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Colorados fitness industry starting to reawaken, but some studios will never reopen – Loveland Reporter-Herald

Posted: June 16, 2020 at 2:51 pm


Buying Barre Forte in LoHi was the realization of a dream years in the making for Sage Fennig. She had longed to own a business that empowers people and makes them feel good about themselves, but only 15 days after she took ownership in March, her dream took a nightmare turn when Colorados fitness industry was shut down due to the coronavirus.

I live right down the street, Fennig said. Ive lived in downtown Denver for the past 16 years, so I really know the area. I know the clientele really well. If I had a dream situation, this was it. Then COVID-19 happened.

Twelve weeks after being shut down, Fennig reopened this past Monday. According to state guidelines, she can only operate at 25% of capacity, which for her studio means five students with one instructor. For Monday evenings class, five came to the studio while eight more participated online.

In the studio, it felt like a reunion.

Its kind of like family to me, member Sherry Ewing said. Im just really excited to be back and see everyone. I think its a good step to start moving forward. Its all about the community, just being together, seeing each other, having those conversations. Its just wonderful.

Ewing felt relatively safe, too.

I feel more safe coming to the studio than I do grocery shopping, she said.

Gyms, fitness studios and rec centers across Colorado are beginning to reopen in limited fashion under strict guidelines, but many are not. Gyms and rec centers managed by the cities of Denver and Lakewood remain closed until further notice, while Englewoods two rec centers will reopen next week. In Arvada, the Apex Recreation District has begun staged reopenings of its facilities.

Denver recreation centers remain closed due to the public gathering limitations, physical distancing, and cleaning and disinfecting requirements, according to Cyndi Karvaski, a public information officer for Denver Parks and Recreation.

But the Englewood Rec Center will reopen on Monday, by reservation only, for hour-long workout blocks. Each block will be followed by 15 minutes of cleaning with spray sanitizers by workers, according to Englewood senior recreation supervisor Allison Boyd, and the facility will be closed from 1 to 4 p.m. for deeper cleaning. A similar plan will be followed at Englewoods Malley Rec Center, a facility for people 55 and over.

The new state guidelines allow gyms to operate at up to 25% capacity or 50 people, whichever is fewer. Complicating matters is that some counties have received variances with different sets of rules. In Lakewood, officials are still trying to determine whether they can open any rec centers before August.

The city is working to balance the ability to operate safely under the limitations, recall employees from furloughs to open the facilities, and pay the cost of operating the facilities with limited users at a time when the citys revenues have dropped significantly, said Stacie Oulton, a public information officer for the city of Lakewood.

Planet Fitness gyms inCastle Rock, Loveland, Parker and Greeley have reopened, and all but one Denver location will open next week. Fourteen metro-area 24 Hour Fitness gyms are scheduled to reopen June 22, according to the corporate website.

Kindness Yoga will begin a phased reopening on July 1 with only one location operating at first, the South Broadway studio. Members received an email this week from Kindness conceding that we face the reality that not all nine studios will be reopening, but founder Patrick Harrington said no decisions have been made on which ones will close permanently.

Evo Rock + Fitness in Louisville will reopen on Monday, June 15..G1 Climbing + Fitness, a new facility in Broomfield that had been open for a month when gyms were closed by the state, reopened June 4 the day the new state guidelines went into effect. Earth Treks climbing gyms will reopen June 22.

Some studios will never reopen, though, and their owners are devastated.

Before the pandemic, Andora Freedom owned three Samadhi Yoga locations that she said were thriving. But after 18 years in business, she is shutting the businesses down.

It was much more than a yoga center, Freedom said. It was a spiritual center. It was peoples church, it was peoples sacred space. If your life was falling apart, you could go, you could just cry. You would be held in the energy of the space. Those people now are giving me the hope that one day Im going to get a life back, because now my life is destroyed. Ive got nothing left, and I dont know how the hell Im going to get through this.

She says she has been through a hellish experience and blames government officials state and federal for lack of support.

Its deeply upsetting to me because I find that my greatest responsibility is creating a sense of community for people, and I find that to be vital for peoples thriving, Freedom said. Knowing that I can no longer be that for people, thats pretty devastating.

Another studio that will not come back is Flex Yoga + Barre. Co-owner Sarah Mellick said the financial numbers just really werent there to operate within the severely limited capacity restrictions mandated by the state.

It was not an easy decision, Mellick said. So much has been put into the space and the community, and theres a lot of emotion behind it. Its hard to go out on terms that werent necessarily yours. When we closed doors on March 16, never in a million years did I imagine that it would be for good. We all thought it was just going to be a few weeks and we would be back up and running.

Freedom said she would be surprised if any yoga studios make it through this transition, and long-term financial viability is still a worry for Fennig despite the excitement of reopening her Barre Forte location on Monday. She has spent $1,000 to enhance her online streaming equipment in hopes of generating more revenue.

Were not going to cut it moving forward if we have to maintain at 25% and are not able to make up some lost revenue through live streaming and on demand-services or outdoor classes, Fennig said. I dont know if were ever going to truly make it, and if I am going to be able to fully see out my dream, no matter how hard I work.

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Colorados fitness industry starting to reawaken, but some studios will never reopen - Loveland Reporter-Herald

In sickness and in health: North Spokane couple weds in front yard during pandemic – The Spokesman-Review

Posted: May 18, 2020 at 2:54 pm


Nothing was going to stop Tony and Nikki Barbee from getting married on Sunday not a worldwide pandemic and certainly not a little bit of rain.

The couple tied the knot Sunday afternoon in their front yard as friends and family watched from the sidewalk.

The couple met about 5 years ago when Tony started working at Costco in Kirkland and Nikki helped train him.

I started working there and she taught me how to do the book table at Costco, Tony said with a chuckle.

The pair had great banter and often quoted Monty Python and the Holy Grail to each other.

Nikki made the first move by buying a copy of the movie for Tony.

They quickly began falling for each other. In fact, their first dance was to the classic Tom Petty tune, Free Fallin.

Tony has three kids, Aadin, 15, Evelynne, 10 and Tony Jr., 9. Nikki has a 12-year-old son, Brayden Webster.

Nikki has swooped in and loved Tonys kids like theyre hers, and Tony does the same, said Dallas Hoy, a bridesmaid and sister-in-law, Dallas Hoy. Its just really sweet to watch.

Nikki said she knew Tony was the one their first Mothers Day as a couple. Despite their constant banter, Tony found a moment to be sincere.

The pair were joking around and Tony said, Yeah, its cause I love you, Nikki recounted.

It just made my heart melt obviously and I was like, this guy is a keeper, Nikki said.

Nikkis mother agreed.

Hes just always been really attentive, even with her son, said Nadine Webster. They feed on each others craziness. Its just fun.

A few years later, Tony couldnt stand being away from Spokane anymore and decided he needed to move back.

She stood by me through everything, ups, downs, moving, Tony said.

Last year, Tony planned a vacation to Mexico to propose.

I planned the whole trip just to ask her to marry me, Tony said.

Nikki had noticed Tony mentioning marriage a bit more in the months before the vacation and had an inkling a proposal was coming, but wasnt quite sure when.

But when Tony got down on one knee on the beach, Nikki was overjoyed.

The couple came back to Spokane and started planning their wedding.

We had everything already paid for and paid off, Tony said. We were going to have Veraci Pizza cater and we had a spot on the South Hill.

They planned on having about 160 people attend, but at the beginning of April it was obvious they would have to cancel the gathering. The couple decided the nuptials just couldnt be postponed.

