Author Archives: Fredricko

Working and autism

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Editor's note: A little over a decade ago, California officials raised an alarm about the growing number of children being diagnosed with autism. The Star examined the struggles of several Ventura County children who were part of that surge in 2000. In this series, we look at what has happened to them as they've come of age.

More on mobile: 2000: Special report - Children in Disorder

Q: What percentage of autistic adults work?

A: About 55 percent of young adults with autism spectrum disorders had held paid employment in the first six years after high school, according to a study published in May. In a review of studies from the 1980s through the mid-2000s, about 25 percent of autistic adults were employed, autism authority Patricia Howlin reported. The studies covered a period when autism was more strictly defined than it is now.

Q: What kinds of jobs do they hold?

A: Some held responsible positions that paid well, but most were menial jobs, such as kitchen hands, unskilled factory workers or backroom supermarket staff, Howlin wrote. In the Southern California area today, autistic adults work in fast-food restaurants, grocery stores, movie theaters and offices, employment specialists said. Some run their own businesses. Media production and computer jobs could be a growth area. They can receive preference for federal jobs under the government's hiring policies for people with severe disabilities. Some are noted for their success, including Temple Grandin, a professor whose life inspired a television movie. Historically, many have worked in sheltered workshops or have done piece work, earning less than minimum wage.

Q: What are the obstacles?

A: Communication problems and social skills are blamed for unsuccessful interviews and problems on the job. People with autism may need routine, have difficulty making eye contact and misunderstand expressions or facial cues, such as a wink or nod. Employers fear they will have outbursts, although not all do. Behavioral interventions have reduced such problems, educators say. Job coaches boost chances of success, as does finding the right match between job and employee.

Q: What's being done about it?

A: Specialists at UC Santa Barbara's Koegel Autism Center are tackling the issues from a research and counseling standpoint. They're working with people who are having trouble preparing for careers because of social issues and studying procedures to ease the passage to adulthood.

See the rest here:
Working and autism

A Hole-Based Taxonomy for Theories of Aging

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Something to think about for today: SENS, the Strategies for Engineered Negligible Senescence is not put forward as a theory of aging, but it is a theory of aging, one that pulls from many other partial attempts to explain aging. It purports to describe, as best we know, the detailed mechanisms that lie at the root of degenerative aging - but is presented (and currently running) as a program of research and development to reverse aging. That is the testable part of the theory, if you like: implement SENS and we should see rejuvenation. If this comes to pass, then it is true that SENS as laid out at present does describe all forms of fundamental damage that cause aging. If not, then SENS is either wrong or, more likely, incomplete - there is some other form of damage that is important and unconnected to those already discovered.

(No new form of fundamental change or damage related to aging has been identified in the past 25 years, across a time of raging progress in biotechnology, which should gives us some confidence that there are no others. There is always room to argue, however, and science is anything but static).

There are, it has to be said, a great many theories of aging. Following this line of thinking, it occurs to me that we can classify most theories of aging according to where they stand with respect to the hole we find ourselves in - that hole being the inconvenient fact that we're all aging to death, and progressively increasing suffering and pain lies in each of our personal futures.

I see three broad buckets for this hole-based taxonomy:

  • How did we get into this hole?
  • What is going on in here?
  • How do we get out of this hole?

How did we get into this hole?

Evolutionary theories of aging seek to explain how we came to age the way we do. Here the proposed mechanisms of aging inform the discussion and modeling of plausible evolutionary processes that would produce them - as well as the staggering variety in lifespan and pace of aging that exists in the natural world. I see this as scientific dispassion at its finest: "Look at the interesting way in which we're all dying! Fascinating, no? We should take some time to think about how this came to pass."

What is going on in here?

Other theories of aging focus on modeling how aging happens: what are the exact mechanisms? Many different approaches to these theories exist. Consider, for example, those that describe aging at the high level, such as in the use of reliability theory to frame aging in the form of a systems failure model. At the other end of the room we have things like the mitochondrial free radical theory of aging, which proposes detailed and particular mechanisms in cells and cellular components that lead to damage and then the larger-scale manifestations of aging.

How do we get out of this hole?

So here we return to SENS, a meta-theory of aging that pulls from many of the mechanism-focused theories of aging proposed over the past century. Until the advent of SENS there really wasn't any sort of contingent in the scientific community whose members presented a theory of aging as something more like a theory on how to defeat aging - to prevent and treat aging with therapies, reverse frailty in the old by removing its root causes, and stop the young from becoming aged.

So we are in a hole, no arguing that. Getting out does require some understanding of the hole in order to best direct efforts - but the scientific community is far and away past the point at which we could be effectively working our way out. Spending all our time gathering more knowledge is no longer good strategy. We in fact don't need to know all that much about how we got here, nor exactly how fundamental causes of aging spiral outward to create the thousand and one causes of death we observe in old people. What SENS tells us is that we just need to know what those root causes are and how to fix them. Additional information is useful, and will probably improve efficiency, but it is not absolutely necessary and nowhere near as important as just forging ahead to get the job done. The test of SENS as a theory aging is for the research community to get out there and actually fix the problems that are killing us.

