They say the boys of summer are baseball players. So I guess this would make me one of the girls of summer. All my life I grew up with boys around. I had one sister, and she also hung out with the boys. I was the competitive one; I did not care if it was against guys or girls. This may be the reason that in the summertime I played baseball with the boys.

I have been playing baseball for the last 20 years. I play competitively against the boys. I have always said if a boy can do it, so can I. I have a mean arm on me, and can play with the best of them. Since being diagnosed with multiple sclerosis, though, I can no longer bat. I cannot run as fast as I need to in order to be able to bat. This is the reason that we use a pinch hitter in my place.

I have compiled a list of ways that keep me in the game even with my multiple sclerosis:

Tip number one

I have to maintain a cool body temperature. In order to do this I drink plenty of water. I maintain enough water to keep me hydrated and cool. I wear bright colors in order to keep the sun rays off of me as well.

The reason that playing baseball is still important to me even with multiple sclerosis is that I want to show the boys I can still strike them out. This is something that I have always taken great pride in being able to do. I told myself that I would never give up playing baseball, unless I ended up in a wheelchair. Well, I have not ended up in a wheelchair, so I still look forward to striking the boys out.

Tip number two

I always stretch before every game. I always spend about 15 minutes warming up before a game because it loosens up the muscles. This allows me to stay in the game longer. It also means that I get to make the boys suffer. I can still throw a mean fastball as long as I’m warmed up. This is the reason I stick to warming up for 15 minutes.

Tip number three

Even though I’m still competitive on the mound, it does not mean I can overdo it. The saying “no pain, no gain” is a saying I do not listen to when it comes to my multiple sclerosis. I know I’m still in pretty good shape for somebody that has a disability like multiple sclerosis, but I know not to overdo it. The mentality of sitting out the game when my multiple sclerosis has the best of me is what has allowed me to endure 20 years of this sport.

Go here to read the rest:
Multiple Sclerosis and Baseball: Top 5 Tips to Staying in the Game

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I grew up cycling in the summertime. This is the reason I still love cycling. It provides me with a great form of exercise for my multiple sclerosis as well. I have cycled in some beautiful places all across the United States as both a child and an adult.

This is the reason I will take you on a 5-stop tour for cyclist. These are 5 of the top places that I have either been cycling as a child or an adult. These 5 stops are also the most memorable stops that I have made in my lifetime.

Stop number one

I grew up in the Hudson Valley area in New York. This is one of the reasons that I love to revisit this area as one of my cycling destinations. The one park that I have returned time and time again to ride through is Minnewaska State Park. This is one of the most beautiful places to go cycling in New York’s Hudson Valley area.

The reason I love this park so much is that it offers some of the most beautiful landscaping in New York. As I ride through this park I enjoy stopping and looking over the cliffs at the scenery below. It offers views of the surrounding lakes. As I continue to ride through the park I eventually arrive at my favorite spot. This is the wonderful waterfall that runs through the park.

This allows me time to stop and reflect as an adult who is fighting multiple sclerosis. This is the reason I always find the time to stop by this waterfall.

Stop number two

I was born and raised in Palm Springs, Calif.; this is the reason it is stop number two on my tour. My favorite stop in the Palm Springs region is Joshua Tree National Park. This ride is one that allows me to reflect, while riding through this park. I always tend to forget about my multiple sclerosis while riding in this park. There are miles of ground to cover and for me the longer I’m able to ride on these trails the better I feel about my accomplishments in life.

Stop number three

Murrells Inlet, S.C., is my third stop on this cycling tour. In particularly I will be heading straight for Huntington Beach State Park. This is a ride that blows my mind every time I take it. Huntington Beach State Park is known for its alligators, and, boy, have I ever seen them. These are creatures that put fear into me. The only time I do not seem to fear these creatures is when I ride in this park.

Continued here:
Cycling With Multiple Sclerosis: 5 Stop Tour

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I have spent my entire life playing sports both competitively and for fun. I idolized another athlete, though, that had multiple sclerosis and was supposed to represent America in the 1988 Olympics as a cyclist. This athlete’s name is Maureen Manley. She lost her Olympic dream, which is the reason I always wanted to be like her and one day make it.

Since this is the year of the Olympics, I will look at another type of Olympic Games. The Olympic Games I will look at will focus on the Olympics that people with disabilities are able to compete in. These Olympic Games are the Paralympics. The Paralympics are played alongside the Olympic Games, which come every four years.