Nothing was going to stop her from being my wife today, Tony said. Thats what we had planned and I wasnt going to wait any longer than that.

So, they decided on a front yard wedding at their North Spokane home.

Nikki wore a strapless white dress with red pumps and a red ribbon at the end of her braided hair. The dress was a steal for $50 at Goodwill.

I hope the rain goes away, Nikki said while she was getting dressed. I dont want to get my dress wet.

It rained all afternoon, but moments before the ceremony began at 5 p.m. the clouds cleared.

Tony stood nervously waiting under a canopy.

Honestly, I couldt wait, Nikki said. Just looking and seeing his face was probably the best moment of it right there.

Tony described the moment as just happy, just all happy.

The ceremony was short, but sentimental, with a few jokes and lots of laughs.

Moments after Kenny Carlson, the pastor, pronounced them husband and wife, the couples 3-year-old nephew Presley screamed, They did it! eliciting cheers from the family.

Its better than we could have ever thought, Tony said.

That statement sums up not only the wedding day but the couples relationship, according to Tonys brother Matt.

From the first time Tony ever mentioned her he has never talked about any girl like that, Matt said.The first time I ever met her, I finally felt like I had a sister.

Matts wife, Hoy, agreed.

When I first met Nikki it just made sense, Hoy said. She and him, theyre both complete absolute weirdos, which is why theyre perfect together.

Tonys parents, Kim and Jeri Barbee, couldnt agree more.

We call her the Energizer bunny, Kim said.

Shes just a light, a positive light, Jeri added.

Despite all that energy and positivity, it has been a tough season for the couple, who were set to open their business, Vintage Slice Pizza Co., before the pandemic put things on hold.

The couple both worked for the food truck when they lived in Western Washington, and told the former owner if he ever wanted to sell the 1953 blue GMC pickup with a wood fire pizza oven in the back, that they would buy it.

We fell in love with making pizzas, and each other, Tony said.

Now, the pair has to wait until Washington reopens to get the rest of their permits.

Even with the setbacks and change of plans, the couple is excited for married life.

Weve lived together for four years and are raising our kids together, and I mean its just another day but were married now, Nikki said.

The couple danced to Tom Petty in the middle of the street as friends and family tearfully looked on.

Some even drove across the state to be there.

The fact that they were here made me realize how special and loved both of us are, Nikki said.

While their wedding wasnt quite what they expected, it was not only a celebration of love but indicative of the positive and resilient people the Barbees are.

This wedding is such a good representation of them as a couple, Hoy said. The two of them together will take any poor, negative situation and make the best out of it.

Originally posted here:
In sickness and in health: North Spokane couple weds in front yard during pandemic - The Spokesman-Review

Furry Friends Provide Big Benefits

Posted: June 20, 2018 at 4:48 pm



Photo credit: Pixabay

The first feelings of puppy love are probably distant memories for many older adults, but that doesn’t mean they can’t experience those same sentiments -- although the expression may be more literal than figurative this time around if their object of affection actually happens to be a furry friend.

And, if they consider animals an important part of their lives, they are far from alone. Indeed, 84.6 American households, or 68 percent, included a pet according to the 2017-2018 American Pet Products Association National Pet Owners Survey, up from 56 percent in 1998 in the poll’s first year.

Given the mental and physical perks pets offer, it’s no surprise those numbers are on the rise. Owning a pet can help your heart health, and not just because some pet owners are more physically active. In fact, simply sitting quietly and stroking a pet lowers people’s blood pressure and pulse rate. Along those same lines, interacting with animals can also reduce stress and anxiety levels.

Walking the Dog

And the benefits increase when your factor movement into the mix. A small study that focused on adults age 65 and older found dog owners walked about 23 minutes longer each day than non-dog owners and took an additional 2,760 steps. Dog owners also had eight fewer continuous periods of sitting down, according to the research cited in a story from Health magazine.

And other research shows the extra activity can translate directly into better health. According to a study cited by U.S. News & World Report, seniors who owned dogs and took them on regular walks were found to have lower body mass indexes, fewer visits to the doctor, and spent less time sedentary than those who did not have a dog or those who had dogs, but did not walk them.

But owning a dog doesn’t always equate to higher activity levels. If you are considering a canine companion, it’s important to find one that’s well-suited to your habits and abilities. For instance, if you really want an exercise partner, you should find a dog who enjoys walks and isn’t too large for you to manage safely.

Part-Time Pet Care

Also, keep in mind that you don’t have to be a dog owner to find a furry workout buddy. For instance, you can sign up as a service provider for a pet sitting and dog walking service. Joining such a network will not only encourage you to get some exercise outdoors, it will give you your dose of dog cuddles without the responsibilities and costs that can come with full-time pet ownership, which can be especially appealing if you like to travel or live in a space that doesn’t allow dogs. Pet sitting and dog walking can also be a great way to expand your social circle to include other animal lovers in your area.

In addition, animals themselves can play an important role in social support systems. In fact, studies have shown pet owners tend to have higher self-esteem and more extroverted than non-owners. And you don’t have to share a home with a pet to reap some of the same benefits. Animals are increasingly being used in a variety of settings, including hospitals and schools to help humans heal faster, adopt healthy habits, or overcome anxieties.

While you may not need formal animal therapy, working as a dog walker and pet sitter may provide many of the same benefits. You’ll be forced to become more of an entrepreneurial extrovert because you’ll be introduced to new people and challenges -- such as setting your own rates and schedule. And you’ll be getting more exercise all while earning extra money and enjoying the physical and mental benefits that come with animal interaction.

So, whether you own and care for your own pet or spend time doting over other people’s dogs, you can be sure your labor of love won’t go unrewarded.

CT Nutrition Consultants – Registered Dietitian

Posted: July 12, 2017 at 7:45 pm


CT Nutrition Consultants are a group of registered dietitians dedicated to helping you improve your health and prevent or reverse disease through nutrition. Our goal is to educate and empower people to move toward better food choices. Our services are geared towards YOU! Our counseling is specific to meet your individual needs.

CT Nutrition Consultants is owned and operated by Mary Ellen Campbell, M.S., R.D., CD-N who has been a registered dietitian for twenty years plus. She has spent many years as a clinical dietitian in hospitals and has counseled patients with coronary artery disease, diabetes, high blood pressure, obesity celiac disease, irritable bowel and bariatric surgery.

Nutrition Services

You realize the importance of making informed food choices and developing sound eating and fitness habits. Registered dietitian nutritionists . . . are the food and nutrition experts. We are here to help you find accurate information to support your healthy lifestyle.

What is a Registered Dietitian?

Registered dietitians, or RDs, are the food and nutrition experts, translating the science of nutrition into practical solutions for healthy living. When you need food and nutrition information based on fact or need to know how a healthy diet improves health and fights disease a registered dietitian can provide you with sound, easy-to-follow nutrition advice. In addition to holding a bachelor's degree, a RD must fulfill a specially designed, accredited nutrition curriculum, pass a rigorous registration exam; and complete 1200 hours of supervised practice through an accredited program.

Registered dietitians play a vital role in the management of your health. As nutrition experts, dietitians must remain abreast of the current literature to provide accurate, medically appropriate information.

