Author Archives: Fredricko

Comments on Chemopreservation Versus Cryopreservation

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There is some ongoing interest in plastination (or chemopreservation) as a possible alternative to cryonics (or cryopreservation) - though not yet enough for an initiative to arise that offers that service. Here is commentary on this topic: "Even if chemopreservation can be demonstrated to preserve the intricate wiring of the brain, it can be safely assumed that there will not be a massive change in demand for brain preservation technologies ... As a consequence, providers of chemopreservation will most likely operate in the same environment as providers of cryonics. That means that, as a general rule, there will be a delay between pronouncement of legal death and the start of procedures. ... There is an understandable tendency to compare brain preservation protocols under ideal conditions and favor the method that produces the best preservation. But support for either technology cannot be solely based on results produces under controlled lab conditions. Personal survival technologies should be evaluated under conditions that are most likely to be encountered by organizations that will offer them. ... One interesting aspect of the cryonics vs chemopreservation debate, though, is that it appears that some people simply feel more comfortable with one of the approaches. People who have shown the slightest interest in human cryopreservation can get really excited about the idea of chemical brain preservation. This indicates that if both approaches would be pursued actively, the growth of chemopreservation would not necessarily be at the expense of cryonics but there would be a growth in the total number of people making bio-preservation arrangements aimed at personal survival. [But] chemopreservation is not at the stage where it can be responsibly offered. The growth of this field requires a committed group of individuals who will research, develop, and implement this program. Chemopreservation does not need to be perfected before being offered (neither was cryonics) but so far most advocacy has been mostly at the conceptual level."

Link: http://www.evidencebasedcryonics.org/2012/06/20/chemopreservation-in-the-real-world/

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http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Calorie Restriction Reduces Loss of Synaptic Plasticity

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Another of the many benefits of calorie restriction is outlined in this paper: "The author focused on the functional decline of synapses in the brain with aging to understand the underlying mechanisms and to ameliorate the deficits. The first attempt was to unravel the neuronal functions of gangliosides so that gangliosides could be used for enhancing synaptic activity. The second attempt was to elicit the neuronal plasticity in aged animals through enriched environmental stimulation and nutritional intervention. Environmental stimuli were revealed neurochemically and morphologically to develop synapses leading to enhanced cognitive function. Dietary restriction as a nutritional intervention restored the altered metabolism of neuronal membranes with aging, providing a possible explanation for the longevity effect of dietary restriction. These results obtained with aging and dementia models of animals would benefit aged people."

Link: https://www.jstage.jst.go.jp/article/pjab/88/6/88_PJA8806B-04/_article

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http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Perverse Incentives and Underestimations of Future Longevity

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We life in an age of change and rapid scientific innovation in medicine. That in and of itself might be enough to explain why historical actuarial predictions of longevity have been low in comparison to the actual outcome: extrapolation of existing trends tends to do poorly in the face of consistently unpredictable innovation.

Nonetheless, a large industry is focused on getting these numbers right, or as close to right as is possible, as vast sums are promised to older folk, either as political entitlements or honestly obligated as a result of insurance contracts. Betting against increasing longevity seems like a fool's game, but nonetheless there is a lot of money to be made in that business - many large entities want to be protected from what is known as longevity risk, the risk that life spans will rise faster than expected and thus financial obligations will spiral out of control. Large entities are willing to pay for that insurance service, and taking on risk for a percentage is very much the core business of finance.

In theory the people taking on that risk for a percentage know what they are doing, and they are the ones funding efforts to understand the risk - which in this case means models for future increases in human longevity due to advances in medicine and biotechnology. In practice? The risk gets sliced and diced and parceled out among the players in finance, that much is true. But I'm sure we all see the present results of that undertaking in other large industries, such as housing: when there is enough money involved the business becomes one of lies and politics, the fine art of pocketing profits, taking on unknown risks for short term gain, steering government policies, and raiding the public treasury to cover losses when it all goes south. When buying politicians and policy is a reasonable cost judged against the cost of contracts, buying politicians and policy becomes a part of doing business - and very lucrative, since it allows risk-bearers to try for the upside with the expectation that they will be bailed out if it fails.

Thus a web of perverse incentives grows, benefiting the connected few at the expense of the many. In the course of all of this, there is an increasing pressure (and ability) to obscure or water down unfavorable data, especially when the interests of profiteers and government appointees coincide. Again, we've all seen this come to pass numerous times in recent years and prior decades. It is the way of the world, and just as much so when it comes to the future of human longevity:

In 1981, the United Kingdom (UK) Office for National Statistics estimated that male life expectancy at birth would rise to 74 by 2031. It hit that age in 1994. In 2002, the 2031 estimate was 81, but we are now expected to pass that in 2019. This systematic underestimation of official life expectancy increases occurs around the world. It is not an accident. It is deliberate. Politicians put pressure on official agencies to do this, so that the full cost of longevity increases does not fall on them or the current generation of voters. The reason is clear: If more accurate and hence higher projection of life expectancy were produced today, then social security contributions would have to rise now rather than later - and this would be politically very unpopular.