I have always competed at the highest level I could with the dreams of making the Olympics. This dream was stripped away in 2006 with my diagnosis of multiple sclerosis, though. I knew that I was not able to compete with healthy bodied people the way that I once was able to. This dream being taken away did not take away the drive to still be the best at the sports I participate in, though.

There are a number of sports that I will follow at the Paralympics, since I have participated in these sports at some point in my life.

Wheelchair Basketball

I played basketball in junior high and high school. I still like to play games such as horse and around the world. With my multiple sclerosis, running has been removed from my life even though I still go for walks. Since I’m not bound to a wheelchair, the game of wheelchair basketball is not something I can compete in. I will be watching the wheelchair basketball players, as I still love the game of basketball.

Paralympic Shooting

I was in the United States Navy in 2000, which where I first fell in love with shooting. The shooting range was my favorite part of boot camp. I learned that I was actually a pretty good shooter while in the Navy, but now enjoy going target practicing in the summertime when it is nice outside. I had dreams of one day participating in the Olympic Games as a marksman for the United States. This dream was stripped away after my diagnosis of multiple sclerosis, though. This is the reason that I will be following the Paralympic shooters.

Paralympic Cycling-Road

I grew up riding bikes and fell in love with the sport of cycling. I do not enjoy track cycling, though. I have multiple sclerosis and like the feeling of the open road versus track cycling as I have a fear that I will be in a crash with countless other cyclist. For this reason I stick to road cycling. I look forward to seeing the road cycling events being held at the Paralympics this year in London.

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Dreams of Olympic and Paralympic Games Stripped Away by Multiple Sclerosis

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Swimming in the summertime is one of my favorite activities. There are a lot of reasons that I enjoy going for swims in the summertime, and there are plenty of benefits to swimming for me since I have multiple sclerosis. I try and swim at least three times a week in the summertime since it allows me to choose between a swimming pool and a lake.

The benefits, for me, are both health and social benefits.

Benefit number one

Social interaction is the first reason I love to swim. I’m able to interact with people that are perfectly healthy, and people that have medical conditions like me. Since I’m not able to work any longer I choose to swim to get my source of social interaction.

I have met many new friends swimming at the local swimming pool. Without these friends my life would be more difficult since I would be closed up inside my house. I spend time going out to eat, and just talking with these friends. My new-found friends have given a sense that not all is lost in my life, even though I have multiple sclerosis.

Benefit number two

Strength training is easiest for me to accomplish through swimming. While I enjoy other strength training exercises like cycling, scuba diving, and walking, swimming is the easiest on my body. I’m able to build strength in my arms and legs through this one healthy exercise. The strength training of swimming comes from the motions in swinging my arms and kicking my legs.

Before I got back into swimming I had to use a walker to get around. Since I started strength training through swimming I have regained my strength and am now able to walk freely. I no longer require the use of a walker or a cane on a daily basis. There are times that my multiple sclerosis is so bad, though, I do use my cane to get around.

Benefit number three

It is easy to become relaxed while swimming. With my multiple sclerosis, high levels of stress are not good for me. High levels of stress can lead me to a relapse in my multiple sclerosis. This is another reason I love to swim. Swimming allows me to relax, therefore bringing down my stress level.

Read more from the original source:
Top Five Ways Swimming is Beneficial to People With Multiple Sclerosis

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Researchers have demonstrated modest progress towards the goal of making the body’s existing cell populations rebuild damaged cartilage in situ:

A small molecule dubbed kartogenin encourages stem cells to take on the characteristics of cells that make cartilage, a new study shows. And treatment with kartogenin allowed many mice with arthritis-like cartilage damage in a knee to regain the ability to use the joint without pain. … The new approach taps into mesenchymal stem cells, which naturally reside in cartilage and give rise to cells that make connective tissue. These include chondrocytes, the only cells in the body that manufacture cartilage.

…

“In the blue-sky scenario, this would be a locally delivered therapy that would target stem cells already there,” says study coauthor Kristen Johnson, a molecular biologist at the Genomics Institute of the Novartis Research Foundation in San Diego. Johnson and her colleagues screened 22,000 compounds in cartilage and found that one, kartogenin, induced stem cells to take on the characteristics of chondrocytes. The molecule turned on genes that make cartilage components called aggrecan and collagen II. Tests of mice with cartilage damage similar to osteoarthritis showed that kartogenin injections lowered levels of a protein called cartilage oligomeric matrix protein. People with osteoarthritis have an excess of the protein, which is considered a marker of disease severity. Kartogenin also enabled mice with knee injuries to regain weight-bearing capacity on the joint within 42 days.