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

Genetic Hotspots for Diseases of Aging

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Some interesting results from genetic research: scientists "have shown definitively that a small number of places in the human genome are associated with a large number and variety of diseases. In particular, several diseases of aging are associated with a locus which is more famous for its role in preventing cancer. For this analysis, [researchers] cataloged results from several hundred human Genome-Wide Association Studies (GWAS) from the National Human Genome Research Institute. These results provided an unbiased means to determine if varied different diseases mapped to common 'hotspot' regions of the human genome. This analysis showed that two different genomic locations are associated with two major subcategories of human disease. ... More than 90 percent of the genome lacked any disease loci. Surprisingly, however, lots of diseases mapped to two specific loci, which soared above all of the others in terms of multi-disease risk. The first locus at chromosome 6p21, is where the major histocompatibility (MHC) locus resides. The MHC is critical for tissue typing for organ and bone marrow transplantation, and was known to be an important disease risk locus before genome-wide studies were available. Genes at this locus determine susceptibility to a wide variety of autoimmune diseases ... The second place where disease associations clustered is the INK4/ARF (or CDKN2a) tumor suppressor locus [also known as p16]. This area, in particular, was the location for diseases associated with aging: atherosclerosis, heart attacks, stroke, Type II diabetes, glaucoma and various cancers. ... The finding that INK4/ARF is associated with lots of cancer, and MHC is associated with lots of diseases of immunity is not surprising - these associations were known. What is surprising is the diversity of diseases mapping to just two small places: 30 percent of all tested human diseases mapped to one of these two places. This means that genotypes at these loci determine a substantial fraction of a person's resistance or susceptibility to multiple independent diseases. ... In addition to the MHC and INK4/ARF loci, five less significant hotspot loci were also identified. Of the seven total hotspot loci, however, all contained genes associated with either immunity or cellular senescence. Cellular senescence is a permanent form of cellular growth arrest, and it is an important means whereby normal cells are prevented from becoming cancerous. It has been long known that senescent cells accumulate with aging, and may cause aspects of aging. This new analysis provides evidence that genetic differences in an individual's ability to regulate the immune response and activate cellular senescence determine their susceptibility to many seemingly disparate diseases."

Link: http://news.unchealthcare.org/news/2012/september/diseases-of-aging-map-to-a-few-hotspots-on-the-human-genome

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

A Look at the Allen Institute for Brain Science

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A comprehensive understanding of the brain is an important line item for future medical development, as the research community will have to develop ways to repair the brain and reverse aspects of its aging while preserving the structures that encode the mind. Here is a look at one of the higher profile projects of recent years: "Paul Allen, the 59-year-old Microsoft cofounder [has] plowed $500 million into the Allen Institute for Brain Science, a medical Manhattan Project that he hopes will dwarf his contribution as one of the founding fathers of software. The institute, scattered through three buildings in Seattle's hip Fremont neighborhood, is primarily focused on creating tools, such as the mouse laser, which is technically a new type of microscope, that will allow scientists to understand how the soft, fleshy matter inside the human skull can give rise to the wondrous, mysterious creative power of the human mind. ... His first $100 million investment in the Allen Institute resulted in a gigantic computer map of how genes work in the brains of mice, a tool that other scientists have used to pinpoint genes that may play a role in multiple sclerosis, memory and eating disorders in people. Another $100 million went to creating a similar map of the human brain, already resulting in new theories about how the brain works, as well as maps of the developing mouse brain and mouse spinal cord. These have become essential tools for neuroscientists everywhere. Now Allen, the 20th-richest man in America, with an estimated net worth of $15 billion, has committed another $300 million for projects that will make his institute more than just a maker of tools for other scientists, hiring several of the top minds in neuroscience to spearhead them. One effort will try to understand the mouse visual cortex as a way to understand how nerve cells work in brains in general. Other projects aim to isolate all the kinds of cells in the brain and use stem cells to learn how they develop. Scientists think there may be 1,000 of these basic building blocks, but they don't even know that. 'In software,' Allen says, 'we call it reverse engineering.'"

Link: http://www.forbes.com/sites/matthewherper/2012/09/18/inside-paul-allens-quest-to-reverse-engineer-the-brain/

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

Considering Senescent Astrocytes in Alzheimer's Disease

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A few days back, I pointed out research that indicates brain cells increasingly become senescent with age. This is a challenge: we want to get rid of senescent cells and prevent their buildup because the harm they cause contributes to degenerative aging, but the obvious way to do that is through targeted destruction via one of the many types of cell-targeting and cell-killing technologies presently under development. This is fine and well for tissues like skin and muscle, in which cells turn over and are replaced - but in the brain and nervous system there are many small but vital populations of cells that are never replaced across the normal human life span. The cells you are born with last a lifetime, and some fraction of those cells contain the data that makes up the mind.