The powers that be and their predecessors have accomplished what powers that be always manage in the end: to set up a system of wealth transfers and entitlements that is both unsustainable and stands in opposition to true progress. Thus the modern spectacle of people trying to argue that increases in human longevity are a bad thing! The collapse will come, the promises that cannot be kept will be broken, that much is certain - although it is true that modern innovations in fiat currencies have allowed the game to go on for a good deal longer and become a good deal more destructive than was usually the case in the past. But eventually they will run out of other people's money to loot. Along the way to that end those who are trying to prop up the house of cards will undoubtedly build a great deal more in the ways of lies, waste, and other unpleasantness.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Enriched Skim Milk Good for Gout, Study Suggests

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(HealthDay News) -- If you have gout, drinking enriched skim milk may help reduce the frequency of painful flare-ups, new research suggests.

The new study included 120 patients who had experienced at least two flare-ups in the previous four months. They were divided into three treatment groups that consumed either lactose powder, skim milk powder or skim milk powder enriched with glycomacropeptide (GMP) and G600 milk fat extract (G600).

Gout, a common form of arthritis, is caused by uric acid buildup in blood. Often, the big toe is the first place where gout strikes. Previous research has shown a higher risk for gout among people who consume fewer dairy products, and earlier work suggested that GMP and G600 tone down the inflammatory response to gout crystals.

The powders were mixed in roughly 8 ounces of water as a vanilla-flavored shake and consumed once a day. The patients recorded their flare-ups and went to a rheumatology clinic once a month. Read more…

Cardiofy Heart Care Supplement

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Speaker offers insights into Parkinson's

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FAIRMONT - It wasn't until celebrities such as Michael J. Fox and Muhammad Ali announced they had Parkinson's Disease that the public began to learn more about this life-altering disease.

While not a terminal illness, Parkinson's does affect the quality of life for those diagnosed.

"About one in 100 people over the age of 60 are diagnosed with Parkinson's Disease," said Rose Wichmann, manager of Struthers Parkinson's Center in Golden Valley. "It goes to two in 100 people over the age of 70. That's more than MS, more than muscular dystrophy and more than ALS-Lou Gehrig's Disease."

Wichmann was in Fairmont on Thursday speaking to a Parkinson's support group at Grace Lutheran Church. She mentioned there are several different types of Parkinson's Disease, and that every person diagnosed has slightly different symptoms.

"Not everyone has the tremors that people associate with Parkinson's," Wichmann said. "We have an acronym called 'TRAP' that lists the four main symptoms, and two or more of these need to be confirmed before receiving a diagnosis."

While tremors are well-associated with Parkinson's, other symptoms are less noticeable, such as rigidity and stiffness in the muscles. There is also the absence or slowing of movements, and posture changes, such as curling over instead of sitting or standing up straight.

"There are about 15 percent of those diagnosed with Parkinson's that never have a tremor," Wichmann said. "But what causes Parkinson's is a group of cells at the base of the brain that produce dopamine. As we age, those cells start to disappear, and about 60 to 80 percent of those disappear before displaying symptoms of Parkinsons."

Dopamine is a chemical that allows the delivery of messages through the brain. Lack of dopamine means signals are not moving as smoothly.

"We say that automatic is broken," Wichmann said. "Those movements you don't even think about, like walking, or rolling over in your sleep. Blinking also goes away, so Parkinson's sufferers have more of a stare. There is a loss of facial expressions because you don't think about if you're going to smile. It's easy for Parkinson's people to be misunderstood because you can't read their facial expressions anymore."

There are also problems with balance.

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Speaker offers insights into Parkinson's

Speaker offers insights into Parkinson’s

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FAIRMONT - It wasn't until celebrities such as Michael J. Fox and Muhammad Ali announced they had Parkinson's Disease that the public began to learn more about this life-altering disease.

While not a terminal illness, Parkinson's does affect the quality of life for those diagnosed.

"About one in 100 people over the age of 60 are diagnosed with Parkinson's Disease," said Rose Wichmann, manager of Struthers Parkinson's Center in Golden Valley. "It goes to two in 100 people over the age of 70. That's more than MS, more than muscular dystrophy and more than ALS-Lou Gehrig's Disease."

Wichmann was in Fairmont on Thursday speaking to a Parkinson's support group at Grace Lutheran Church. She mentioned there are several different types of Parkinson's Disease, and that every person diagnosed has slightly different symptoms.