As a long term goal for tissue engineering, controlling existing cell populations sufficiently well to rebuild lost or damaged structures in the body is preferable to strategies that involve surgery – such as, for example, building cartilage outside the body and then implanting it. Both avenues are under development at this time.

One consequence of an increased focus on controlling stem cells in the body is that researchers must find ways to reverse the stem cell decline that comes with aging. If stem cell populations are generally less effective, then therapies based on directing those cells may be of limited benefit. Given that most of the regenerative therapies we can envisage will be of greatest use to the elderly, the people who bear the most damage and bodily dysfunction, and who are generally the wealthiest portion of the population, there is a strong financial incentive to find ways to build working therapies for that market. This is why I see the regenerative medicine community blending in at the edges with the longevity science community in the years to come – many of the goals are much the same.

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

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Enlarge Michael Rossato-Bennett

Joe, a nursing home resident, broke into song during a personalized music session. His story and others are documented in the film Alive Inside.

Joe, a nursing home resident, broke into song during a personalized music session. His story and others are documented in the film Alive Inside.

Henry, an elderly Alzheimer’s patient in an American nursing home, recently became a viral star. In a short video that has been viewed millions of times online, he starts out slumped over and unresponsive but undergoes a remarkable transformation as he listens to music on a pair of headphones.

The clip is part of a documentary called Alive Inside, which follows social worker Dan Cohen as he creates personalized iPod playlists for people in elder care facilities, hoping to reconnect them with the music they love. Cohen tells NPR’s Melissa Block that the video of Henry is a great example of the link between music and memory.

“He is able to actually answer questions and speak about his youth, and this is sort of the magic of music that’s familiar for those with dementia,” Cohen says. “Even though Alzheimer’s and various forms of dementia will ravage many parts of the brain, long-term memory of music from when one was young remains very often. So if you tap that, you really get that kind of awakening response. It’s pretty exciting to see.”

Cohen says his goal is to make access to personalized music the standard of care at nursing facilities. An early concern, he says, was that headphones might isolate the patients even further. But when he first implemented the project on a large scale in 2008, putting 200 iPods in four facilities around New York, he got the opposite result: a flood of stories from the staff about increased socialization.

“People wanted to share their music with others: ‘Here, you’ve gotta listen to this,’ or ‘What was the name of that song?’ ” Cohen says. “The music is great, but to me, perhaps the even bigger win is people having better and more relationships with those around them.”

Get the playlist right. Find out the person’s tastes and create a varied mix: no more than five to seven songs per artist. Have them weed out tracks that are so-so, so you end up with 100 or 200 songs that all resonate.

Keep it simple. Make sure the elder knows how to use the player, or that someone nearby can help. Use over-ear headphones rather than earbuds, which can fall out.

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For Elders With Dementia, Musical Awakenings

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Much like the practice of calorie restriction, exercise changes everything for the better in most people – it is far more effective in improving and sustaining long term health for the majority of us than any presently available medical technology. We need the future of better medicines that will achieve what good living cannot, such as rejuvenation of the elderly, absolute prevention of age-related disease, and radical life extension, but in the meanwhile it makes sense to make the most of present and proven methodologies to better out position as much as possible. People in the middle of life today will be cutting it fine under the most optimistic estimates for the development of working rejuvenation biotechnology – every year counts when it comes to either making future technology arrive more rapidly or being able to wait for longer.

The present phase of rapid development in biotechnology is uncovering a great deal of new knowledge when it comes to the workings of exercise: how exactly, down to the level of cells and signals, it improves health and life expectancy. For example, here is a paper on exercise and the brain:

The benefits of exercise and physical fitness on mental health and cognitive performance are well documented … Animal studies have also demonstrated that exercise or physical activity produces very specific changes in the brain that are distinct from those produced by learning or novel experiences. … Recently, studies have been carried out in humans using non-invasive brain imaging techniques to investigate exercise-related changes in brain structure. Such studies provide compelling evidence for the powerful effects of exercise on the brain, but also raise several questions. For example, do structural changes occur throughout the brain or are they limited to specific brain regions? What aspects of brain architecture are specifically modified by physical activity? On what time scale do these changes occur, and how persistent are they when exercise is discontinued? Do specific preconditions such as aging, disease, or genetic phenotypes make individuals more or less susceptible to activity-based brain changes?