Thus it begins to seem likely that we can't just rampage through and destroy everything that looks like a senescent cell: possible therapies to address cell senescence as a contribution to aging will have to be more discriminating, and so more complex and costly to develop.

Following on in this topic, I noticed an open access paper today that examines the role of cellular senescence of astrocyte, the support cells of the brain, in Alzheimer's disease (AD). Unlike the research I noted above, the biochemical signatures of senescence examined here are the same as those used in last year's mouse study showing benefits resulting from a (necessarily) convoluted way of destroying senescent cells as they emerge - which of course starts the mind wandering on what might be going on in the brain of these mice. Astrocytes can perhaps be replaced without harming the mind or important nervous cells, but what about other cells in the brain?

In any case, here is the paper:

Astrocyte Senescence as a Component of Alzheimer's Disease

A recent development in the basic biology of aging, with possible implications for AD, is the recognition that senescent cells accumulate in vivo. Although senescent cells increase with age in several tissues, little is known about the potential appearance of senescent cells in the brain. The senescence process is an irreversible growth arrest that can be triggered by various events including telomere dysfunction, DNA damage, oxidative stress, and oncogene activation. Although it was once thought that senescent cells simply lack function, it is now known that senescent cells are functionally altered. They secrete cytokines and proteases that profoundly affect neighboring cells, and may contribute to age-related declines in organ function.

...

Astrocytes comprise a highly abundant population of glial cells, the function of which is critical for the support of neuronal homeostasis. ... Impairment of these functions through any disturbance in astrocyte integrity is likely to impact multiple aspects of brain physiology. Interestingly, astrocytes undergo a functional decline with age in vivo that parallels functional declines in vitro. We demonstrated that in response to oxidative stress and exhaustive replication, human astrocytes activate a senescence program.

...

The importance of senescent astrocytes in age-related dementia has been the subject of recent discussion, but to date, there is little evidence to suggest that senescent astrocytes accumulate in the brain. In this study, we examined brain tissue from aged individuals and patients with AD to determine whether senescent astrocytes are present in these individuals. Our results demonstrate that senescent astrocytes accumulate in aged brain, and further, in brain from patients with AD.

Furthermore, since A? peptides induce mitochondrial dysfunction, oxidative stress, and alterations in the metabolic phenotype of astrocytes; we examined whether A? peptides initiate the senescence response in these cells. In vitro, we found that exposure of astrocytes to A?1-42 triggers senescence and that senescent astrocytes produce high quantities of interleukin-6 (IL-6), a cytokine known to be increased in the [central nervous system] of AD patients. Based on this evidence, we propose that accumulation of senescent astrocytes may be one age-related risk factor for sporadic AD.

As I mentioned in the last post on this subject, this all seems to point to the likely need for ways to reverse cellular senescence, not just selectively destroy senescent cells - at least for some populations of nerve cells. One open question here is whether fixing all the known fundamental forms of cellular damage (as described in the Strategies for Engineered Negligible Senescence) would be sufficient to achieve this end.

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

Considering Senescent Astrocytes in Alzheimer’s Disease

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A few days back, I pointed out research that indicates brain cells increasingly become senescent with age. This is a challenge: we want to get rid of senescent cells and prevent their buildup because the harm they cause contributes to degenerative aging, but the obvious way to do that is through targeted destruction via one of the many types of cell-targeting and cell-killing technologies presently under development. This is fine and well for tissues like skin and muscle, in which cells turn over and are replaced - but in the brain and nervous system there are many small but vital populations of cells that are never replaced across the normal human life span. The cells you are born with last a lifetime, and some fraction of those cells contain the data that makes up the mind.

Thus it begins to seem likely that we can't just rampage through and destroy everything that looks like a senescent cell: possible therapies to address cell senescence as a contribution to aging will have to be more discriminating, and so more complex and costly to develop.

Following on in this topic, I noticed an open access paper today that examines the role of cellular senescence of astrocyte, the support cells of the brain, in Alzheimer's disease (AD). Unlike the research I noted above, the biochemical signatures of senescence examined here are the same as those used in last year's mouse study showing benefits resulting from a (necessarily) convoluted way of destroying senescent cells as they emerge - which of course starts the mind wandering on what might be going on in the brain of these mice. Astrocytes can perhaps be replaced without harming the mind or important nervous cells, but what about other cells in the brain?

In any case, here is the paper:

Astrocyte Senescence as a Component of Alzheimer's Disease

A recent development in the basic biology of aging, with possible implications for AD, is the recognition that senescent cells accumulate in vivo. Although senescent cells increase with age in several tissues, little is known about the potential appearance of senescent cells in the brain. The senescence process is an irreversible growth arrest that can be triggered by various events including telomere dysfunction, DNA damage, oxidative stress, and oncogene activation. Although it was once thought that senescent cells simply lack function, it is now known that senescent cells are functionally altered. They secrete cytokines and proteases that profoundly affect neighboring cells, and may contribute to age-related declines in organ function.