Original post:
CT Nutrition Consultants - Registered Dietitian

Channel Update – Fitness & Football Videos Only! – Video

Posted: August 10, 2014 at 9:44 pm



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Measuring the Impact of Cytomegalovirus in Younger People

Posted: September 1, 2013 at 2:49 am


Cytomegalovirus (CMV) is one of the less immediately harmful members of the family of herpesviruses. It is very prevalent: most people have it in their system by the time they are old, but probably never even noticed, as the symptoms for a healthy individual are essentially nonexistent. Nonetheless like all herpesviruses CMV is very successful at remaining within the body after initial exposure, establishing a life-long infection despite the best efforts of the immune system to get rid of it. The recurring campaigns waged against CMV by your immune cells appear to have a long-term cost: we have evolved to support a given number of immune cells as adults, and as ever more of those immune cells become specialized to a specific pathogen, such as CMV, there is ever less space left in the inventory for cells that can tackle new threats or keep up with all the other jobs of the immune system, such as destroying precancerous and senescent cells.

If you eye the publications of an open access journal like Immunity and Ageing, you'll see a steady flow of papers looking at the role of CMV in age-related immune system decline, a fair-sized component of the frailty of old age. There are a range of possible approaches to this problem, but the most direct and potentially effective don't actually involve doing anything about CMV itself. Instead there are proposals to either add large numbers of new, fresh, and capable immune cells to the body or eliminate the CMV-specialized cells to free up space. Both of these approaches are quite near-term: only a a couple of years would be needed to develop a viable prototype therapy from where we are now, were a research group fully funded and tasked with the effort. Both the ability to culture immune cells and the ability to destroy specific cells in the body based on their surface markers are progressing rapidly.

Some research groups are working on a vaccine for CMV - but a successful vaccine won't do much good for those high percentage of adults in much of the world who have been infected for a long time. Their immune systems are already badly misconfigured as a result of the extended exposure. So tackling CMV isn't a good enough approach on its own, as it only stops the very slow pace of ongoing harm.

Here is a paper to suggest that the progressive disarray in the immune system caused by CMV starts early, even while young.

Rudimentary signs of immunosenescence in Cytomegalovirus-seropositive healthy young adults

Ageing is associated with a decline in immune competence termed immunosenescence. In the elderly, this process results in an accumulation of differentiated 'effector' phenotype memory T cells, predominantly driven by Cytomegalovirus (CMV) infection.

Here, we asked whether CMV also drives immunity towards a senescent profile in healthy young adults. One hundred and fifty-eight individuals (age 21?±?3 years, body mass index 22.7?±?2.7) were assessed for CMV serostatus, the numbers/proportions of CD4+ and CD8+ late differentiated/effector memory cells, plasma interleukin-6 (IL-6) and antibody responses to an in vivo antigen challenge (half-dose influenza vaccine). Thirty percent (48/158) of participants were CMV+.

A higher lymphocyte and CD8+ count and a lower CD4/CD8 ratio were observed in CMV+ people. Eight percent (4/58) of CMV+ individuals exhibited a CD4/CD8 ratio of less than 1.0, whereas no CMV- donor showed an inverted ratio. The numbers of late differentiated/effector memory cells were?~fourfold higher in CMV+ people. Plasma IL-6 was higher in CMV+ donors and showed a positive association with the numbers of CD8+CD28- cells. Finally, there was a significant negative correlation between [vaccine response and the levels of CMV particles present]. This reduced vaccination response was associated with greater numbers of total late differentiated/effector memory cells.

This study observed marked changes in the immune profile of young adults infected with CMV, suggesting that this virus may underlie rudimentary aspects of immunosenescence even in a chronologically young population.

Source:
https://www.fightaging.org/archives/2013/08/measuring-the-impact-of-cytomegalovirus-in-younger-people.php

Decreased mTOR Expression Provides 20% Mean Life Span Extension in Mice

Posted: at 2:49 am


Mammalian (or mechanistic, depending on who you ask) target of rapamycin (mTOR) is the most likely candidate for the next round of billion-dollar research funding devoted to the search for drugs that can slow aging. It will be a repeat of the overhyped and ultimately largely futile interest in sirtuin research, which generated knowledge but nothing of real practical application, except that this time there is far more compelling evidence that manipulation of mTOR actually extends life in laboratory animals. Though as always, there are those who believe that this is not in fact the case - that mTOR alteration only reduces cancer risk, rather than impacting the processes of aging per se. Just as resveratrol and resveratrol-derivatives are the compounds of choice for those investigating sirtuin biology, so rapamycin and rapamycin-derivatives are the compounds of choice for research groups focused on manipulating mTOR and its related signaling networks. I would imagine that we're in for another decade or so of overhyped claims and public and research community interest in what is in fact an inefficient, expensive, and time-consuming path towards only slightly extending healthy life.

Drugs to slow aging through alterations to metabolism are not the path to radical life extension. Slowing aging does nothing for people already old. The research community should focus instead on rejuvenation through therapies that repair and remove the cellular damage that causes aging, an approach that can actually meaningfully help the aged when realized. For all that rejuvenation is the obviously superior research strategy, however, it's taking time to convince the world of that truth. Time spent on trying to slow aging is little different in outcome to time spent investigating the details of aging but choosing to do nothing about it: a few years here and there, and nothing that is as effective as simple exercise and calorie restriction. There's no such thing as useless knowledge in the long term, but we already know enough to work effectively on human rejuvenation.

The new study quoted below will no doubt bolster the prospects of those groups presently raising funds for attempts to slow aging or further develop drug candidates derived from rapamycin. While looking at the results, however, you might compare them with plain old calorie restriction in mice, something that can produce twice the extension of healthy life shown here.

Mutant Mice Live Longer

MTOR is a kinase involved in myriad cellular processes, from autophagy to protein synthesis. Genetic studies of TOR in other organisms, such as yeast and flies, have implicated a role for the enzyme in lifespan. In mammals, however, mTOR is required for survival, making a knockout mouse model unfeasible. So the National Heart, Lung and Blood Institute's Toren Finkel and his colleagues decided to use a mouse in which transcription was only partially disrupted, reducing the levels of mTOR to about 25 percent of the normal amount.

All else being equal, the researchers found that normal mice typically lived 26 months, while those with less mTOR survived around 30 months. Finkel said the increase in lifespan was greater than other researchers have seen using the immunosuppressant rapamycin to inhibit mTOR. It's possible that having mTOR reduced beginning in the womb, rather than at middle age, could explain the disparity. Additionally, this new mutant affected the levels of both forms of mTOR - mTORC1 and mTORC2 complexes - rather than preferentially impacting one, as rapamycin would.

The paper on this research is open access, so head on over and take a look. I think you'll find it interesting. In particular note the author's cautions regarding the size of the life extension effect and the life span of the control mice in the discussion section: the number of mice used isn't large, and it's possible that the controls were just randomly a slightly short-lived group.

Increased Mammalian Lifespan and a Segmental and Tissue-Specific Slowing of Aging after Genetic Reduction of mTOR Expression

We analyzed aging parameters using a mechanistic target of rapamycin (mTOR) hypomorphic mouse model. Mice with two hypomorphic (mTOR?/?) alleles are viable but express mTOR at approximately 25% of wild-type levels. These animals demonstrate reduced mTORC1 and mTORC2 activity and exhibit an approximately 20% increase in median survival. While mTOR?/? mice are smaller than wild-type mice, these animals do not demonstrate any alterations in normalized food intake, glucose homeostasis, or metabolic rate. Consistent with their increased lifespan, mTOR?/? mice exhibited a reduction in a number of aging tissue biomarkers. Functional assessment suggested that, as mTOR?/? mice age, they exhibit a marked functional preservation in many, but not all, organ systems. Thus, in a mammalian model, while reducing mTOR expression markedly increases overall lifespan, it affects the age-dependent decline in tissue and organ function in a segmental fashion.