"Not everyone has the tremors that people associate with Parkinson's," Wichmann said. "We have an acronym called 'TRAP' that lists the four main symptoms, and two or more of these need to be confirmed before receiving a diagnosis."

While tremors are well-associated with Parkinson's, other symptoms are less noticeable, such as rigidity and stiffness in the muscles. There is also the absence or slowing of movements, and posture changes, such as curling over instead of sitting or standing up straight.

"There are about 15 percent of those diagnosed with Parkinson's that never have a tremor," Wichmann said. "But what causes Parkinson's is a group of cells at the base of the brain that produce dopamine. As we age, those cells start to disappear, and about 60 to 80 percent of those disappear before displaying symptoms of Parkinsons."

Dopamine is a chemical that allows the delivery of messages through the brain. Lack of dopamine means signals are not moving as smoothly.

"We say that automatic is broken," Wichmann said. "Those movements you don't even think about, like walking, or rolling over in your sleep. Blinking also goes away, so Parkinson's sufferers have more of a stare. There is a loss of facial expressions because you don't think about if you're going to smile. It's easy for Parkinson's people to be misunderstood because you can't read their facial expressions anymore."

There are also problems with balance.

The rest is here:
Speaker offers insights into Parkinson's

Higher Parkinson’s Risk Linked to Certain Solvents

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Increased risks for Parkinsons disease have been linked to some solvents. Parkinsons disease is a progressive, degenerative central nervous system disorder that typically affects motor skills and speech, among other functions and, while not fatal, complications can be deadly. The cause is unknown and there is no cure.

Samuel M. Goldman, M.D., M.P.H., of The Parkinsons Institute in Sunnyvale, California, and colleagues, conducted a so-called discordant twin pair design study involving 99 pairs of twins. The study was conducted to determine if exposure to specific solvents is linked to increased risks for Parkinsons disease. Participant interviews involved task-specific and lifetime occupation and hobby questions, said Medical Xpress. The study was published in the Annals of Neurology.

The researchers found that exposure to trichloroethylene (TCE) was associated with a significantly increased risk of Parkinsons disease and saw a trend for significance for exposure to the chemicals perchloroethylene (PERC) and carbon tetrachloride (CCl4). Although the present work focused on occupational exposures, solvents are ubiquitous in the environment, and this is particularly true for those implicated in this studyTCE, PERC, and CCl4, the authors wrote, according to Medical Xpress. Our findings require replication in other populations with well-characterized exposures, but the potential public health implications are considerable, the team authored.

Weve also written that over the past several years, the agricultural pesticide paraquat has been linked to Parkinsons, posing a risk to agricultural workers who toil in fields where the pesticide is sprayed, as well as to people living near the fields.

Other research revealed that people exposed at their workplaces to ziram, maneb, and paraquat tripled their risk of Parkinsons; workplace exposure to both ziram and paraquat nearly doubled Parkinsons risk; and people who worked with either paraquat or the pesticide rotenone were 2.5 times likelier to develop Parkinsons disease.

Another study found that some medications, notably the amphetamines Benzedrine or Dexedrine, used to treat attention deficit hyperactivity disorder (ADHD) and help patients achieve more defined focus and increase clarity and awareness, could also place those patients at risk for Parkinsons disease.

We recently wrote that another study found an association with glyphosate, the active ingredient in Monsatos Roundup, and Parkinsons disease and Parkinsons-related brain disorders. According to a report from the Organic Authority, Roundup is the best-selling pesticide in the world and is the companion chemical application to many of the companys genetically modified seeds including corn, soy, canola and cotton.

According to Digital Journal, this is just the latest study to find a link between glyphosate and Parkinsons-like disorders. For example, a 2011 report published in the journal Parkinsonism Related Disorders, detailed the case of a 44-year-old women with Parkinsons-like symptoms after sustaining long-term chemical exposure to glyphosate for three years as a worker in a chemical factory.

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Higher Parkinson’s Risk Linked to Certain Solvents

BUSM researchers identify role of FOXO1 gene in Parkinson's disease

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Public release date: 28-Jun-2012 [ | E-mail | Share ]

Contact: Jenny Eriksen Leary jenny.eriksen@bmc.org 617-638-6841 Boston University Medical Center

(Boston) A recent study led by researchers at Boston University School of Medicine (BUSM) revealed that the FOXO1 gene may play an important role in the pathological mechanisms of Parkinson's disease. These findings are published online in PLoS Genetics, a peer-reviewed open-access journal published by the Public Library of Science.

The study was led by Alexandra Dumitriu, PhD, a postdoctoral associate in the department of neurology at BUSM. Richard Myers, PhD, professor of neurology at BUSM, is the study's senior author.