...

Astrocytes comprise a highly abundant population of glial cells, the function of which is critical for the support of neuronal homeostasis. ... Impairment of these functions through any disturbance in astrocyte integrity is likely to impact multiple aspects of brain physiology. Interestingly, astrocytes undergo a functional decline with age in vivo that parallels functional declines in vitro. We demonstrated that in response to oxidative stress and exhaustive replication, human astrocytes activate a senescence program.

...

The importance of senescent astrocytes in age-related dementia has been the subject of recent discussion, but to date, there is little evidence to suggest that senescent astrocytes accumulate in the brain. In this study, we examined brain tissue from aged individuals and patients with AD to determine whether senescent astrocytes are present in these individuals. Our results demonstrate that senescent astrocytes accumulate in aged brain, and further, in brain from patients with AD.

Furthermore, since A? peptides induce mitochondrial dysfunction, oxidative stress, and alterations in the metabolic phenotype of astrocytes; we examined whether A? peptides initiate the senescence response in these cells. In vitro, we found that exposure of astrocytes to A?1-42 triggers senescence and that senescent astrocytes produce high quantities of interleukin-6 (IL-6), a cytokine known to be increased in the [central nervous system] of AD patients. Based on this evidence, we propose that accumulation of senescent astrocytes may be one age-related risk factor for sporadic AD.

As I mentioned in the last post on this subject, this all seems to point to the likely need for ways to reverse cellular senescence, not just selectively destroy senescent cells - at least for some populations of nerve cells. One open question here is whether fixing all the known fundamental forms of cellular damage (as described in the Strategies for Engineered Negligible Senescence) would be sufficient to achieve this end.

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

Correlating Progressive Frailty in Aging With Parental Longevity

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A nice demonstration of the degree to which the pace of aging is inherited - but remember that for the vast majority of us, lifestyle choices have more influence than genes, while progress in medical technology trumps all such concerns: "Various measures incorporated in geriatric assessment have found their way into frailty indices (FIs), which have been used as indicators of survival/mortality and longevity. Our goal is to understand the genetic basis of healthy aging to enhance its evidence base and utility. We constructed a FI as a quantitative measure of healthy aging and examined its characteristics and potential for genetic analyses. Two groups were selected from two separate studies. One group (OLLP for offspring of long-lived parents) consisted of unrelated participants at least one of whose parents was age 90 or older, and the other group of unrelated participants (OSLP for offspring of short-lived parents), both of whose parents died before age 76. FI(34) scores were computed from 34 common health variables and compared between the two groups. The FI(34) was better correlated than chronological age with mortality. The mean FI(34) value of the OSLP was 31% higher than that of the OLLP. The FI(34) increased exponentially, at an instantaneous rate that accelerated 2.0% annually in the OLLP and 2.7 % in the OSLP consequently yielding a 63% larger accumulation in the latter group. The results suggest that accumulation of health deficiencies over the life course is not the same in the two groups, likely due to inheritance related to parental longevity. Consistent with this, [sibling pairs] were significantly correlated regarding FI(34) scores, and heritability of the FI(34) was estimated to be 0.39. ... Variation in the FI(34) is, in part, due to genetic variation; thus, the FI(34) can be a phenotypic measure suitable for genetic analyses of healthy aging."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22986583

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

Reproducing Research Results: Removing a Scientific Roadblock

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The California stem cell agency faces
no easy task in trying to translate basic research findings into
something that can be used to treat patients and be sold commercially.

Even clinical trials, which only begin
long after the basic research is done and which involve more ordinary
therapeutic treatments than stem cells, fail at an astonishing rate.
Only one out of five that enter the clinical trial gauntlet
successfully finish the second stage, according to industry data
cited last spring by Pat Olson, executive director of scientific activities at the stem cell agency. And
then come even more challenges.
But at a much earlier stage of
research there is the “problem of irreproducible results,” in the
words of writer Monya Baker of the journal Nature. Baker last month reported on
moves by a firm called Science Exchange in Palo Alto, Ca., to
do something to ease the problem and speed up preclinical research.
The effort is called the Reproducibility Initiative and also involves
PLOS and figshare, an open science Internet project.
Elizabeth Iorns
Science Exchange Photo
Science Exchange is headed by Elizabeth
Iorns, a scientist and co-founder of the firm. She wrote about  test-tube-to-clinic translation issues in a recent article in New
Scientist that was headlined, “Is medical science built on shaky
foundations?”
Iorns said,

“One goal of scientific publication
is to share results in enough detail to allow other research teams to
reproduce them and build on them. However, many recent reports have
raised the alarm that a shocking amount of the published literature
in fields ranging from cancer biology to psychology is not
reproducible.”