…

Although relatively few studies exist on the effects of aerobic activity on the brain structure of healthy, younger individuals, there is a wealth of data demonstrating the cognitive benefits of frequent aerobic exercise throughout the lifespan – perhaps none more convincing than a recent study of 1.2 million Swedish military conscripts that showed a strong correlation between fitness and intelligence. Much work remains to be done to determine what level of aerobic activity is required for cognitive and brain health to be maximized, but it seems likely this level is well above that of the average individual.

You might compare that conclusion with data on life expectancy in athletes:

• Atheletes Live Longer, Probably the Exercise
• Putting Upper Bounds on Longevity Derived From Exercise

But equally, it seems clear that even moderate regular exercise has great benefits – the 80/20 point is probably somewhere in the vicinity of the venerable recommendation of 30 minutes of some aerobic activity. Sadly, even that level of exercise is probably “well above that of the average individual” in the wealthier nations.

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

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An example of work that lays the foundations for lung tissue engineering, which has been lagging behind advances for other organs: “How do you grow stem cells into lungs? The question has puzzled scientists for years. First you need the right recipe, and it took [researchers] seven years of trial and error and painstaking science to come up with it. … Some tissues, like muscle and nerves, are relatively easy to grow, but others, including liver, lung, thyroid, and pancreas, have been much more difficult. These troublesome tissues all spring from the endoderm, the innermost layer of an early embryo. The endoderm forms when an embryo is about three weeks old and differentiates into organs as early as five weeks. Somehow, in these two weeks the endoderm transforms into differentiated organs as diverse as the lungs and the stomach. … [Researchers] decided to create a knock-in reporter gene that would glow green during the ‘fate decision’ – the moment when the stem cells expressed a gene called Nkx2-1 and thereby took a step toward becoming lungs. This allowed the team to track the cells as they developed, mapping each of the six critical decisions on the path to lung tissue. … Once [the] team had grown what appeared to be lung cells, they had to make sure they had the recipe right. They took samples of mouse lungs and rinsed them with detergent until they became cell-free lung-shaped scaffolds. They seeded one lung with 15-day-old homegrown lung cells that they had purified from stem cells. As a control, they seeded another lung with undifferentiated embryonic stem cells. Within 10 days after seeding, the lung cells organized themselves and populated the lung, creating a pattern recognizable [as] lung tissue. … A happy side effect of the discovery was that the scientists also mapped out the road from stem cell to thyroid. [The] thyroid, it turns out, also comes from the endoderm layer, deriving from a progenitor that expresses the same key gene as lung progenitors. [The] work will likely have a huge impact on lung stem cell researchers, who have been waiting for a discovery like this to propel their research on inherited lung disease.”

Link: http://www.bu.edu/today/2012/from-stem-cells-to-lung-cells/

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An interesting experiment, especially when compared with work on brain aging that focuses on levels of cell proliferation: “During the past decade, it has become increasingly clear that consistent changes in the levels of expression of a small cohort of genes accompany the aging of mammalian tissues. In many cases, these changes have been shown to generate features that are characteristic of the senescent phenotype. Previously, a small pilot study indicated that some of these changes might be reversed in rat liver, if the liver cells became malignant and were proliferating. The present study has tested the hypothesis that inducing proliferation in old rat liver can reset the levels of expression of these age-related genes to that observed in young tissue. A microarray approach was used to identify genes that exhibited the greatest changes in their expression during aging. The levels of expression of these markers were then examined in transcriptomes of both proliferating hepatomas from old animals and old rat liver lobes that had regenerated after partial hepatectomy but were again quiescent. We have found evidence that over 20% of the aging-related genes had their levels of expression reset to young levels by stimulating proliferation, even in cells that had undergone a limited number of cell cycles and then become quiescent again. Moreover, our network analysis [may] provide insights into mechanisms involved in longevity and regeneration that are distinct from cancer.”