According to the Parkinson's Disease Foundation, 60,000 Americans are diagnosed with Parkinson's disease each year and approximately one million Americans are currently living with the disease.

Parkinson's disease is a complex neurodegenerative disorder characterized by a buildup of proteins in nerve cells that lead to their inability to communicate with one another, causing motor function issues, including tremors and slowness in movement, as well as dementia. The substantia nigra is an area of the midbrain that helps control movement, and previous research has shown that this area of the brain loses neurons as Parkinson's disease progresses.

The researchers analyzed gene expression differences in brain tissue between 27 samples with known Parkinson's disease and 26 samples from neurologically healthy controls. This data set represents the largest number of brain samples used in a whole-genome expression study of Parkinson's disease to date. The novel aspect of this study is represented by the researchers' emphasis on removing possible sources of variation by minimizing the differences among samples. They used only male brain tissue samples that showed no significant marks of Alzheimer's disease pathology, one of the frequently co-occurring neurological diseases in Parkinson's disease patients. The samples also had similar tissue quality and were from the brain's prefrontal cortex, one of the less studied areas for the disease. The prefrontal cortex does not show neuronal death to the same extent as the substantia nigra, although it displays molecular and pathological modifications during the disease process, while also being responsible for the dementia present in a large proportion of Parkinson's disease patients.

Results of the expression experiment showed that the gene FOXO1 had increased expression in the brain tissue samples with known Parkinson's disease. FOXO1 is a transcriptional regulator that can modify the expression of other genes. Further examination of the FOXO1 gene showed that two single-nucleotide polymorphisms (SNPs), or DNA sequence variations, were significantly associated with age at onset of Parkinson's disease.

"Our hypothesis is that FOXO1 acts in a protective manner by activating genes and pathways that fight the neurodegeneration processes," said Dumitriu. "If this is correct, there could be potential to explore FOXO1 as a therapeutic drug target for Parkinson's disease."

###

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BUSM researchers identify role of FOXO1 gene in Parkinson's disease

BUSM researchers identify role of FOXO1 gene in Parkinson’s disease

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Public release date: 28-Jun-2012 [ | E-mail | Share ]

Contact: Jenny Eriksen Leary jenny.eriksen@bmc.org 617-638-6841 Boston University Medical Center

(Boston) A recent study led by researchers at Boston University School of Medicine (BUSM) revealed that the FOXO1 gene may play an important role in the pathological mechanisms of Parkinson's disease. These findings are published online in PLoS Genetics, a peer-reviewed open-access journal published by the Public Library of Science.

The study was led by Alexandra Dumitriu, PhD, a postdoctoral associate in the department of neurology at BUSM. Richard Myers, PhD, professor of neurology at BUSM, is the study's senior author.

According to the Parkinson's Disease Foundation, 60,000 Americans are diagnosed with Parkinson's disease each year and approximately one million Americans are currently living with the disease.

Parkinson's disease is a complex neurodegenerative disorder characterized by a buildup of proteins in nerve cells that lead to their inability to communicate with one another, causing motor function issues, including tremors and slowness in movement, as well as dementia. The substantia nigra is an area of the midbrain that helps control movement, and previous research has shown that this area of the brain loses neurons as Parkinson's disease progresses.

The researchers analyzed gene expression differences in brain tissue between 27 samples with known Parkinson's disease and 26 samples from neurologically healthy controls. This data set represents the largest number of brain samples used in a whole-genome expression study of Parkinson's disease to date. The novel aspect of this study is represented by the researchers' emphasis on removing possible sources of variation by minimizing the differences among samples. They used only male brain tissue samples that showed no significant marks of Alzheimer's disease pathology, one of the frequently co-occurring neurological diseases in Parkinson's disease patients. The samples also had similar tissue quality and were from the brain's prefrontal cortex, one of the less studied areas for the disease. The prefrontal cortex does not show neuronal death to the same extent as the substantia nigra, although it displays molecular and pathological modifications during the disease process, while also being responsible for the dementia present in a large proportion of Parkinson's disease patients.

Results of the expression experiment showed that the gene FOXO1 had increased expression in the brain tissue samples with known Parkinson's disease. FOXO1 is a transcriptional regulator that can modify the expression of other genes. Further examination of the FOXO1 gene showed that two single-nucleotide polymorphisms (SNPs), or DNA sequence variations, were significantly associated with age at onset of Parkinson's disease.

"Our hypothesis is that FOXO1 acts in a protective manner by activating genes and pathways that fight the neurodegeneration processes," said Dumitriu. "If this is correct, there could be potential to explore FOXO1 as a therapeutic drug target for Parkinson's disease."