Iorns cited studies in Nature that
reported that Bayer cannot “replicate about two-thirds of published
studies identifying possible drug targets” and that Amgen failed at
even a higher rate. It could not “replicate 47 of 53 highly
promising results they examined.”
The California Stem Cell Report earlier
this week asked Iorns for her thoughts on the implications for the
California stem cell agency, whose motto is "Turning stem cells into cures." Here is the full text of her response.

“First, I think it is important to
accept that there is a crisis affecting preclinical research. Recent
studies estimate that 70% of preclinical research cannot be
reproduced. This is the research that should form the foundation upon
which new discoveries can be made to enhance health, lengthen life,
and reduce the burdens of illness and disability. The
irreproducibility of preclinical research is a significant impediment
to the achievement of these goals. To solve this problem requires
immediate and concrete action. It is not enough to make
recommendations and issue guidelines to researchers. Funders must act
to ensure they fund researchers to produce high quality reproducible
research. One such way to do so, is to reward, or require,
independent validation of results. The reproducibility initiative
provides a mechanism for independent validation, allowing the
identification of high quality reproducible research. It is vital
that funders act now to address this problem, to prevent the wasted
time and money that is currently spent funding non-reproducible
research and to prevent the erosion of public trust and support for
research.”

Source:
http://californiastemcellreport.blogspot.com/feeds/posts/default?alt=rss

Parkinson's researcher at NIH is first honored with award named for Jay Van Andel

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GRAND RAPIDS, MI A National Institutes of Health researcher who has uncovered genetic causes of Parkinsons disease today became the first to receive an honor named after Amway co-founder Jay Van Andel.

Dr. Andrew Singleton was honored with the Jay Van Andel Award for Outstanding Academic Achievement in Parkinsons Disease Research during a research symposium at Van Andel Institute.

Jay Van Andel, who died of the effects of Parkinsons in 2004, would have been pleased with the first recipient of the award named after him, said his son, David Van Andel, VAI chairman and chief executive officer.

Dr. Andrew Singleton is the type of scientist he would have envisioned honoring bold, pioneering and working to make a difference in human lives, David Van Andel said.

Singletons accomplishments include the discovery of a duplication and triplication of a gene that causes a severe, early-onset form of Parkinsons.

Scientists already knew that a few extremely rare mutant forms of the protein were bad, but Dr. Singleton showed us that too much of the normal protein also has ramifications, Van Andel said.

Singleton also led a group of researchers that identified mutations in a gene as a cause of familial Parkinsons disease.

His discoveries opened new fields of Parkinsons research, Van Andel said. Singletons lab has research programs investigating genetic diversity and the consequences of genetic alterations.

VAI today began a two-day symposium bringing together experts in Parkinsons disease research to showcase the latest developments.

This is truly a gathering of some of the worlds greatest minds in Parkinsons disease research, said Dr. Patrik Brundin, the chair of the Jay Van Andel Translational Parkinsons Disease Research Laboratory. The research shared at the conference will become the building blocks for therapies that may be commonplace a decade from now.

Read the original here:
Parkinson's researcher at NIH is first honored with award named for Jay Van Andel

Parkinson’s researcher at NIH is first honored with award named for Jay Van Andel

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GRAND RAPIDS, MI A National Institutes of Health researcher who has uncovered genetic causes of Parkinsons disease today became the first to receive an honor named after Amway co-founder Jay Van Andel.

Dr. Andrew Singleton was honored with the Jay Van Andel Award for Outstanding Academic Achievement in Parkinsons Disease Research during a research symposium at Van Andel Institute.

Jay Van Andel, who died of the effects of Parkinsons in 2004, would have been pleased with the first recipient of the award named after him, said his son, David Van Andel, VAI chairman and chief executive officer.

Dr. Andrew Singleton is the type of scientist he would have envisioned honoring bold, pioneering and working to make a difference in human lives, David Van Andel said.

Singletons accomplishments include the discovery of a duplication and triplication of a gene that causes a severe, early-onset form of Parkinsons.

Scientists already knew that a few extremely rare mutant forms of the protein were bad, but Dr. Singleton showed us that too much of the normal protein also has ramifications, Van Andel said.

Singleton also led a group of researchers that identified mutations in a gene as a cause of familial Parkinsons disease.

His discoveries opened new fields of Parkinsons research, Van Andel said. Singletons lab has research programs investigating genetic diversity and the consequences of genetic alterations.

VAI today began a two-day symposium bringing together experts in Parkinsons disease research to showcase the latest developments.

This is truly a gathering of some of the worlds greatest minds in Parkinsons disease research, said Dr. Patrik Brundin, the chair of the Jay Van Andel Translational Parkinsons Disease Research Laboratory. The research shared at the conference will become the building blocks for therapies that may be commonplace a decade from now.