Link: http://www.ncbi.nlm.nih.gov/pubmed/22477361

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Via ScienceDaily: “Individuals who suffer from autoimmune diseases also display a tendency to develop atherosclerosis – the condition popularly known as hardening of the arteries. Clinical researchers [have] now discovered a mechanism which helps to explain the connection between the two types of disorder. The link is provided by a specific class of immune cells called plasmacytoid dendritic cells (pDCs). … Using laboratory mice as an experimental model, the researchers were able to show that pDCs contribute to early steps in the formation of athersclerotic lesions in the blood vessels. Stimulation of pDCs causes them to secrete large amounts of interferons, proteins that strongly stimulate inflammatory processes. The protein that induces the release of interferons is produced by immune cells that accumulate specifically at sites of inflammation, and mice that are unable to produce this protein also have fewer plaques. Stimulation of pDCs in turn leads to an increase in the numbers of macrophages present in plaques. Macrophages normally act as a clean-up crew, removing cell debris and fatty deposits by ingesting and degrading them. However, they can also ‘overindulge,’ taking up more fat than they can digest. When this happens, they turn into so-called foam cells that promote rather than combat atherosclerosis. In addition, activated, mature pDCs can initiate an immune response against certain molecules found in atherosclerotic lesions, which further exacerbates the whole process. … The newly discovered involvement of pDCs in the development of atherosclerosis [reveals] why the stimulation of pDC that is characteristic of autoimmune diseases contributes to the progression of atherosclerosis. The findings also suggest new approaches to the treatment of chronic inflammation that could be useful for a whole range of diseases.”

Link: http://www.sciencedaily.com/releases/2012/04/120404102943.htm

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Progress in the tissue engineering of cell structures for use as research tools, and later as the basis for therapies: “Three-dimensional clusters of pancreatic beta-cells that live much longer and secrete more insulin than single cells grown in the laboratory are valuable new tools for studying pancreatic diseases such as diabetes and for testing novel therapies. This cutting-edge advance is described in [an open access paper] … Finding a solution for the culturing and final transplantation of pancreatic cells will be an enormous breakthrough for the treatment of diabetes … Growing pancreatic cells in the laboratory is challenging, in part because to survive and function normally they require cell-cell contact. [Researchers] developed an innovative method that uses photolithography to create microwell cell culture environments that support the formation of 3-D pancreatic beta-cell clusters and control the size of the cell aggregates. They describe the ability to remove these cell clusters from the microwells and encapsulate them in hydrogels for subsequent testing or implantation.”

Link: http://www.sciencecodex.com/new_method_yields_insulinproducing_pancreatic_cell_clusters-89204

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An open access review paper: “Several studies suggest that an increase in adult neurogenesis has beneficial effects on emotional behavior and cognitive performance including learning and memory. The observation that aging has a negative effect on the proliferation of neural stem cells has prompted several laboratories to investigate new systems to artificially increase neurogenesis in senescent animals as a means to compensate for age-related cognitive decline. … recent evidences indicate that the relative abundance of stem cells in certain organs does not necessarily correlate with their impact on organ function. Specifically, the mammalian brain is perhaps the organ with the lowest regenerative potential but the one in which the signs of aging are more manifested. Using the words of the renaissance writer Michel de Montaigne, ‘age imprints more wrinkles on the mind than it does on the face’ indicating that age-related cognitive decline has the highest impact on the quality of life. To which extent this decline is dependent on neural stem and progenitor cells (together referred to as NSCs) is hard to tell but growing evidences indicate that, despite their negligible numbers, the few resident NSCs that are located in specific brain regions, most notably the subgranular zone of the hippocampus, seem to play a major role in cognitive functions such as learning, memory, and emotional behavior by generating, through intermediate progenitors, neurons that are constantly added to the brain circuitry throughout life. … the available data strongly suggests that aging almost exclusively acts at the level of NSC proliferation. Yet, the many contradicting results and uncertainties on identifying the exact causes of this ‘decreased proliferation’ [need] to be fully acknowledged in order to give a rigorous and meaningful direction to this relatively new field. … The fact that NSCs can efficiently respond to physiological and pathological stimuli to increase neurogenesis indicates that stimulation of endogenous NSCs offers a promising alternative to transplantation approaches that until now were intensely investigated.”