Source:
https://www.fightaging.org/archives/2013/08/decreased-mtor-expression-provides-20-mean-life-span-extension-in-mice.php

A Collagen Patch to Spur Heart Tissue Repair

Posted: at 2:49 am


Building patches for damaged hearts is a popular implementation in tissue engineering at the moment: it's an achievable stepping stone on the way to more complex goals, such as the creation of entire organs starting from only a patient's stem cells, something that still lies in the future. Progress towards a long-term goal in any field requires useful intermediary products, as they help pull in the greater support and funding needed for the next phase of research and development.

When heart cells die from lack of blood flow during a heart attack, replacing those dead cells is vital to the heart muscle's recovery. But muscle tissue in the adult human heart has a limited capacity to heal, which has spurred researchers to try to give the healing process a boost. Various methods of transplanting healthy cells into a damaged heart have been tried, but have yet to yield consistent success in promoting healing.

Now, [researchers] have developed a patch composed of structurally modified collagen that can be grafted onto damaged heart tissue. Their studies in mice have demonstrated that the patch not only speeds generation of new cells and blood vessels in the damaged area, it also limits the degree of tissue damage resulting from the original trauma. The key [is] that the patch doesn't seek to replace the dead heart-muscle cells. Instead, it replaces the epicardium, the outer layer of heart tissue, which is not muscle tissue, but which protects and supports the heart muscle, or myocardium.

The epicardium - or its artificial replacement - has to allow the cell migration and proliferation needed to rebuild damaged tissue, as well as be sufficiently permeable to allow nutrients and cellular waste to pass through the network of blood vessels that weaves through it. The mesh-like structure of collagen fibers in the patch has those attributes, serving to support and guide new growth. Because the patch is made of acellular collagen, meaning it contains no cells, recipient animals do not need to be immunosuppressed to avoid rejection. With time, the collagen gets absorbed into the organ.

Link: http://www.eurekalert.org/pub_releases/2013-08/sumc-scp082613.php

Source:
https://www.fightaging.org/archives/2013/08/a-collagen-patch-to-spur-heart-tissue-repair.php

Statin Use Correlates With Higher Telomerase Activity

Posted: at 2:49 am


There has been interest in extending increasing telomerase expression as a means to slow aging for some years. The available tools other than gene therapy are sparse on the ground, however. Telomerase extends telomere length, the caps of repeating DNA sequences at the ends of chromosomes that shorten with each cell division. Telomerase may have other roles that more directly impact aging, however, such as an influence on mitochondrial function.

Shorter telomeres in at least some tissues correlate with stress and ill health and aging, but this is a very dynamic system - average telomere length can change in either direction on a short time scale. It is far from clear that progressively shorter telomere length is a cause of aging rather than just a reflection of other changes and damage, and the same goes for natural variations in levels of telomerase in the body. While increasing expression of telomerase is shown to extend life in mice, that may or may not have anything to do with telomere length, and mouse telomerase biology is quite different from that of humans.

So all this said, it was only a matter of time before researchers evaluated all the existing approved drugs for treatment of age-related conditions to see if any of them altered telomerase activity. There are regulatory incentives to beware of here, however, in that it is much cheaper for research institutions to try to find marginal new uses of already approved drugs than to work on new and radically better medical technologies that would then have to go through the exceedingly and unnecessarily expensive approval process. So don't expect anything of great practical use to result from this:

Not only do statins extend lives by lowering cholesterol levels and reducing the risks of cardiovascular disease, but new research [suggests] that they may extend lifespans as well. Specifically, statins may reduce the rate at which telomeres shorten, a key factor in the natural aging process. This opens the door for using statins, or derivatives of statins, as an anti-aging therapy. "By telomerase activation, statins may represent a new molecular switch able to slow down senescent cells in our tissues and be able to lead healthy lifespan extension."

To make this discovery, Paolisso and colleagues worked with two groups of subjects. The first group was under chronic statin therapy, and the second group (control), did not use statins. When researchers measured telomerase activity in both groups, those undergoing statin treatment had higher telomerase activity in their white blood cells, which was associated with lower telomeres shortening along with aging as compared to the control group. This strongly highlights the role of telomerase activation in preventing the excessive accumulation of short telomeres.

"The great thing about statins is that they reduce risks for cardiovascular disease significantly and are generally safe for most people. The bad thing is that statins do have side effects, like muscle injury. But if it is confirmed that statins might actually slow aging itself - and not just the symptoms of aging - then statins are much more powerful drugs than we ever thought."

Link: http://www.eurekalert.org/pub_releases/2013-08/foas-sms082913.php

Source:
https://www.fightaging.org/archives/2013/08/statin-use-correlates-with-higher-telomerase-activity.php

Children of Long-Lived Parents Have Better Immune Systems

Posted: at 2:49 am


The immune system declines greatly with aging, and poor immune response is an important component of age-related frailty: old people become vulnerable to infections that the young can shrug off with ease. So we might expect to see that long-lived people have better immune systems, and that whatever underlying mechanisms cause that difference are to some degree inherited.

People may reach the upper limits of the human life span at least partly because they have maintained more appropriate immune function, avoiding changes to immunity termed "immunosenescence." Exceptionally long-lived people may be enriched for genes that contribute to their longevity, some of which may bear on immune function. Centenarian offspring would be expected to inherit some of these, which might be reflected in their resistance to immunosenescence, and contribute to their potential longevity. We have tested this hypothesis by comparing centenarian offspring with age-matched controls. We report differences in the numbers and proportions of both CD4+ and CD8+ early- and late-differentiated T cells, as well as potentially senescent CD8+ T cells, suggesting that the adaptive T-cell arm of the immune system is more "youthful" in centenarian offspring than controls. This might reflect a superior ability to mount effective responses against newly encountered antigens and thus contribute to better protection against infection and to greater longevity.

The goal of future medicine is to make inherited differences of this nature irrelevant. There are a number of promising approaches that may remove much of the age-related decline of immune function: regrow the atrophied thymus, where immune cells are cultured; create new immune cells in the clinic and infuse them regularly into older people; destroy the population of over-specialized memory cells that exist in the elderly, thus freeing up space for effective immune cells that can combat new threats.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23974207

Source:
https://www.fightaging.org/archives/2013/08/children-of-long-lived-parents-have-better-immune-systems.php

A Two-Part Report on Global Futures 2045

Posted: August 25, 2013 at 2:53 am


The 2045 Initiative is a fairly young but comparatively well-backed effort to generate more support for and technological progress towards non-biological means of human life extension: artificial bodies, and ultimately artificial brains, built to be far more resilient and maintainable than our present evolved equipment. There is some debate over whether this is an efficient course in comparison to medical research, but that end of the futurist community already primarily interested in strong artificial intelligence seem to like where this is going.

There is a lot of fascinating groundwork in reverse-engineering the human brain presently under way, and it's clear that neuroscience is going to become an interesting place to be over the next few decades. However, I remain unconvinced that any of this is going to help us get over the initial hurdles to extending human longevity, meaning the frailty and short life span of the human body and physical structures that support the mind, soon enough to matter. Artificial intelligence and human minds running on machinery will certainly come to pass, and I will be surprised if the latter fails to happen in the laboratory prior to 2050 given the pace at which available processing power is growing. However, and this is important, over that time scale most of us doing the writing and the reading here and now are dead without some means of medical treatment for aging. This is one of the reasons why I pay less attention to neuroscience and mind-machine interface development than I do to repair biotechnologies for the causes of aging.

The Global Futures 2045 conference series is a part of the 2045 Initiative advocacy, and the most recent event took place a couple of months ago. I noted some of the media reports at the time. A two part report published earlier this month is quoted below and focuses more on the presentations than did past articles in the popular press, which I think is a good thing.