Read the original here:
Parkinson's researcher at NIH is first honored with award named for Jay Van Andel

Parkinson's Drug Mirapex Under Safety Review

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Parkinsons Disease and Restless Legs Syndrome Drug Under Review for Heart Failure Risk

Sept. 19, 2012 -- The FDA is investigating a possible risk of heart failure linked to Mirapex, a drug used to treat Parkinson's disease and restless legs syndrome.

Officials say recent studies suggest a potential raised risk of heart failure with the use of Mirapex, but further review of research is needed.

The FDAs safety alert stops short of an official warning announcement for the drug. The agency has not concluded that Mirapex raises the risk of heart failure.

Instead, the FDA says it is working with Mirapexs manufacturer to clarify the risk of heart failure and will update the public when more information is available.

Meanwhile, officials say people taking Mirapex should continue to take the drug as prescribed and contact their health care provider with any questions or concerns.

The alert comes after the FDA pooled results from clinical trials, and analysis suggests heart failure was more common among people taking Mirapex than those taking a placebo.

They also evaluated two population studies that suggested a higher risk of new cases of heart failure among Mirapex users. However, officials say limitations of the studies make it difficult for them to determine whether the risk was related to Mirapex or other factors.

The FDA is continuing to review safety data on Mirapex.

Officials recommend people taking the drug contact a health care professional if they experience any symptoms of heart failure while taking Mirapex, such as:

Excerpt from:
Parkinson's Drug Mirapex Under Safety Review

Parkinson’s Drug Mirapex Under Safety Review

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Parkinsons Disease and Restless Legs Syndrome Drug Under Review for Heart Failure Risk

Sept. 19, 2012 -- The FDA is investigating a possible risk of heart failure linked to Mirapex, a drug used to treat Parkinson's disease and restless legs syndrome.

Officials say recent studies suggest a potential raised risk of heart failure with the use of Mirapex, but further review of research is needed.

The FDAs safety alert stops short of an official warning announcement for the drug. The agency has not concluded that Mirapex raises the risk of heart failure.

Instead, the FDA says it is working with Mirapexs manufacturer to clarify the risk of heart failure and will update the public when more information is available.

Meanwhile, officials say people taking Mirapex should continue to take the drug as prescribed and contact their health care provider with any questions or concerns.

The alert comes after the FDA pooled results from clinical trials, and analysis suggests heart failure was more common among people taking Mirapex than those taking a placebo.

They also evaluated two population studies that suggested a higher risk of new cases of heart failure among Mirapex users. However, officials say limitations of the studies make it difficult for them to determine whether the risk was related to Mirapex or other factors.

The FDA is continuing to review safety data on Mirapex.

Officials recommend people taking the drug contact a health care professional if they experience any symptoms of heart failure while taking Mirapex, such as:

Excerpt from:
Parkinson's Drug Mirapex Under Safety Review

Research and Markets: Global Parkinson's Disease Drug Pipeline Capsule – 2012 Update

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/6lkdr4/global) has announced the addition of the "Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update" report to their offering.

Fore Pharma's latest report 'Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update' provides most up-to-date information on key Research and Development activities (R&D) in the global Parkinson's Disease market. It covers active Parkinson's Disease pipeline molecules in various stages of clinical trials, preclinical research, and drug discovery.

This report helps executives track competitors pipeline molecules. The information presented in this report can be used for identifying partners, evaluating opportunities, formulating business development strategies, executing in-licensing and out-licensing deals.

The report provides information on pipeline molecules by company and mechanism of action across the R&D stages. It also provides information on pipeline molecules developed in leading geographies (North America and Europe). Licensing activities are thoroughly captured in this report.

Key Features of the Report:

- Parkinson's Disease: Overview

- Parkinson's Disease Pipeline Overview

- Parkinson's Disease Phase 3 Clinical Trial Pipeline Insights

- Parkinson's Disease Phase 2 Clinical Trial Pipeline Insights

Originally posted here:
Research and Markets: Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update

Research and Markets: Global Parkinson’s Disease Drug Pipeline Capsule – 2012 Update

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/6lkdr4/global) has announced the addition of the "Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update" report to their offering.

Fore Pharma's latest report 'Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update' provides most up-to-date information on key Research and Development activities (R&D) in the global Parkinson's Disease market. It covers active Parkinson's Disease pipeline molecules in various stages of clinical trials, preclinical research, and drug discovery.

This report helps executives track competitors pipeline molecules. The information presented in this report can be used for identifying partners, evaluating opportunities, formulating business development strategies, executing in-licensing and out-licensing deals.

The report provides information on pipeline molecules by company and mechanism of action across the R&D stages. It also provides information on pipeline molecules developed in leading geographies (North America and Europe). Licensing activities are thoroughly captured in this report.

