains Dr. Ji-Woong Lee, who recently completed his doctorate at the Max-Planck-Institut für Kohlenforschung under the supervision of Professor Benjamin List, head of the Institute's Homogenous Catalysis Group. "As opposed to this, our method can give simple textiles microscopic functionalities," explains the Korean scientist. Together with his colleagues, Dr. Lee armed pieces of nylon with catalysts. The latter can be imagined as chemical tools which fulfil various tasks during chemical reactions.

Excellent yields, little wear and tear

For their tests, the Mühlheim-based researchers used three organic catalysts: a base (dimethylaminopyridine, DMAP), a sulfonic acid and a catalyst which functions as both an acid and a base. The latter is used in the pharmaceuticals industry to steer a reaction to one of two products, which are chemically completely identical. The two forms have mirror-image structures, like a left and right hand, but only one variant has the desired medical effect. Up to now, the catalyst that generates this variant could only be used in dissolved form and then had to be separated again. The complicated separation process could be avoided using a catalyst immobilised on fabric.

To attach the catalysts to the nylon fibres, the chemists irradiated the textile to which a catalyst was applied with UV light for five minutes -- but no longer, as this would impede the activity of the catalyst and its immobilisation on the nylon. A comparable process did not exist up to now.

The catalysts, which were practically interwoven with the fabric, displayed all of the characteristics that the chemists expect from such a system: the result of the chemical reactions which the scientists undertook with the catalyst-loaded nylon strips is impressive. 

All three catalysts converted around 90 percent of the source materials to the desired products. And the catalyst which is used in the pharmaceutical industry and only generates one out of two mirror-image molecules, achieved a success rate of over 95 percent without showing any major signs of wear and tear. Ji-Woong Lee carried out several hundred test-runs and observed that the catalysts relinquished little of their functionality.

A large surface makes chemical reactions more efficient

Compared with other ways of immobilising catalysts, "organotextile catalysis" has several advantages: in particular, it provides the reagents with a larger surface than other supports, for example plastic spheres or foils -- the larger the surface, the more efficiently a reaction proceeds. Moreover, nylon is flexible and very inexpensive. Dry textiles loaded with catalysts are easy to transport, which means that it is simpler to meet the requirements for some chemical processes where it is practically impossible to set up sophisticated chemical systems. For example, organotextile catalysis could help in the treatment of water in locations where people are cut off from the water supply.

"Our method enables the low-cost production of long-term functionalised textiles without causing any pollution," says Ji-Woong Lee. He is entirely convinced that the process can be applied in several scientific areas -- and industrial processes. "In addition to chemistry, these could include biology, the materials science and pharmaceutics."

Source: Max-Planck-Institut für Kohlenforschung

Credit score can also describe health status

It appears the same behaviors that ruin credit ruin health too. Credit: © Ivelin Radkov / Fotolia

A credit score doesn't just reduce a person's entire financial history down to a single number and somehow predict their credit-worthiness.

It might also be saying something about a person's health status, too, according to a new analysis from a long-term study of the physical and mental health of more than 1,000 New Zealanders who have been monitored continuously from birth to age 38.

The latest paper from the study, appearing this week in the Proceedings of the National Academy of Sciences, has found a strong relationship between low credit scores and poor cardiovascular health.

This doesn't mean that poor financial management hurts your health, post-doctoral researcher Salomon Israel of Duke University is quick to point out. It's that the sort of personal attributes that can lead to a poor credit score can also contribute to poor health.

This and other studies from the Dunedin Multidisciplinary Health and Development Study in New Zealand have found that self-control, planning ahead and perseverance are attributes that predict both better financial status and better health.

"What it comes down to is that people who don't take care of their money don't take care of their health," said study leader Terrie Moffitt, who is the Nannerl O. Keohane university professor of psychology and neuroscience at Duke. She said this study confirms what the insurance and financial industries may already understand.

Backtracking into the data on these study participants, the researchers found that about 20% of the relationship between credit scores and heart health was accounted for by the attitudes, behaviors and competencies displayed by the study members when they were younger than age 10.

"We're showing that these things take root early in life," Israel said.

Harvard economist David Laibson, who was not involved in the research, said the study "fundamentally transforms our understanding of the psychological factors that connect our health and wealth."

Lamar Pierce, an associate professor of organization & strategy at Washington University in St. Louis, agreed. "This study is important because it identifies common cognitive foundations long before financial and physical health problems emerge," said Pierce, who was not involved in this study. "It provides hope that early life intervention can impede the development of life-long patterns of illness and financial struggle."

Using a standard measure called the Framingham cardiovascular risk score, the Duke researchers estimated the "heart age" of their participants, based on blood pressure, cholesterol levels, blood sugar and smoking habits. At age 38, the participants' Framingham "heart ages" ranged from 22 to 85 years. Participants with higher credit scores had younger "heart ages." The components of the Dunedin study's human capital measure -- educational attainment, cognitive ability and self-control -- each predicted higher credit scores and younger heart age.