The world according to Itskov: Futurists convene at GF2045 (Part 1)

The development of brain-computer interfaces (BCIs) to allow paralyzed individuals to control various external prosthetic devices, such as a remote robotic arm, was another key topic at GF2045. A very recent example of the BCI research Carmena and Maharbiz discussed is Neural Dust: An Ultrasonic, Low Power Solution for Chronic Brain-Machine Interfaces. The theoretical pre-print paper proposes neural dust - thousands of ultra-miniaturized, free-floating, independent sensor nodes that detect and report local extracellular electrophysiological data - with neural dust power and communication links established through a subcranial interrogator. With the purpose being to enable "massive scaling in the number of neural recordings from the brain while providing a path towards truly chronic BMI," the researchers' goal is "an implantable neural interface system that remains viable for a lifetime."

In Making Minds Morally: the Research Ethics of Brain Emulation, Dr. Anders Sandberg - a Computational Neuroscientist, and James Martin Research Fellow at the Future of Humanity Institute at Oxford University, and Research Associate at the Oxford Neuroethics Center - addressed the social and ethical impact of cognitive enhancement and whole brain emulation. "We want to get to the future," Sandberg said in his talk, "but that implies that the future had better be a good place. Otherwise, there wouldn't be a point in getting there - but that would mean in turn that the methods we're going to use to get to the future had better be good as well."

The world according to Itskov: Futurists convene at GF2045 (Part 2)

Dr. Theodore Berger gave the most groundbreaking presentation of the Congress - one that also received a standing ovation. In Engineering Memories: A Cognitive Neural Prosthesis for Restoring and Enhancing Memory Function, Berger discussed his extraordinary research in the development of biomimetic models of hippocampus to serve as neural prostheses for restoring and enhancing memory and other cognitive functions. Berger and his colleagues have successfully replaced the hippocampus - a component of the cortex found in humans and other vertebrates that transforms short-term memory into long-term memory - with a biomimetic VLSI (Very Large-Scale Integrated circuit) device programmed with the mathematical transformations performed by the biological hippocampus.

Dr. Randal Koene, neuroscientist, neuroengineer and science director of the 2045 Initiative, has been focusing on the functional reconstruction of neural tissue since 1994. In his Whole Brain Emulation: Reverse Engineering A Mind presentation and soon-to-be published book with the same title, Koene describes the process of progressing from our current condition to a possible substrate-independent mind achieved by whole brain emulation and cites a wide range of research, including the work of fellow GF2045 presenters.

Source:
https://www.fightaging.org/archives/2013/08/a-two-part-report-on-global-futures-2045.php

The Next Few Years of Research Into Alzheimer’s Disease

Posted: at 2:53 am


A conservative view of what lies ahead for Alzheimer's disease (AD) research sees incremental progress resulting from new and better investigative biotechnologies:

In the recently published work "The Biology of Alzheimer Disease" (2012), most of what is known about AD today is described in detail. The book culminates in a chapter called Alzheimer Disease in 2020, where the editors extol "the remarkable advances in unraveling the biological underpinnings of Alzheimer disease...during the last 25 years," and yet also recognize that "we have made only the smallest of dents in the development of truly disease modifying treatments." So what can we reasonably expect over the course of the next 7 years or so? Will we bang our heads against the wall of discovery, or will there be enormous breakthroughs in identification and treatment of AD?

Though a definitive diagnosis of AD is only possible upon postmortem histopathological examination of the brain, a thorough review of the book leads me to believe that the greatest progress currently being made is in developing assays to diagnose AD at earlier stages. It is now known that neuropathological changes associated with AD may begin decades before symptoms manifest. This, coupled with the uncertainty inherent in a clinical diagnosis of AD, has driven a search for diagnostic markers. Two particular approaches have shown the most promise: brain imaging and the identification of fluid biomarkers of AD.

The authors anticipate that advances in whole-genome and exome sequencing will lead to a better understanding of all of the genes that contribute to overall genetic risk of AD. Additionally, improved ability to sense and detect the proteins that aggregate in AD and to distinguish these different assembly forms and to correlate the various conformations with cellular, synaptic, and brain network dysfunction should be forthcoming in the next few years. Lastly, we will continue to improve our understanding of the cell biology of neurodegeneration as well as cell-cell interactions and inflammation, providing new insights into what is important and what is not in AD pathogenesis and how it differs across individuals, which will lead, in turn, to improved clinical trials and treatment strategies.

Link: http://www.alcor.org/magazine/2013/08/21/alzheimer-disease-in-2020/

Source:
https://www.fightaging.org/archives/2013/08/the-next-few-years-of-research-into-alzheimers-disease.php

A Look Back at Some of the Roots of Modern Thought on Radical Life Extension

Posted: at 2:53 am


The modern movements of transhumanism and support for longevity science have deep roots: you can find early expressions of the ideas of human enhancement and overcoming natural limits on our biology in a range of writings from past centuries. These ideas became more commonplace and more complex over time as the prospects for technology caught up with our desires:

Immanuel Kant (1724-1804) was an 18th century philosopher, one of the earliest philosophers belonging to the enlightenment tradition, and often considered the father of German Idealism. Kant is remembered today more for his moral philosophy than his contributions to metaphysics and epistemology (Rohlf 2010). His contributions to the field of life-extension, however, remain almost completely unexplored, despite the fact that certain claims made in his Theory of Ethics arguably qualify him as a historical antecedent of the contemporary social movement and academic discipline of life-extension.

Marquis du Condorcet (1743-1794), another historical antecedent the modern longevity movement, appears to have originated the "idea of progress" in the context of the enlightenment, which became an ideological cornerstone of the enlightenment tradition. In Sketch for a Historical Picture of the Progress of the Human Mind, Condorcet not only conceives of the idea of progress in perhaps the first form it would take within the enlightenment tradition, but also explicates its link to indefinite life-extension, which was not an existing movement or academic discipline at the time of his writing:

"Would it be absurd now to suppose that the improvement of the human race should be regarded as capable of unlimited progress? That a time will come when death would result only from extraordinary accidents or the more and more gradual wearing out of vitality, and that, finally, the duration of the average interval between birth and wearing out has itself no specific limit whatsoever? No doubt man will not become immortal, but cannot the span constantly increase between the moment he begins to live and the time when naturally, without illness or accident, he finds life a burden?"

It is this very notion of infinite progress towards endlessly-perfectible states, carried forward after Condorcet by Kant and other members of the enlightenment tradition, that also underlies Kant's own ties to the contemporary field of life-extension. Kant's claim, made in his Theory of Ethics, that to retain morality we must have comprehensively unending lives - that is, we must never, ever die - I will argue qualifies him as a historical antecedent of the contemporary life-extension movement.

Link: http://hplusmagazine.com/2013/08/21/immanuel-kant-morality-necessitates-immortality/

Source:
https://www.fightaging.org/archives/2013/08/a-look-back-at-some-of-the-roots-of-modern-thought-on-radical-life-extension.php

Damaging the Biology of Mice to Make them Age More Rapidly Often Tells Us Little of Use

Posted: at 2:53 am


Aging is damage: it is the accumulation of broken and obstructed protein machinery and nanoscale structures inside and around our cells. Living beings come with many varied repair systems, so the processes by which damage grows and eventually overwhelms those repair systems is far from straightforward. In that sense aging isn't like the wearing of stone by the weather, or the failure of a non-repairing mechanical system like a car - but it's still all about damage. At the highest level the same mathematical models of damage and component loss that work just fine as aids to understanding failure in complex non-repairing systems like electronics also work just fine for aging.