Key Features of the Report:

- Parkinson's Disease: Overview

- Parkinson's Disease Pipeline Overview

- Parkinson's Disease Phase 3 Clinical Trial Pipeline Insights

- Parkinson's Disease Phase 2 Clinical Trial Pipeline Insights

Originally posted here:
Research and Markets: Global Parkinson's Disease Drug Pipeline Capsule - 2012 Update

Former Longhorn Earl Campbell gives donation to National Multiple Sclerosis Society

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By Liz Farmer

A scholarship supported by University of Texas football legend Earl Campbell and his son Tyler Campbell could make it easier for students affected by multiple sclerosis to finish college.

Earl Campbell, NFL Hall of Fame running back and Heisman Trophy winner, announced Tuesday that he and his son have raised $60,000 for the nonprofit National Multiple Sclerosis Society to provide scholarships for college students who have MS or who have a parent with MS. The society reports it has awarded $187,000 in scholarships to 22 Texas students this year.

MS is a chronic disease of the central nervous system that interrupts information flow between the body and the brain with symptoms including limb numbness, paralysis and vision loss. Campbell's son was diagnosed with MS while at San Diego State University.

The Campbells raised part of the scholarship funds through sales of "The Unstoppable Earl Campbell," a Warner Bros. piece of art signed by Earl Campbell that depicts him in UT gear running a football past cartoon characters including Bugs Bunny and Yosemite Sam.

"I feel very happy that my son and our family has done something to give back," Earl Campbell said. Some money came from benefits such as the Flavors of Austin, which featured local food and drinks. Tyler Campbell said raising money for scholarships is great but he's not satisfied.

"We have to put this disease to rest," he said.

Scholarship recipient Justin Williams is studying for a degree in neurobiology at UT and said he wants to treat people such as his grandmother and father, who both have MS. "My dad's doctor made me truly believe a doctor could change someone's life," Williams said. "I can't thank Earl and Tyler enough."

Bridgette Kieffer, who also got a scholarship, said her mother was diagnosed with MS a few months before she was born. Kieffer said she is pursuing a degree in sociology and English.

"I knew that (college) may not be a possibility because of the cost of medical bills," Kieffer said. "The scholarship has given my family hope and showed us that there's more to life."

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Former Longhorn Earl Campbell gives donation to National Multiple Sclerosis Society

Local Woman Joins Battle Against Multiple Sclerosis

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Twin Falls, Idaho (KMVT-TV) Tammy Lynard of Filer was diagnosed with multiple sclerosis seven years ago.

She says her brain sends messages that her muscles don't always get. She tires easily and the heat bothers her. Lynard takes a shot every day, but she wants to help find a cure for MS.

Lynard says, "It was kind of a shock when you first hear about it. You try to get as much information as possible. You see the neurologist, they get you on therapies, hopefully as soon as possible. Hopefully the therapies help you live a better life."

Like any other medical condition, MS can affect different people to different degrees. Lynard says one out of every 300 people in idaho have multiple sclerosis.

Lynard says, "The MS Society is great with information, they tell you how to get involved, what to do. I heard about the Walk that first year, and I met a lot of people. I found out there's a lot of people in this area that have the disease. In fact, we're one of the highest in the nation."

You can sign up for Saturday's "Walk MS" in Twin Falls online at walkmsidaho.org , or you can call 1 (800) FIGHT MS, and select option two.

Walk MS will be held this Saturday at the Twin Falls Visitor Center near the Perrine Bridge. Registration starts this Saturday at 8:30 a.m., and the walk begins at ten o'clock.

Walk MS is free to participate in, but the organizers encourage you to raise some money to benefit the cause.

Sept. 19, 2012.

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Local Woman Joins Battle Against Multiple Sclerosis

Multiple sclerosis patients, doctors appreciate help from Ann Romney, Michelle Obama

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By Irene Maher, Times Staff Writer Irene MaherTampa Bay Times In Print: Monday, September 17, 2012

Regardless of your political leanings, at least one group of Americans was grateful for the Republican and Democratic National Conventions: Those affected by MS.

People with multiple sclerosis appreciated the shout-out from Ann Romney, wife of presidential nominee Mitt Romney, at the Republican National Convention in Tampa and from first lady Michelle Obama with the Democrats a week later in Charlotte, N.C.

Romney has been living with MS since 1998. Obama's father lived with the disease for about 30 years before his death at age 66. Both women related how their lives were affected by MS.

That kind of exposure does more than increase awareness of an often misunderstood disease that afflicts 400,000 Americans, experts said.

"In the case of Ann Romney, seeing someone at the podium, in the national spotlight, living an obviously busy, active life allows others to see how much you can accomplish with MS," said Dr. Stanley Krolczyk, director of the multiple sclerosis division in the department of neurology at USF Health. "It puts a different face on the disease when celebrities, like Montel Williams and Clay Walker, for example, go public and talk about living with MS."

Jzon Livingston Sr., a patient of Krolczyk's, agrees. The 33-year-old self-employed IT administrator was diagnosed with MS four years ago. With treatment, he's been able to continue working and keep up with his three children, ages 15, 13 and 11. Livingston was moved when Obama described watching the decline in her father.