###

Excerpt from:
BUSM researchers identify role of FOXO1 gene in Parkinson's disease

Research and Markets: Handbook of Parkinson's Disease – Blue-Ribbon Guide

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/lb6wfj/handbook_of_parkin) has announced the addition of the "Handbook of Parkinson's Disease" book to their offering.

This blue-ribbon guide has long prevailed as one of the leading resources on Parkinson's Disease (PD). Fully updated with practical and engaging chapters on pathology, neurochemistry, etiology, and breakthrough research, this source spans every essential topic related to the identification, assessment, and treatment of PD. Reflecting the many advances that have taken place in the management of PD, this source promotes a multidisciplinary approach to care and supplies new sections on the latest pharmacologic, surgical, and rehabilitative therapies, as well as essential diagnostic, imaging, and nonmotor management strategies for PD.

Key Topics Covered:

Early Iconography of Parkinson's Disease

Epidemiology of Parkinsonism

Differential Diagnosis of Parkinsonism

Pathophysiology and Clinical Assessment of Parkinsonian Symptoms and Signs

Autonomic Dysfunction and Management

Sleep Dysfunction in Parkinson's Disease

Originally posted here:
Research and Markets: Handbook of Parkinson's Disease - Blue-Ribbon Guide

Research and Markets: Handbook of Parkinson’s Disease – Blue-Ribbon Guide

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/lb6wfj/handbook_of_parkin) has announced the addition of the "Handbook of Parkinson's Disease" book to their offering.

This blue-ribbon guide has long prevailed as one of the leading resources on Parkinson's Disease (PD). Fully updated with practical and engaging chapters on pathology, neurochemistry, etiology, and breakthrough research, this source spans every essential topic related to the identification, assessment, and treatment of PD. Reflecting the many advances that have taken place in the management of PD, this source promotes a multidisciplinary approach to care and supplies new sections on the latest pharmacologic, surgical, and rehabilitative therapies, as well as essential diagnostic, imaging, and nonmotor management strategies for PD.

Key Topics Covered:

Early Iconography of Parkinson's Disease

Epidemiology of Parkinsonism

Differential Diagnosis of Parkinsonism

Pathophysiology and Clinical Assessment of Parkinsonian Symptoms and Signs

Autonomic Dysfunction and Management

Sleep Dysfunction in Parkinson's Disease

Originally posted here:
Research and Markets: Handbook of Parkinson's Disease - Blue-Ribbon Guide

Mayo Clinic Uses New Approach To Reverse Multiple Sclerosis In Mice Models

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Mayo Clinic researchers have successfully used smaller, folded DNA molecules to stimulate regeneration and repair of nerve coatings in mice that mimic multiple sclerosis (MS). They say the finding, published today in the journal PLoS ONE, suggests new possible therapies for MS patients.

"The problem has been to find a way to encourage the nervous system to regenerate its own myelin (the coating on the nerves) so nerve cells can recover from an MS attack," says L. James Maher III, Ph.D., Mayo Clinic biochemist and senior author on the paper. "We show here that these small molecules, called aptamers, can stimulate repair in the mice we are studying."

More than 200,000 people have multiple sclerosis. There is no cure and no effective therapy to stop progression or repair damage to the myelin sheath that surrounds and protects the nerves. Without that protection, nerve fibers will be damaged, leading to declining mobility and cognitive function, and other debilitating complications.

MS researchers, including Mayo neurologist Moses Rodriguez, M.D., a co-author on this paper, have focused on monoclonal antibodies in mice to stimulate myelin repair. The Rodriguez and Maher teams, working together, have determined that the aptamers are not only effective, but they are easy and cheap to synthesize an important point for drug developers. They also are stable and not likely to cause an immune response. This new approach must be validated in other mouse models to see if it might be a candidate for human clinical trials.

The monoclonal antibodies used in earlier research are large and complex, but were shown to promote both cell signaling and remyelination of central nervous system lesions in mice. The aptamers used in this study are less than one-tenth the size of antibodies and are single-strands of DNA containing only 40 nucleotide units.

The research was supported by Mayo Clinic and the National Multiple Sclerosis Society. Co-authors include Branislav Nastasijevic, Brent Wright, Ph.D., John Smestad, and Arthur Warrington, Ph.D., all of Mayo Clinic.

SOURCE: Mayo Clinic

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Mayo Clinic Uses New Approach To Reverse Multiple Sclerosis In Mice Models

New approach to reverse multiple sclerosis in mice models

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ScienceDaily (June 28, 2012) Mayo Clinic researchers have successfully used smaller, folded DNA molecules to stimulate regeneration and repair of nerve coatings in mice that mimic multiple sclerosis (MS). They say the finding, published June 28 in the journal PLoS ONE, suggests new possible therapies for MS patients.