The idea of checking credit scores against the detailed personal data in the Dunedin study came from a conversation Moffitt had with her seatmate on a plane about a decade ago. When she told her travelling companion from the life insurance industry that she studied self-control and life outcomes, he said, "We do that too, but we use credit scores."

"The thing that's so compelling about credit scores is that they're both predictive and retrospective," said co-author Avshalom Caspi, the Edward M. Arnett professor of psychology and neuroscience, psychiatry & behavioral sciences at Duke. "They offer a window on the future, but also a window on the past."

In recent years, credit scores have been used for pre-employment screening and many other functions beyond their original intent, Israel said. This study seems to bear out their usefulness as a proxy for a person's reliability and steadfastness, and in turn how healthy they may be.

"Our findings suggest that life insurance companies that acquire an applicant's credit score are also indirectly acquiring information about that applicant's educational attainment, intelligence and personality, right back to childhood," the authors wrote.

The link might work the other way as well. In less developed countries where credit scores aren't available, a Harvard team has been experimenting with using a 40-minute personality quiz to assess candidates' credit-worthiness for microloans.

This research was supported by the New Zealand Health Research Council, US National Institute on Aging (AG032282, T32-AG000029), the UK Medical Research Council (MR/K00381X) the Jacobs Foundation and the Yad Hanadiv Rothschild Foundation.

Source: Duke University

Targeted culling of deer controls disease with little effect on hunting

A new study found that the targeted culling of deer prevents the rampant spread of chronic wasting disease to healthy deer.

Chronic wasting disease, the deer-equivalent of mad cow disease, has crept across the U.S. landscape from west to east. It appeared first in captive mule deer in Colorado in the late 1960s. By 1981, it had escaped to the wild. It reached the Midwest by 2002. Little is known about its potential to infect humans.

The effort to keep chronic wasting disease in check in Illinois is a success, report researchers Nohra Mateus-Pinilla, left, a wildlife veterinary epidemiologist with the Illinois Natural History Survey; U. of I. animal sciences professor Jan Novakofski; and postdoctoral researcher Michelle Green.

Now researchers at the University of Illinois offer a first look at the long-term effectiveness of the practice of culling deer in areas affected by CWD to keep the disease in check. Their study appears in the journal Preventive Veterinary Medicine.

Each year, the Illinois Department of Natural Resources tests 7,000 (hunted, culled or incidentally killed) deer for CWD infection, conducts aerial surveillance to see where deer congregate and sends in sharpshooters to cull deer at the sites with disease, said Jan Novakofski, a professor of animal sciences at the University of Illinois and an author of the study.

"We know a lot about how far deer typically move," he said. "If they're sick, they're going to spread the disease that far. So if you find a deer that's sick, you draw that small circle and you shoot there."

Novakofski called this approach "a textbook scientific strategy for control. You reduce contact and you reduce the spread of infection with the smallest overall impact on healthy deer."

He and his colleagues at the Illinois Natural History Survey (part of the Prairie Research Institute at the U. of I.) found that the strategy worked: The prevalence of CWD in tested Illinois deer remained at about 1 percent from 2002 to 2012.

The team also found that hunters were killing more deer each year in each region of the state (north, central and south) regardless of CWD and CWD management. Statewide, the number of deer killed by hunters went from 147,830 in 2001, before the appearance of CWD, to 181,451 in 2012. The only exception: Two counties out of 10 with cases of CWD saw a reduction in hunter harvest over the same period.

"We wanted to know whether Illinois hunters have fewer deer to hunt now than they did before CWD," said Nohra Mateus-Pinilla, a wildlife veterinary epidemiologist at the INHS who led the study with postdoctoral researcher Mary Beth Manjerovic. "We found that hunter harvest has increased, and the prevalence of CWD has been maintained at low levels for 10 years in Illinois."

This finding answers a long-time complaint by some hunters that the culling of deer makes it harder for them to find deer to shoot, Novakofski said.
"Since 2001, hunter harvest of deer has increased similarly in the northern region of Illinois, where CWD occurs, and the rest of the state, where there is no disease or sharpshooting," he said.

In the two Illinois counties with fewer deer, "the reductions were 11 to 20 percent," Manjerovic said.

The team compared the Illinois experience with that of Wisconsin, which changed its CWD-management strategy from one that relied on culling to one that consisted primarily of allowing hunters to thin deer herds, the researchers said. Wisconsin saw a striking increase of infection in CWD-tested deer after it did that, the team found.

"In the early years in Wisconsin, (CWD prevalence) was still about 1 percent, just as it was in Illinois," Manjerovic said. "Then the strategy changed. Since 2007, CWD prevalence has increased to about 5 percent."

"We can't find an environmental or other variable that explains the increase in prevalence except a change in management," Novakofski said.

The numbers may not seem alarming to some, said postdoctoral researcher and co-author Michelle Green. But the trend is of concern, she said.