"That's what the average person needs to know about MS. It's a hard disease to have," he said. "Without knowledge of how it can affect lives, there's no understanding. Without understanding, there's no action."

Multiple sclerosis is a chronic disease of the central nervous system that targets the brain, spinal cord and optic nerves. It can range from mild to severe, where the patient is paralyzed or blind. The disease is unpredictable, and symptoms may start suddenly and persist, then resolve. Sometimes, it seems to be dormant and patients may go months or years without a flare-up. Others, though, have symptoms all the time.

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Multiple sclerosis patients, doctors appreciate help from Ann Romney, Michelle Obama

Intern – European Multiple Sclerosis Platform

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European Multiple Sclerosis Platform is looking for an intern

The Brussels-based European Multiple Sclerosis Platform (EMSP) is looking for a full-time, paid internship to support the organisation from September 2012 onwards in its Public Affairs and Communications efforts. The envisaged duration of the internship is 6 months, with a possible 3-month extension. The intern will provide support on flagship projects of the EMSP (e.g. further development of our YOUTH project) and contribute to the EMSP's website / web alert as key external communication tools.

Profilea background in communication or EU studies outstanding communication skills and excellent English excellent drafting skills; track-record in contributing to print and online publications a good understanding of European policies and the workings of the EU institutions

Interpersonal skills flexible, can-do attitude well-organised team player yet autonomous

Qualified candidates should submit their CV and cover letter in English to the attention of Christoph Thalheim, Deputy CEO and Director of External Affairs at christoph.thalheim@emsp.org. by the 25th September at the latest. Please note that only short listed candidates will be contacted.

About EMSP The EMSP is representing the interests of 38 national MS societies /patient organisations at the European level, working towards equitable treatment and support for persons with MS throughout Europe. Multiple Sclerosis is the most common debilitating neurological disease of young and middle aged people in Europe. More than 600,000 Europeans are affected.

2012 European voice. All rights reserved.

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Intern - European Multiple Sclerosis Platform

Pill shows promise in suppressing multiple sclerosis relapses

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A new oral medication to treat patients in the early stages of multiple sclerosis has shown considerable promise in two clinical trials, researchers announced Wednesday.

The medication is on track to become just the third oral drug available to MS patients, and potentially the safest and most effective, experts said. The second oral drug, called Aubagio, was approved just last week.

MS was virtually untreatable only two decades ago, but today nine "disease modifying" drugs are available for early-stage patients; a half-dozen more are in the late stages of development. Most patients in the early stage of the disease, a form called relapsing-remitting MS, take drugs intravenously.

The two new studies, published online in The New England Journal of Medicine, found that the drug BG-12, developed by Biogen Idec, reduced relapse rates in patients with relapsing MS by about 50 percent.

The drug also significantly reduced the frequency of new brain lesions often associated with these attacks, and slowed the progression of disease compared with a placebo.

The studies were Phase 3 trials, a last step on the road to drug approval. The Food and Drug Administration is required to make a decision about the drug's approval before the end of this year.

"This drug is clearly quite effective in managing disease and reducing disability, and the safety profile looks quite good," said Timothy Coetzee, the chief research officer at the

Multiple sclerosis is often a progressive disease in which the immune system damages neurons in the brain and spinal cord.

A majority of people with MS have relapsing-remitting MS, characterized by flare-ups that cause lesions in the brain to develop and neurological symptoms to emerge or worsen. Eventually, more than half of patients develop a progressive form of MS, leading to permanent disabilities.

Interferons, the drugs most commonly used in relapsing MS, reduce relapses by about 30 percent, and have not been shown to slow the progression of the disease and disability. The newly approved Aubagio also reduces relapses by about 30 percent, and it has the advantage of being an oral drug.

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Pill shows promise in suppressing multiple sclerosis relapses

Remembering dementia's toll in Warranwood

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FOR Christmas in 2005, Diana Fayle's mother Jan Riley drove herself to Warranwood to celebrate with her family.

"But by 2006, she didn't even know what the telephone was or how to use it,'' Ms Fayle said.

Mrs Riley, 69, had dementia - and the illness progressed quickly.

"Mum first started showing signs of memory loss in 2004, but by 2006 we knew there was something wrong,'' she said.

A piano teacher for more than 40 years, Mrs Riley's students began calling Ms Fayle about strange things that were happening during lessons.

The family first put in programs such as home help to keep Mrs Riley at home, but it was soon apparent she needed more care.

"She got to the point where she didn't know the difference between day and night,'' Ms Fayle said.

With a new baby herself, Ms Fayle said it was difficult finding the right home for her mother.

"We wanted to do what was right and best for her, and that meant making difficult decisions,'' she said.

"Finding the right nursing home was paramount.''

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Remembering dementia's toll in Warranwood