Every so often a research group feels the need to publicize work in which they damage mice or other laboratory species in ways that cause them to live shorter lives. There are many very subtle ways to alter genes, such as those involved in DNA repair, that produce what is arguably accelerated aging. (Though not everyone thinks that these forms of life span reduction are in fact accelerated aging, but that's a debate for another time and place). The point here is that I think you have to beware of taking it at face value that these research results are relevant to normal aging, or relevant to extending healthy life. You can damage mice with a hammer if you so choose, and it will certainly shorten their life spans, but examining the results won't tell you anything about aging. Similarly, it's the case that near all of the possible ways of interfering in mouse biology via genes and metabolic operation in order to reduce life span are just as irrelevant.

Here is an example of this sort of thing: researchers are producing mice with additional damage in their mitochondria, a component of cellular biology known to be important in all sorts of metabolic processes, and considered to be important in aging, and showing that these mice don't live as long. I don't think that the authors can show that they've proved much of relevance to aging with this study as constructed, however, for the reasons noted above.

Mutations of mitochondrial DNA can hasten offspring's ageing process

In ageing research, mitochondria have been scrutinized by researchers for a long time already. The mitochondria in a cell contain thousand of copies of a circular DNA genome. These encode, for instance, proteins that are important for the enzymes of the respiratory chain. Whereas the DNA within the nucleus comes from both parents, the mitochondrial DNA (mtDNA) only includes maternal genes, as mitochondria are transmitted to offspring via the oocyte and not via sperm cells. As the numerous DNA molecules within a cell's mitochondria mutate independently from each other, normal and damaged mtDNA molecules are passed to the next generation.

To examine which effects mtDNA damage exerts on offspring, researchers used a mouse model. Mice that inherited mutations of mtDNA from their mother not only died quicker compared to those without inherited defects, but also showed premature ageing effects like reduced body mass or a decrease in male's fertility. Moreover, these rodents were prone to heart muscle disease.

As the researchers discovered, mutations of mtDNA not only can accelerate ageing but also impair development: In mice that, in addition to their inherited defects, accumulated mutations of mtDNA during their lifetime, researchers found disturbances of brain development. They conclude that defects of mtDNA that are inherited and those that are acquired later in life add up and finally reach a critical number.

To show relevance, you really need to demonstrate life extension - meaning repair mechanisms for mitochondrial DNA rather than damage mechanisms should be the focus. To shorten life spans through various forms of damage is unlikely to provide anything more than hints and inference when it comes to ways to extend life.

Source:
https://www.fightaging.org/archives/2013/08/damaging-the-biology-of-mice-to-make-them-age-more-rapidly-often-tells-us-little-of-use.php

Calorie Restriction as a Means to Augment Cancer Therapies

Posted: at 2:53 am


Long term calorie restriction lowers the risk of cancer in addition to extending life in laboratory animals. Here researchers show that short term calorie restriction appears to augment the effectiveness of treatments for an existing cancer:

While previous studies suggest a connection between caloric intake and the development of cancer, scientific evidence about the effect of caloric intake on the efficacy of cancer treatment has been rather limited to date. When humans and animals consume calories, the body metabolizes food to produce energy and assist in the building of proteins. When fewer calories are consumed, the amount of nutrients available to the body's cells is reduced, slowing the metabolic process and limiting the function of some proteins. These characteristics of calorie restriction have led researchers to hypothesize that reducing caloric intake could potentially help inhibit the overexpression of the protein Mcl-1, an alteration associated with several cancers.

Researchers conducted a series of experiments in mice developing lymphoma resembling Burkitt's lymphoma and diffuse large B-cell lymphoma, two human cancers of the white blood cells. The team began by separating the mice into two categories: those who would receive a regular diet and those who would receive a reduced-calorie diet (75 percent of normal intake) for the duration of the experiment. After the mice consumed either a regular or a reduced-calorie diet for one week, researchers then further divided the mice into four groups according to the treatment they would receive for the following 10 days. Of the two groups of mice that received a normal diet, one (the control group) did not receive treatment and the other received treatment with an experimental targeted therapy, ABT-737, designed to induce cancer cell death. Of the two groups of mice who received a reduced-calorie diet, one did not receive treatment and the other received ABT-737. On day 17 of the experiment, both treatment and calorie restriction ended, and mice had access to as much food as they desired.

Investigators observed that neither treatment with ABT-737 nor calorie restriction alone increased the survival of mice over that of the other mice; however, the combination of ABT-737 and calorie restriction did. Median survival was 30 days in the control group that received a regular diet and no treatment, 33 days in mice that received a regular diet and treatment with ABT-737, 30 days in mice that received a reduced-calorie diet without treatment, and 41 days in mice that received a reduced-calorie diet and treatment with ABT-737. Shortly after this experimental period, investigators also observed that the combination of calorie restriction and ABT-737 reduced the number of circulating lymphoma cells in the mice, suggesting that the combination sensitized the lymphoma cells to treatment.

Link: http://hematology.org/News/2013/10958.aspx

Source:
https://www.fightaging.org/archives/2013/08/calorie-restriction-as-a-means-to-augment-cancer-therapies.php

Life Without Ageing: Aubrey de Grey and Tom Kirkwood to Debate Longevity Science at the British Science Festival

Posted: August 18, 2013 at 2:55 am


The British Science Festival will be held in Newcastle a few weeks from now. One of the events has Aubrey de Grey of the SENS Research Foundation, advocate and coordinator for rejuvenation research, debating Tom Kirkwood, one of the leading figures in the mainstream faction of the aging research community who think that there isn't much hope for rapid progress to rejuvenation. Those researchers see the best available path forward as one of modestly slowing aging through replication of known metabolic or genetic alterations associated with natural variations in longevity, such as those involved in the response to calorie restriction - but even this will be a long time in realization, a slow grind towards incremental improvements.

I agree with the viewpoint that attempts to safely slow aging in humans will be very hard indeed. Success requires a much greater understanding of metabolism and aging than presently exists, and it's not unreasonable to suggest that decades and many billions of dollars lie between us and even the first prototype drugs to slightly slow aging. However, slowing aging by altering genes and metabolism is not the only approach that can be taken - indeed it's probably the worst of viable scientific approaches to extending healthy life. It's exceedingly costly, produces marginal results, and therapies that can slow ongoing aging are of little to no use for people who are already old and frail.

In this Kirkwood represents the old mainstream of standardized drug discovery and marginal, unambitious process in medicine. De Grey represents the disruptive future of medical technology, his SENS vision and ongoing research being one of a number of entirely new paradigms for health and aging that are winning over an increasing fraction of the research community. The times are changing, and every new wave of development is met by skepticism from those in the mature industries it will replace. We should aim for rejuvenation through periodic repair of cellular damage: it will like take no longer, will quite possibly be cheaper than trying alter ourselves to slow aging, and will be very beneficial for people who are already old when these therapies are introduced.

Life Without Ageing - Two Contrasting Visions Of An Ageing World


EVENT: Life Without Ageing - Two contrasting visions of an ageing world
DATE: Monday 9th September TIME: 13.00 - 14.30
VENUE: Fine Art Building Lecture Theatre, Newcastle, UK

Is a cure for ageing within reach in our own lifetimes?