"CWD is a prion disease (like mad cow disease) and it's 100 percent fatal. 
There's no current way that we can actually make the deer better, so it's important that we keep it from spreading too far throughout the population," she said. "And then there's also the connection to mad cow disease. We don't have enough information yet to really understand what the impact to human health could be."

"We all hope that there is never a case of chronic wasting disease in humans. We all hope that it never spreads to people or agricultural animals," Novakofski said. "If it ever does, the investment in maintaining prevalence at a low level in Illinois will be repaid a thousand-fold."

Source: University of Illinois at Urbana-Champaign

Scrapie could breach the species barrier

Scrapie is a neurodegenerative disease that has been known for centuries and which affects sheep and goats. Credit: INRA/Florent Giffard

INRA scientists have shown for the first time that the pathogens responsible for scrapie in small ruminants (prions) have the potential to convert the human prion protein from a healthy state to a pathological state. In mice models reproducing the human species barrier, this prion induces a disease similar to Creutzfeldt-Jakob disease. These primary results published in Nature Communications on 16 December 2014, stress the necessity to reassess the transmission of this disease to humans.

Scrapie is a neurodegenerative disease that has been known for centuries and which affects sheep and goats. Similar to Bovine Spongiform Encephalopathy (BSE) or mad cow disease, scrapie is caused by a transmissible pathogen protein called prion.

However, and contrary to BSE[1], epidemiological studies have never been able to establish a link between this disease and the occurrence of prion diseases in humans. "Risks of transmitting scrapie to humans (zoonose) were hitherto considered negligible because of the species barrier that naturally prevents prion propagation between species," said Olivier 

Andreoletti, INRA scientist who led the present study.

Researchers at INRA studied the permeability of the human transmission barrier to pathogens responsible for scrapie, using animal models specifically developed for this purpose. This approach previously allowed the confirmation of the zoonotic nature of prions responsible for BSE in cows and of the variant of Creutzfeldt-Jakob disease in humans (vCJD).

Unexpectedly, in these rodent models, certain pathogens responsible for scrapie were able to cross the transmission barrier. Moreover, the pathogens that propagated through this barrier were undistinguishable from the prions causing the sporadic form of Creutzfeldt-Jakob disease (sCJD). This data suggest a potential link between the occurrence of certain sCJD and these animal prions.

"Since CJD is scarce, about 1 case per million and per year, and incubation periods are usually long -several decades- it is extremely difficult for epidemiological studies to try and make this link," explains Olivier Andreoletti.

In their conclusions, the authors stress the fact that CJD cases are rare though scrapie has been circulating for centuries in small ruminants for which we eat the meat. Even if in future studies scrapie is finally confirmed to have a zoonotic potential, the authors consider that this disease does not constitute a new major risk for public health.

Source: INRA-France

Lead in teeth can tell a body's tale, study finds

Revealing information UF geology professor George Kamenov has published research that shows trace amounts of lead in modern and historical human teeth can give clues about where they came from. Credit: Ray Carson/UF Photography

Your teeth can tell stories about you, and not just that you always forget to floss.

A study led by University of Florida geology researcher George D. Kamenov showed that trace amounts of lead in modern and historical human teeth can give clues about where they came from. The paper will be published in the August issue of Science of The Total Environment.

The discovery could help police solve cold cases, Kamenov said. For instance, if an unidentified decomposed body is found, testing the lead in the teeth could immediately help focus the investigation on a certain geographic area. That way, law enforcement can avoid wasting resources checking for missing persons in the wrong places.

"We can use this pollution signal to figure out where these people came from," he said.
Lead is composed of four variants, called isotopes. The amount of those isotopes fluctuates in different rocks, soils and ores -- and, therefore, regions of the world.

Mining and other pollution-causing activities release that lead into the environment, and it accumulates in children's bodies as they grow because kids inhale dust and ingest soil when they put their hands in their mouths.

Tooth enamel, which develops during childhood, locks in the lead signals and preserves them.
"When you grow up, you record the signal of the local environment," Kamenov said. "If you move somewhere else, your isotope will be distinct from the local population."
Even different teeth can reveal certain facts.

First molar enamel is finished forming by age 3, so it provides information about birth and toddler years. Incisor and canine enamel starts later and finishes around age 5, so it gives insight into early childhood. The third molar enamel does not start forming until age 8, so it indicates late childhood residences.

Lead analysis can also tell what time period a body is from.

Modern and historical teeth have different signals, according to the study. The natural composition of lead changed over the past century because of mining and the use of leaded gasoline, so there's a clear distinction between modern and historical human exposure.

Using that information, archaeologists can identify early European bodies in New World areas.
"You can go back in time, look at archaeological sites and try to reconstruct human migration," Kamenov said.

But modern American teeth are like no others in the world, according to the study. Whereas available data for areas such as South America overlap with Europe, American teeth can be identified anywhere due to usage of ores with distinct isotope signals in the United States.
"What's in the environment goes into your body," Kamenov said

Source: University of Florida.