"The problem has been to find a way to encourage the nervous system to regenerate its own myelin (the coating on the nerves) so nerve cells can recover from an MS attack," says L. James Maher III, Ph.D., Mayo Clinic biochemist and senior author on the paper. "We show here that these small molecules, called aptamers, can stimulate repair in the mice we are studying."

More than 200,000 people have multiple sclerosis. There is no cure and no effective therapy to stop progression or repair damage to the myelin sheath that surrounds and protects the nerves. Without that protection, nerve fibers will be damaged, leading to declining mobility and cognitive function, and other debilitating complications.

MS researchers, including Mayo neurologist Moses Rodriguez, M.D., a co-author on this paper, have focused on monoclonal antibodies in mice to stimulate myelin repair. The Rodriguez and Maher teams, working together, have determined that the aptamers are not only effective, but they are easy and cheap to synthesize -- an important point for drug developers. They also are stable and not likely to cause an immune response. This new approach must be validated in other mouse models to see if it might be a candidate for human clinical trials.

The monoclonal antibodies used in earlier research are large and complex, but were shown to promote both cell signaling and remyelination of central nervous system lesions in mice. The aptamers used in this study are less than one-tenth the size of antibodies and are single-strands of DNA containing only 40 nucleotide units.

The research was supported by Mayo Clinic and the National Multiple Sclerosis Society. Co-authors include Branislav Nastasijevic, Brent Wright, Ph.D., John Smestad, and Arthur Warrington, Ph.D., all of Mayo Clinic.

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The above story is reprinted from materials provided by Mayo Clinic.

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New approach to reverse multiple sclerosis in mice models

Cancer Risk Lower In Multiple Sclerosis Patients

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Editor's Choice Main Category: Cancer / Oncology Also Included In: Colorectal Cancer;Multiple Sclerosis Article Date: 28 Jun 2012 - 9:00 PDT

Current ratings for: Cancer Risk Lower In Multiple Sclerosis Patients

3 (2 votes)

The study, conducted by researchers at the University of British Columbia and Vancouver Coastal Health, is published in the journal Brain.

Lead author of the study Elaine Kingwell, a postdoctoral fellow in the UBC Faculty of Medicine and Brain Research Center at UBC and VCH Research Institute, explained:

After comparing diagnoses of cancer in MS patients in British Columbia with those of the general public, the researchers discovered that MS patients were less likely to develop cancer. In particular MS patients had a lower risk of developing colorectal cancer. However, the team found that these patients had a slightly increased risk of developing brain and bladder cancer, although this increase was not significant. Furthermore, the risk for non-melanoma skin cancer was significantly higher among patients with relapsing-onset MS.

The researchers note that further studies are required in order to understand why MS patients have a reduced overall risk of developing cancer.

The researchers also found that MS patients who developed cancer usually had larger tumors at time of diagnosis. They state that more researcher is needed to find out why some tumors might be caught later in individuals with MS.

Helen Tremlett, associate professor in the UBC Faculty of Medicine, said: "Because the symptoms of MS can be broad and include feelings of fatigue, it's possible the symptoms of cancer are being masked or overlooked."

Tremlett states that MS patients and their physicians should continue to follow cancer screening guidelines, regardless of the study findings. A follow-up study is planned in order for the researchers to determine if cancer mortality rates are altered in MS patients.

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Cancer Risk Lower In Multiple Sclerosis Patients

Dementia: Not a normal part of aging

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By GARY LEBLANC | Common Sense Caregiving Published: June 28, 2012 Updated: June 28, 2012 - 12:00 AM

I recently had a conversation with a fellow caregiver that is caring for his elderly mother who is suffering from some type of dementia. He told me that her primary physician diagnosed her with "Old Brain." I almost fell out of my chair. What kind of medical diagnosis is that?

Dementia is not a normal part of aging. For example, my own mother is 93 years old and as sharp as a whip! I believe this is the way we are all meant to live out our golden years.

If our loved ones show signs of dementia, something is causing it and if their doctors aren't going to investigate it, I suggest we take them to a neurologist right away. In the case of Alzheimer's Disease, it's the disease that has brought on the symptoms of dementia. (Yes. Dementia is a symptom.)

A good analogy to use when explaining the term dementia is "fever." Fever refers to an elevated temperature, indicating that the person is sick, but it does not explain what is causing the sickness. So, simply stated, dementia is not a disease; it is one of the symptoms of a disease.

Lewy Body Dementia, Parkinson's Disease, Huntington's Disease I could go on and on, but in all cases it's the diseases themselves that have created the symptom of dementia.

The goal of any truly caring doctor is to discover what is causing it, and the sooner the better. There are even some cases such as Vascular Dementia which can be reversed if caught early enough.

Around the age of 60, everyone starts to develop a little brain shrinkage. This may cause some absent mindedness, but this should not necessarily be mistaken for dementia.