Biomedical gerontologist Dr Aubrey de Grey, Chief Science Officer of the SENS Research Foundation will be joining Professor Tom Kirkwood CBE, Associate Dean for Ageing at Newcastle University to debate a 'Life Without Ageing'. In this event, chaired by Dr Sir Tom Shakespeare, Aubrey de Grey will suggest that a "cure" for ageing is within reach in our own lifetimes, while Tom Kirkwood will argue that such a goal is not only unrealistic but distorts what should be the real research priorities of an ageing world.

Dr de Grey's research proposes that eliminating ageing as a cause of debilitation and death in mankind can be achieved within just a few decades through his proposed 'Strategies for Engineered Negligible Senescence'; a term coined by De Grey in his first book The Mitochondrial Free Radical Theory. Countering this is Professor Kirkwood, a former BBC Reith Lecturer, whose research is around healthy ageing and improving life in old age by looking at the prevention of age associated factors, such as frailty, disability and age related disease, and by helping to change society's attitudes towards ageing.

The tantalising idea of living forever is as old as humanity, but can modern science really hope to consign the ageing process to history? Life Without Ageing promises to be a fascinating insight into modern day ageing research and the opposing visions of an ageing world. At the end of the debate the floor will be opened, giving the audience opportunity to put questions to the speakers and take part in what should be a lively discussion.

If you take a careful look at the festival site page for the debate, you'll see that it's possible to submit questions for the speakers. If you intend to go in person, it looks like registration is required, but it's otherwise a free event.

Source:
https://www.fightaging.org/archives/2013/08/life-without-ageing-aubrey-de-grey-and-tom-kirkwood-to-debate-longevity-science-at-the-british-science-festival.php

A Short Overview of 3-D Printing in Tissue Engineering

Posted: at 2:55 am


Technologies derived from rapid prototyping and 3-D printing will likely play an important role in the future of tissue engineering, just as they are coming to do in many fields:

The field of tissue engineering has deployed several fabrication strategies aimed at bringing cells and structure together to generate tissue. Biomaterial scaffolding - which provides structural support and can be formed into biologically relevant shapes - has been combined with cells to generate hybrid 3-D structures for use as tissue surrogates in vitro and in vivo. Protocols have been developed that enable removal of living cells from native tissues, leaving only a natural scaffolding of extracellular matrix, which can then be re-seeded with cells to reconstruct or partially reconstruct 3-D tissues. Another approach to soft tissue reconstruction has been the development of cell-laden hydrogels, which are often cast into a specific shape and placed into a permissive environment in vitro or in vivo that allows maturation and establishment of tissue-specific characteristics. In recent years, with the advancement of 3-D printing technologies for the on-demand fabrication of complex polymer-based objects, efforts have been underway to adapt 3-D printing technologies and engineer bioprinting instruments that can leverage similar 3-D replication concepts and accommodate the incorporation of living cells.

Organovo's NovoGen MMX Bioprinter precisely dispenses "bio-ink" - tiny building blocks composed of living cells - generating tissues layer-by-layer according to user-defined designs. Built for flexibility, the bioprinter enables fabrication of tissues with a wide array of cellular compositions and geometries; side-by-side comparison of multiple tissue prototypes facilitates optimization and selection of specific designs geared toward a particular application. Working within the confines of an object library, bio-ink building blocks of various shapes, sizes and compositions are assembled into architectures that recapitulate the form of native tissue. Tubes, layered sheets and patterned structures have been bioprinted, yielding 3-D tissues that are free of biomaterial scaffolding and characterized by tissue-like microarchitecture, including the development of intercellular junctions and endothelial networks.

In the short-term, 3-D human tissues are being deployed in the laboratory setting as models of human physiology and pathology; cell-based assays are a mainstay of the drug discovery and development process, and multicellular/multitissue systems may serve as more predictive indicators of clinical outcomes. Longer-term applications of 3-D tissue technologies will extend our knowledge of how to build the smallest functional units of a tissue to the fabrication of larger-scale tissues useful for surgical grafts to repair or replace damaged tissues and organs in the body. What are the next steps in the evolution of bioprinting? The first step is scaling up and down - increasing the resolution of specific features while advancing fabrication hardware and techniques to produce larger-scale tissues. The next, enhancing the complexity of designs - building the tool set that enables conceptual or visual inputs to be translated rapidly to executable bioprinting programs that select from a library of bio-ink building blocks to translate the vision into reality.

Link: http://www.rdmag.com/articles/2013/08/3-d-printing-life-science-applications

Source:
https://www.fightaging.org/archives/2013/08/a-short-overview-of-3-d-printing-in-tissue-engineering.php

Another Way to Improve Memory in Old Mice

Posted: at 2:55 am


In recent years researchers have demonstrated a number of ways to improve memory in old laboratory mice. Here is another:

If you forget where you put your car keys and you can't seem to remember things as well as you used to, the problem may well be with the GluN2B subunits in your NMDA receptors. And don't be surprised if by tomorrow you can't remember the name of those darned subunits. They help you remember things, but you've been losing them almost since the day you were born, and it's only going to get worse. An old adult may have only half as many of them as a younger person.

Cognitive decline with age is a natural part of life, and scientists are tracking the problem down to highly specific components of the brain. Separate from some more serious problems like dementia and Alzheimer's disease, virtually everyone loses memory-making and cognitive abilities as they age. The process is well under way by the age of 40 and picks up speed after that. But of considerable interest: It may not have to be that way. "These are biological processes, and once we fully understand what is going on, we may be able to slow or prevent it."

In recent research [scientists] used a genetic therapy in laboratory mice, in which a virus helped carry complementary DNA into appropriate cells and restored some GluN2B subunits. Tests showed that it helped mice improve their memory and cognitive ability. The NMDA receptor has been known of for decades. [It] plays a role in memory and learning but isn't active all the time - it takes a fairly strong stimulus of some type to turn it on and allow you to remember something. The routine of getting dressed in the morning is ignored and quickly lost to the fog of time, but the day you had an auto accident earns a permanent etching in your memory.

Within the NMDA receptor are various subunits, [and] research keeps pointing back to the GluN2B subunit as one of the most important. Infants and children have lots of them, and as a result are like a sponge in soaking up memories and learning new things. But they gradually dwindle in number with age, and it also appears the ones that are left work less efficiently. "The one thing that does seem fairly clear is that cognitive decline is not inevitable. It's biological, we're finding out why it happens, and it appears there are ways we might be able to slow or stop it, perhaps repair the NMDA receptors. If we can determine how to do that without harm, we will."

Link: http://oregonstate.edu/ua/ncs/archives/2013/aug/cognitive-decline-age-normal-routine-%E2%80%93-not-inevitable

Source:
https://www.fightaging.org/archives/2013/08/another-way-to-improve-memory-in-old-mice.php

SENS Research Foundation Releases 2013 Research Report

Posted: at 2:55 am


The SENS Research Foundation coordinates and conducts research into the baseline technologies needed for human rejuvenation. We age because we become damaged: cells and the structures between cells accumulate broken proteins, waste products, and other forms of harm. The machines of our cells run down, run amok, and run ragged. Eventually that kills us, as damage overwhelms self-repair, but this ugly process of aging to death could be indefinitely postponed given effective means of repairing the forms of damage that are fundamental, those that result from nothing more than the ordinary operation of human metabolism.

SENS stands for the Strategies for Engineered Negligible Senescence, and is a detailed set of theories and supporting evidence regarding which forms of damage and change identified in the old actually cause aging, combined with research plans to develop the foreseeable means to repair these fundamental forms of damage. SENS is a guide to lead us from today, a time in which the research community finally knows enough to be able to lay out a plan like this in detail, to a tomorrow of realized prototype therapies that can rejuvenate old laboratory animals such as mice.