Link: http://impactaging.com/papers/v4/n3/full/100446.html

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An introduction to calorie restriction at h+ Magazine: “In the early twentieth century nutrition researchers found that rats maintained on reduced caloric intake showed lower spontaneous tumors compared to rats fed ad libitum (allowed to eat as much as they chose). Although this work did not address caloric restriction (CR) and aging, it suggested that CR might slow the onset of age-associated disease in rodents. … Numerous follow-up studies demonstrated that a micronutrient adequate CR diet significantly increased the lifespan of many species, largely crossing species boundaries. … While CR increases the lifespans of most species examined, it also suppresses many of the diseases associated with human aging, thus increasing the ‘health-span.’ Over short periods, CR lowers blood pressure, heart rate, and glucose levels, and improves memory in older individuals and measures of cognitive performance in animals. Over longer periods CR significantly reduces the risk for many different types of cancer, age-related brain atrophy, heart disease (and atherosclerosis related diseases), autoimmune disease, and adult onset diabetes. CR appears to lessen the risk for, and attenuates or even reverses the symptoms of Alzheimer’s and possibly Parkinson’s diseases; two major age-related neurodegenerative diseases that cause enormous human suffering. … Interestingly, CR appears to promote the progression of Amyotrophic Lateral Sclerosis (Lou Gehrig’s disease), indicating it does not protect from all human diseases. Aging causes extensive, often organ-specific changes in gene expression patterns. Analysis [has] shown that aging, calorically restricted mice show gene expression patterns resembling those of young animals, compared to ad libitum-fed mice of the same age. CR also lowers cellular oxidative damage by reducing mitochondrial oxygen free radical production, lessens age-related telomere shortening, lowers inflammation, increases DNA damage repair efficiency and lowers damage to DNA and RNA (thus promoting genomic stability), lowers insulin levels while promoting insulin sensitivity, reduces the number of senescent (non-dividing) cells that accumulate with aging, attenuates age-related cellular protein cross-linking, and increases the removal of damaged cellular proteins – a process called ‘autophagy’ which declines with age and plays a role in resistance to infection, cancer, heart disease, and neurodegeneration. “

Link: http://hplusmagazine.com/2012/04/04/caloric-restriction-and-longevity/

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The SENS Foundation research community is steadily gathering momentum in their work on biotechnologies that, once fully realized, will be capable of rejuvenating the old – restoring youthful health, vigor, and function to the formerly declining organs and biological systems in the body. Even before then, the first applications resulting from SENS research will have a significant impact on health and age-related disease, achieved by partially reversing some of the root causes of aging. To go along with the recently released 2011 annual report, the SENS Foundation staff have also published their 2011 research report (in PDF format):

The subtitle on our logo banner reads “advancing rejuvenation biotechnologies”, and in keeping with the dynamic connotations of that statement, we’ve spent 2011 engaged in focused, concrete actions toward embodying it. … We’re excited to be a part of this revolution in scientific innovation, grateful to everyone who has supported us through their generous gifts of time and funding, and delighted to have multiple exciting developments to report on the research front.

There is a lot of material in the report, and I encourage you to read the whole thing – it’s very approachable for the layperson, and a good way to obtain a top to bottom view of the Foundation’s research strategy at present. That more or less encompasses these questions: what exactly causes aging, and what can be done here and now to make progress towards preventing it and reversing it? For example, here’s an excerpt from the GlycoSENS category, research with the potential to reverse the cause of much of the chemical and structural aging of skin, blood vessel walls, and many forms of connective tissue:

The elasticity of the artery wall, the flexibility of the lens of the eye, and the high tensile strength of the ligaments are examples of tissues that rely on maintaining their proper structure. But chemical reactions with other molecules in the extracellular space occasionally result in a chemical bond (a so-called crosslink) between two nearby proteins that were previously free-moving, impairing their ability to slide across or along each other and thereby impairing function. It is the goal of this project to identify chemicals that can react with these crosslinks and break them without reacting with anything that we don’t want to break.

…

In 2011, we established a Center of Excellence for GlycoSENS and other rejuvenation research at Cambridge University and hired postdoctoral student Rhian Grainger to design and perform experiments to develop reagents that can detect proteins bearing glucosepane crosslinks, facilitating further studies on its structure, abundance, and cleavage by small molecules. We also established a collaboration with researchers at Yale University, who will lend their expertise in generating advanced glycation end-products and lead efforts in developing agents which may be able to cleave glucosepane.

There are other projects recently started by the Foundation in other areas of the SENS program. You’ll also find progress reports for the work that has been ongoing for some years: the MitoSENS project to block the contribution of mitochondrial DNA damage to aging, and the LysoSENS biomedical remediation work that is a search for enzymes to safely remove the build up of damaging compounds that the body’s recycling mechanisms cannot cope with on their own.