Here are a couple of scenarios to consider; we all misplace our keys once in a while, but when we're holding our car keys in our hand and forget what they are for . . . or if we forget something in our bedroom and we walk back in there and don't recognize the room we're standing in, that's concern for dementia!

If you or your loved one are experiencing this symptom, please see a doctor right away. Now, don't let the word "Alzheimer's" be the first thing to pop into your head. There are many probable causes including: vitamin B deficiency, medication side-effects, depression, just to name a few. All avenues should be explored right away.

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Dementia: Not a normal part of aging

Dementia has robbed me of my freedom, says Thunderbirds creator Gerry Anderson

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He said he did not even know his mental condition was deteriorating and described how the diagnosis came as a shock.

I dont think I realised at all, he told BBC Berkshire.

I don't think I realised at all. It was my wife Mary who began to notice that I would do something quite daft like putting the kettle in the sink and waiting for it to boil.

"Finally I was persuaded to go and see the doctor and eventually I was confronted with the traditional test - a piece of paper with drawings on it, taking a pencil and copying them.

"I thought 'Why are they doing this? A child could do this'.

"But when I started to copy the drawings, that wasn't the case.

"I started to get in a muddle. That's when I began to realise that there was something wrong."

He said not being able to drive anymore was the bitterest blow of all because he could not get to Pinewood from his home in Henley-on-Thames.

This depressed me enormously because my film work was my life.

Suddenly my life was cut off. Since I've had Alzheimer's I've realised how debilitating it is. It can affect your life in so many ways that you don't think about, he said.

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Dementia has robbed me of my freedom, says Thunderbirds creator Gerry Anderson

ABC News Profiles BalanceWear® and the Benefits for Multiple Sclerosis Patients

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SAN FRANCISCO--(BUSINESS WIRE)--

Wow, Its like looking at a miracle, isnt it, said Cheryl Jennings, co-anchor of ABC 7 News. She was referring to reporter Carolyn Johnsons Health & Science segment on BalanceWear, a semi-custom made orthotic that has helped dramatically improve stability in patients with MS, Parkinsons disease, stroke, TBI, ataxia and other Sensory Based Motor Disorders (SBMD).

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For patients suffering from multiple sclerosis or other degenerative diseases, just controlling their own bodies can be a challenge. But now, a simple device invented in the Bay Area is helping a growing number of those patients move far more smoothly, Johnson says as she introduces viewers to Mary Spencer, a woman who suffers with balance issues caused by Multiple Sclerosis and to physical therapist Cindy Gibson-Horn, creator of BalanceWear.

"You can't tell what direction is what. Your body doesn't know what's up or down," says Mary.

Directional loss is a symptom of several Sensory Based Motor Disorders. As the patient walks, he or she becomes preoccupied with their movements, trying to compensate with every step in order to keep from falling. Gibson-Horn discovered that small, strategically placed weights applied to BalanceWear helps to adjust directional loss. Her research led to the discovery of Balance-Based Torso Weighting (BBTW), a breakthrough that has been noticed by doctors and researchers. Recently, a National Institutes of Health Recovery Grant of just under $400,000 was awarded to Samuel Merritt University (SMU) Physical Therapy Professor Dr. Gail Widener, PT, and Dr. Diane Allen at San Francisco State University to continue research into Balance-Based Torso Weighting (BBTW) and its effects on Multiple Sclerosis (MS) mobility challenges. The first phase of the study validates previous research funded by the National MS Society. The research is currently in its second phase and has led to documented evidence of the efficacy of prior clinical observations.

"If you think about balance, it's the foundation of movement. So you couldn't even sit, unless you had balance," Gibson-Horn tells Johnson. "If the patient has a balance problem, and we can identify the directional losses of balance, then we can treat those imbalances by strategically placing light weights in BalanceWear and immediately you'll know whether or not your patient is going to experience balance improvement."

Steve Cookston, CEO of Motion Therapeutics, the company that manufactures and markets BalanceWear, has spent years in the medical device field. BalanceWear has the remarkable ability to change a persons life by simply being fitted for the vest, says Cookston. It requires no downtime, drugs or special care. It is designed and manufactured to insure that the patients balance is dramatically improved immediately and that is what makes us all enthusiastically committed to this product.

Says Johnson, For Spencer, the results have already been life changing.

"I have the freedom to move without thinking, 'Where do I need to be? How do I need to stand?'" Spencer explains.

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ABC News Profiles BalanceWear® and the Benefits for Multiple Sclerosis Patients

Nighttime leg cramps hurt patient

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Dear Dr. DonohueI have leg cramps at night quite often. They wake me up, and I have to straighten my leg slowly. I do 15 bends, squats, modified push-ups and sit-ups every night. What causes these cramps? What can I do to stop them? I am physically fit and healthy at age 80. R.C.