If fully funded to a level of $100 million / year or so, then SENS is a ten to twenty year project, involving the creation of a large new research community and public support to rival that of the cancer research edifice. It might sound like a massive, unobtainable amount of money, but bear in mind that the National Institute on Aging spends ten times amount that as a yearly budget, a single company engaged in not-so-great-in-the-end research on a single type of drug to slightly slow aging sold for $700 million, and neither of those examples offers any great hope of producing meaningful change in the aging process. To a first approximation the NIA are not funding interventions, only investigations, and much of that work is largely irrelevant in comparison to what might be done by ambitious, funded researchers. Such is life: in large-scale institutions mediocrity rules, and ambitious, high risk work that might produce great change is largely going to go unfunded.

At the end of the SENS road we will have the first form of a medical toolkit to reverse aging - an event that could happen in time to help most of those reading this today. Yet there is still little funding for SENS research: a few million dollars a year, derived from community support and philanthropic donors such as Peter Thiel and Aubrey de Grey. This level of funding will have to increase greatly if we are to see the promise of SENS realized.

In advance of the forthcoming SENS6 conference, the SENS Research Foundation has released their 2013 research report, which as always makes for interesting reading.

SENS Research Report 2013 (PDF)

In May of 2012, a 10-year-old girl was suffering in hospital with a blockage in her portal vein - the major blood vessel that brings nutrients from the digestive tract into the liver. Bypassing the risks of transplantation, Swedish doctors engineered the girl a new, custom replacement. Drawing from earlier human successes with engineered tracheas, a donor's blood vessel was stripped of its cells.The resulting scaffold was seeded with stem cells from the girl's bone marrow, and chemical signals were then used to encourage the cells to grow into a functional portal vein. Thanks to the engineered vessel, the girl's blood tests have normalized, and she is now capable of light gymnastics and mile-and-a-half walks.

This groundbreaking achievement is just one example of what can emerge from a few years of rapid progress in animal models and other precedent-setting tissue engineering projects. It is also an example of the type of work SENS Research Foundation is funding with the goal of applying it to a primary problem of aging: the decline of the immune system. Only a few of us will ever need a new portal vein or trachea - but nearly all of us will need a new thymus, which plays an indispensible role in the immune system. The fine structures and functioning cells of the thymus we were born with will slowly degenerate between our teen years and our sixties; as the organ begins to fail with age, we become increasingly vulnerable to influenza and other common infectious diseases. With SRF support, Wake Forest Institute of Regenerative Medicine researchers are now making rapid progress in work to apply the decellularized-recellularized scaffold method to the thymus in animal models. SRF is excited to be spearheading the adaptation of existing techniques to geriatric medicine, where innovation is so sorely needed. But we know that this alone is not enough to address the emerging health crisis posed by age-related disease, which has surpassed infectious disease as the most pressing health problem facing humanity today.

SENS Research Foundation is currently the only research nonprofit pushing the boundaries of the field toward the molecular level, where much of the damage of aging resides. Treating the symptoms of the resulting pathologies can only take us so far, because the body's repair and maintenance mechanisms continue to deteriorate. SRF's unique dedication to identifying and alleviating the damage that long precedes pathology serves as the basis for much of our work. Our longest-running project in this vein targets age-related macular degeneration, the leading cause of blindness in people over the age of 65. Macular degeneration is caused by the accumulation of a toxic byproduct of the visual cycle called A2E, which builds up in the retinal pigment epithelial (RPE) cells responsible for maintaining the light-sensing cells of the eye. We are working to preserve and restore the health of these cells by fortifying them with new, engineered enzymes capable of clearing A2E deposits. In 2012, scientists in our Research Center identified an enzyme (SENS20) that has since demonstrated efficacy in degrading A2E not only in vitro, but in RPE cells administered an A2E "stress test."

These two critical-path projects, as well as the others described in this Research Report, reflect our ongoing mission to transform the way the world researches and treats age-related disease. Our commitment to developing the industry of restorative medicine begins with proof-of-concept work - but ultimately rests upon creating the rejuvenation biotechnologies that can actually cure these diseases. To accomplish this, in addition to funding and conducting more research into the health problems of aging, we must realize a shift in how these health problems are conceptualized. We must move from seeing age-related illnesses as discrete entities to acknowledging that as we grow older, we become progressively more vulnerable to every single age related disease that exists, because we are all accumulating damage at levels no form of medicine can presently touch. When we reimagine aging, we envision a world where the damage preceding pathology is recognized as a treatable condition in and of itself, and addressed accordingly. SRF is delighted to share our progress toward this end in this Research Report. We hope you will join us in taking the tremendous opportunity at hand to set the new standard for twenty-first century medical research and development.

SENS and the SENS Research Foundation are the seed for what will become the core, central pillar of medicine in the decades ahead. Nothing will be as important to health as maintaining youth by periodic repair of cellular damage. Just like antibiotics today, that will be the primary barrier that stands between us and the ubiquitous suffering and mortality that preceded it. The greater the support given to SENS and SENS-like research, the faster we get to that point.

Source:
https://www.fightaging.org/archives/2013/08/sens-research-foundation-releases-2013-research-report.php

Targeting Redox Biology to Reverse Mitochondrial Dysfunction

Posted: at 2:55 am


Mitochondria are the power plants of the cell, generating chemical fuel stores that can be used to power cellular processes. They are important in aging, and this has a lot to do with the generation of reactive oxygen species (ROS) that happens as a side-effect of their operation. Researchers have shown that benefits to health and longevity can be realized in laboratory animals by targeting antioxidants to mitochondria in order to soak up some ROS before they cause harm. Other research focuses on repairing the damage that mitochondria inflict upon themselves this way, so as to stop it from contributing to degenerative aging.

There is general agreement that mitochondria play an important role in the aging process, but the role of mitochondrial oxidative stress remains controversial. Most previous work looking at mitochondrial oxidative stress has focused on damage to DNA, proteins, and lipids with age or in response to manipulation of cellular antioxidants. The interaction between oxidative damage and aging has been called into question in recent years by studies demonstrating little effect on aging and lifespan in mice with genetically modified antioxidant systems. A notable exception is the life extension and protection against multiple diseases in mice that express catalase in the mitochondria, which suggests that the cellular location and type of reactive oxygen species is an important factor.

Our laboratory is interested in whether redox inhibition of mitochondrial function contributes to age-related energy deficits in vivo in mouse and human skeletal muscle. [We] tested this hypothesis using a mitochondrial targeted peptide, SS-31, known to reduce mitochondrial H2O2 production.

SS-31 reduced the high mitochondrial H2O2 production from aged permeabilized muscle fibers [but] had no effect on young fibers. In the aged mice, one hour after in vivo treatment with SS-31 the cellular redox status [was] more reduced. This was accompanied by improved mitochondrial [function] in vivo in the skeletal muscle, while there was no effect on the mitochondrial energetics in young skeletal muscle. In addition to the improvements in muscle energetics, one hour and one week of SS-31 treatment resulted in improved muscle performance and increased exercise tolerance, respectively, in the old mice.

This rapid reversal of in vivo energy deficits supports the hypothesis that mitochondrial deficits in aged skeletal muscle are, at least in part, due to reversible redox sensitive inhibition. Thus assessing the role of mitochondrial oxidative stress in aging and disease will require careful attention to changes to the in vivo redox environment and the mechanisms by which these changes can affect cell function.

Link: http://impactaging.com/papers/v5/n8/full/100590.html

Source:
https://www.fightaging.org/archives/2013/08/targeting-redox-biology-to-reverse-mitochondrial-dysfunction.php

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