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A devastated Michael J. Fox initially turned to alcohol to cope with his Parkinson’s disease diagnosis.

The Family Ties star discovered he had the degenerative disorder back in 1991 and confesses he took to the bottle to drown his sorrows.

He tells Parade magazine, “For a time I dealt with it with alcohol, which turned out to be a disaster. I’d always been kind of a partier, but this was the first time I was drinking in order not to feel something. It had a dark purpose.”

The actor eventually quit drinking for good and now Fox credits his wife of 23-years, Tracy Pollan, with helping him get sober.

He continues, “About a year after my diagnosis, I woke up one morning and saw (wife) Tracy’s face…She said, ‘Is this what you want?’ Instantly I knew – no, this isn’t what I want or who I am. So I quit drinking in ’92.

“I recognised I had choices about drinking, and that made me realise I had choices about Parkinson’s as well… Acceptance doesn’t mean resignation; it means understanding that something is what it is and that there’s got to be a way through it.”

Fox has been a longtime Parkinson’s disease advocate and in 2000 he founded The Michael J. Fox Foundation, which funds research programmes in the hopes of finding a cure.

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Fox turned to alcohol to cope with Parkinson's disease

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New research at Children’s Hospital Boston and the Immune Disease Institute (IDI) helps explain common cancer mutations caused by DNA chromosomes breaking and fusing back together at the wrong spots to connect two different genes. These chromosomal rearrangements are characteristic of many types of cancers, including leukemias and lymphomas. In work that was published in the February 16 issue of Cell, Dr. Frederick Alt at the Children’s Hospital Boston and Dr. Job Dekker at the University of Massachusetts Medical School have worked out some of the rules about how these rearrangements occur.
The study combined two distinct technologies that each lab developed over the past several years. One technique developed by Dr. Alt’s group that uses high-throughput DNA sequencing to find where chro…

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Kingsley G. Morse Jr. is one of the regulars at the Gerontology Research Group mailing list. He maintains a spreadsheet of all the life span studies in various organisms that he has been able to find, and is generally willing to sell that data at white paper rates, should you happen to be interested. He recently posted a histogram assembled from the study results, which I’m sure you’ll agree is interesting:

The history of working to extend life in laboratory animals – and of studying effects on longevity and mortality in humans – is largely a big null result. Other than calorie restriction, the effects of which were first formally cataloged by scientists in the 1930s, all of the excitement shows up in the past twenty years or so. The successes are a tiny fraction of the studies that showed nothing, or showed a result well within the margin of error, or produced results that could not be replicated. In mammals, mostly mice, the bulk of studies that do extend life significantly fall in to the 15% to 30% life extension bracket – on a par with moderate to severe calorie restriction. Only a few methods have been demonstrated to reach beyond that point.

To a large degree this is because near everything tried to date has been a form of metabolic manipulation – change the operation of metabolism to slow the effective rate at which damage accrues to the organism. I would be surprised to see any great improvement in the length of life lived by laboratory animals until the research community changes strategy to focus on actually repairing and reversing the cellular and molecular damage that causes aging. The difference between slowing aging and repairing aging will be as night and day when it comes to the practical results that can be achieved.

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

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BILL Jones, 76, a retired sheep shearer, former horse racer and trainer and vintage car enthusiast from Williamstown, has been living with Parkinsons disease for more than 10 years.

How did you find out you had Parkinsons disease?

Roughly 11 years ago, I was experiencing a lot of trouble swallowing, so I visited my GP who then referred me to an ear, nose and throat specialist.

The specialist thought I might have Parkinsons disease, so he referred me to a neurologist.

The next day I visited a neurologist, who performed a brain scan, which confirmed I had Parkinsons disease.

How does the disease effect you?

Im a bit slower with my movements, for example, my right leg tends to freeze every now and then.

My leg doesnt receive the message to step forward at times.

Without management, I also experience hand tremors.

How is the disease treated?

View post:
Local Knowledge: Living with Parkinson's disease

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Despite researchers’ best efforts, Parkinson’s disease remains incurable. While there are treatment options that mitigate some symptoms, assigning the right treatment approach can be hit or miss. To better predict the response of Parkinson’s patients to therapy, the Cleveland Clinic has joined consumer genomics company 23andMe in its Parkinson’s Community Research Project. Enrollment in the program will also allow the clinic’s patients to take advantage of 23andMe’s Personal Genome Service.