AnswerNighttime leg cramps are the bane of a significant number of older people. What causes them is a question to which no one has come up with an answer. That hasn't stopped people from suggesting a number of possible causes: low magnesium, low potassium, too little calcium. None of these has been proved.

Some medicines have been implicated as possible causes. Water pills (diuretics) have been cited, as have long-acting beta-2 agonists used for asthma control.

Peripheral artery disease, a common malady of the elderly, is said to be common among people who suffer from nighttime cramps. That's the circulatory problem where there's obstruction to blood flow to the legs because of clogged arteries. The various kinds of arthritis also are said to contribute to nighttime cramping.

Ways to end cramps include doing exercises before going to bed. Leg exercise is particularly important. If you have a stationary bike, it might be one way to conquer cramps. Stretching exercises for the leg muscles also are important. If the calves are cramping, then stand on a stair with your heels projecting off the stair. Lower your heels, and hold that position for 10 seconds. Repeat 10 times at bedtime, and do this exercise three times during the day.

Medicines sometimes can be helpful if nothing else is working. Examples are gabapentin (Neurontin), diltiazem (Cardizem) and a multivitamin containing a mix of B vitamins. Tonic water, because of its quinine content, often is offered as a preventive step.

The booklet on restless leg syndrome and nighttime cramps offers more tips. Readers can obtain a copy by writing: Dr. Donohue No. 306, Box 536475, Orlando, FL 32853-6475. Enclose a check or money order (no cash) for $4.75 with the recipient's printed name and address. Please allow four weeks for delivery.

Dear Dr. DonohueMy husband was diagnosed with ataxia. What is it? R.A.

AnswerAtaxia is uncoordinated muscle movement. For most ataxia patients, it indicates a stumbling walk.

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Nighttime leg cramps hurt patient

Grover Beach boy will get service dog thanks to fundraiser; more that 400 attend event

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By Mike Hodgson/Associate Editor Email a friend Printer friendly

Lucas Appleton, right, plays with Tony Boy during a fundraiser Sunday at Mangos Saloon in Grover Beach. //Phil Klein/Contributor

A Grover Beach boy stricken with Friedreichs ataxia will get his service dog as a result of a fund-raiser that drew more than 400 people Sunday.

Nine-year-old Lucas Appleton, who suffers from the progressively crippling form of muscular dystrophy, managed to spend five hours at the event at Mongos Saloon, said his godmother, Linda McClure, who organized the barbecue that included a prize drawing, musical performances and a bake sale.

It was a huge success, McClure said. Lucas was so happy and so was his brother (William) and mother, Casandra.

We raised enough to get him a dog, with a small amount left over for a van, and were working on that now, she said.

A trained service dog, which costs $12,000 to $15,000, will help Lucas maintain his balance, turn on lights for him, pick up things hes dropped, help him through the familys narrow bathroom door and just be a companion.

McClure said about 450 people and a host of dogs attended the event that started at 10:30 a.m. and continued until Mongos closed that night.

She noted Lucas had asked to have a golden retriever or black Labrador retriever for a service dog, which might not be possible.

But a golden retriever club heard about his request and showed up with all their dogs.

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Grover Beach boy will get service dog thanks to fundraiser; more that 400 attend event

Boy will get service dog thanks to fundraiser

Posted on by

By Mike Hodgson/Associate Editor Email this story Print this story

Lucas Appleton, right, plays with Tony Boy during a fundraiser Sunday at Mangos Saloon in Grover Beach. //Phil Klein/Contributor

A Grover Beach boy stricken with Friedreichs ataxia will get his service dog as a result of a fund-raiser that drew more than 400 people Sunday.

Nine-year-old Lucas Appleton, who suffers from the progressively crippling form of muscular dystrophy, managed to spend five hours at the event at Mongos Saloon, said his godmother, Linda McClure, who organized the barbecue that included a prize drawing, musical performances and a bake sale.

It was a huge success, McClure said. Lucas was so happy and so was his brother (William) and mother, Casandra.

We raised enough to get him a dog, with a small amount left over for a van, and were working on that now, she said.

A trained service dog, which costs $12,000 to $15,000, will help Lucas maintain his balance, turn on lights for him, pick up things hes dropped, help him through the familys narrow bathroom door and just be a companion.

McClure said about 450 people and a host of dogs attended the event that started at 10:30 a.m. and continued until Mongos closed that night.

She noted Lucas had asked to have a golden retriever or black Labrador retriever for a service dog, which might not be possible.

But a golden retriever club heard about his request and showed up with all their dogs.

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Boy will get service dog thanks to fundraiser