23andMe began its Parkinson’s disease collaboration in 2009 when it teamed up with the Michael J. Fox Foundation for Parkinson’s Research and the Parkinson’s Institute and Clinical Center. After roughly 18 months, the collaboration had assembled and analyzed genetic data from more than 3,400 Parkinson’s patients, found 20 previously known genetic associations, and identified two novel loci rs6812193 near SCARB2 and rs11868035 near SREBF1/RA11. Ultimately, the collaboration aims to enroll 10,000 people. To date, 23andMe has enrolled roughly 6,500 patients, and the Cleveland Clinic is planning to add another 1,000 patients.

For clinicians like Andre Machado, director of the Cleveland Clinic’s Center for Neurological Restoration, the ideal scenario is that this large-scale collaboration can produce a roadmap to advance treatments for Parkinson’s patients. “We’re hoping to get data on the progression or responsiveness to a given type of treatment, things that can help us understand maybe in the future how to select treatments that are more likely to work for some patients versus others,” Machado says.

The process starts by reaching out to patients diagnosed with Parkinson’s disease by their neurologists and inviting them to participate. “Because this study aims to find novel genetic variants associated with Parkinson’s disease by way of genome-wide association studies, it is crucial that the group of whose genes are being analyzed have a pure diagnosis of Parkinson’s disease, as opposed to parkinsonism,” says Kathryn Teng, director of the Center for Personalized Healthcare at the Cleveland Clinic. “As with all genome-wide association studies, in order to get pure results, you need to have pure data going into the study.”

One enrollment challenge, Teng says, is that participants might be older, and therefore less comfortable with computers. “The 23andMe model requires electronic enrollment and participation in surveys, so family members may need to assist with the enrollment and data collection if the patient requires assistance,” she adds.

Reaching the desired sample size is also made difficult by a lack of -familiarity with genetic research in some pockets of the target population. “Many may not be aware of the protections offered by the GINA law which protects against discrimination based on genetic information for health insurance and employment,” Teng says. To assuage any anxieties, potential recruits are told that they and their DNA samples will only be identified by a unique code. They are also told that the reports that they receive through 23andMe’s website summarizing the genes identified in their DNA will not be part of their medical record.

To make participation as easy as possible, the Cleveland Clinic has dedicated computer portals set up at locations where Parkinson’s patients are likely to visit, including its various campuses.

Ultimately, Machado says he does not know if 10,000 patients will be a large enough sample size to effectively interrogate the data to make a difference on treatment. However, he adds, the collaboration with 23andMe provides “an opportunity for doing exploration and there is a chance that it will benefit patients down the line.”

More here:
Recruits for Research

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http://www.longevitymedicine.tv/feed/

Posted: Sunday, April 1, 2012 4:00 am | Updated: 4:55 pm, Wed Mar 28, 2012.

OPTIMISM is the focus of this years annual American Parkinson Disease Association East Texas OPTIMISM Walk 2012, scheduled April 28 at the Rose Rudman Recreational Trail in Tyler.

The East Texas Parkinsons walk is an annual effort to raise money for education, research and support services for those affected by Parkinsons disease. The event is sponsored by the APDA East Texas Chapter and the ETMC Movement Disorder Center.

Individuals living with Parkinsons or those whose friends or loved ones have been diagnosed and all individuals who want to support a good cause are invited to join in by registering for or donating to our event today, said Kelly Boutin, walk chairperson and Tyler-area APDA Information and Referral Center coordinator. When everyone works together, great things can be accomplished to ease the burden and find the cure for Parkinsons disease.

The Tyler walk is open to all East Texas residents, and it starts at 11:30 a.m. on April 28 in the Robert E. Lee parking lot near the REL track. Check-in starts at 10 a.m. All activities will conclude at 2 p.m.

Approximately 3.6 million Americans have been diagnosed with Parkinsons disease. Approximately 50,000 new cases are diagnosed each year, and many more may have Parkinsons without realizing it yet.

It predominantly affects older adults, but healthcare providers also see early onset cases, which are estimated at between five and 10 percent of the total Parkinsons population.

For more information, or to support or participate in the Optimism Walk for Parkinsons, visit our chapter website at http://www.etapda.org or contact: Kelly Boutin at 903-596-3618 or kmboutin@etmc.org.

Read more from the original source:
East Texas Optimism Walk for Parkinson’s disease set for April 28

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