Australia is leading the world with the first publicly funded program aimed at reducing the risk of developing dementia.

A new brain health program, Your Brain Matters, will be launched by Alzheimer’s Australia this week.

It was funded by the federal government in the 2012 budget, the first prevention program for dementia in the world to receive public funding, said Alzheimer’s Australia chief executive Glenn Rees.

He said this showed the condition was being treated as a chronic disease, rather than a normal part of ageing.

Mr Rees said the program was a guide to keeping the brain healthy by exercising the mind and body and eating a nutritious diet.

“It’s important to understand that while there is, as yet, no cure for dementia there are things we can all do now – like keeping your brain active, being fit and healthy and looking after your heart – which may help to reduce our risk of developing dementia, or slow cognitive decline in those already diagnosed with dementia,” Mr Rees said in a statement.

He said there was evidence to suggest that if physical inactivity could be reduced in Australia by five per cent every five years, this could cut dementia prevalence by 11 per cent by 2051.

This would equate to about 100,000 fewer Australians living with dementia by addressing just one risk factor, he said.

International Alzheimer’s expert Dr Serge Gauthier, of McGill University in Canada, who is visiting Australia as part of Dementia Awareness Week, said prevention programs were vital to try to stem the incidence of dementia.

About 280,000 Australians have dementia, with this figure set to soar to almost one million by 2050.

View original post here:
National push to prevent dementia

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

COLLIER COUNTY, FL –

A veteran dementia patient was found lying in the woods, nearly dead. Five years later, his family says they finally have justice.

“We needed justice for my grandfather and people needed to be held accountable for their actions,” said Dederick’s granddaughter Lauren Carey, who searched tirelessly for five days to find her missing grandfather.

Then 88-year-old Loren Dederick, who passed away last year, went missing in 2007 after a medical transport mix-up.

A jury found TLC Non-Emergency Medical Transport at fault ordered the company to pay Dederick’s family $700,000 for his injuries and mental anguish.

“He laid there for five days with no food or water and no way out,” said Dederick’s. “He was dirty, ant bites all over, dehydrated and just really scared.”

“He was getting close to the time where he probably couldn’t sustain himself any longer,” said Dederick’s daughter Donna Ward.

The World War II veteran was taken to NCH North Naples hospital for chest pain on September 21, 2007.

When he was released, NCH accidentally gave a TLC transport driver Dederick’s old address, the HarborChase assisted-living facility on Airport-Pulling Road in Naples.

The driver, 44-year-old Dimas Herrera, took Dederick to that wrong address. According to testimony, nurses at the assisted-living center told Herrera that Dederick didn’t live there.

See the original post here:
Dementia patient's family: "We needed justice"

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

By way of following on from yesterday’s thoughts on progress in longevity science, I’ll point out that the August 2012 issue of Rejuvenation Research is available online. The leading editorial by Aubrey de Grey of the SENS Foundation covers much the same set of topics and is presently open access – so head on over and read it while that lasts.

What’s Really Delaying the Defeat of Aging?

In the mid-1990s, when I decided to switch from computer science to gerontology, I recognized that the creation of a credible assault on aging would require solving three basic problems: (1) Creating a credible plan; (2) getting the people best placed to implement it to be interested in doing so; and (3) giving them the financial resources to get on with the job.

I broke the back of the first problem in mid-2000, when I realized that regenerative medicine – repairing the accumulating damage of aging – will probably be far simpler and easier to implement than the alternative followed by most biogerontologists, namely slowing the creation of that damage. By that time, I had also done most of the heavy lifting of item 2 (as I continued to do thereafter), by connecting with leading researchers worldwide, mostly face to face at conferences, and improving their understanding of how their expertise could be productively applied to aging. By way of illustration, quite a few of the most prestigious such people are named on the front cover of this journal as associate editors, and they accepted such a position for that reason. But what about item 3?

Unfortunately, I cannot tell so positive a story with respect to financial resources. Nearly a decade ago, I began to make public predictions of how soon we would achieve success in our crusade. I did so, as I still do, in the manner that (for better or worse) preoccupies the general public, namely in terms of longevity, but I have always been careful to incorporate two key caveats: (1) The level of uncertainty of the time frames, even if only scientific uncertainty is considered, and (2) the reliance of such estimates on adequate funding.

The first of these caveats is often elided, but it is simple: I estimate that we have a 50% chance of achieving the milestone of “robust human rejuvenation” (essentially, the rejuvenation of 60 year olds comprehensively enough that they won’t be biologically 60 again until they’re chronologically 90) within 25 years, but I also estimate that we have at least a 10% chance of not getting there in 100 years. But…that is all subject to the second caveat, namely funding.

Tragically, the level of funding that has been forthcoming during the past decade is only a few percent (at most) of what is necessary. The rate of progress in research to defeat aging has been quite amazing in view of that, but nonetheless, I estimate that it has been only about one-third of what could have been achieved with 10-20 times more money.

Which is much as I said yesterday: there are now plenty of researchers and research groups who would work on building real rejuvenation biotechnology as described in the SENS vision if they were given a budget to do so. That budget is, however, sadly lacking at this time. Millions of dollars are going to SENS and SENS-like research programs these days (which is a big improvement over their non-existence ten years ago) – but a hundred times that flow of resources would be needed to achieve earnest progress at the best possible rate.

One of the logical conclusions emerging from this point of view is that longevity science remains in that stage of growth wherein advocacy and education are the primary drivers of progress. There is sufficient buy-in from the scientific community to make institutional investment in research the bottleneck to progress, and obtaining that funding is a matter of persuasion.

In one sense this is encouraging: it is a characteristic state of affairs during a rapid shift in priorities for any field of human endeavor. Organizations with large sums to place into research tend to be the most conservative portions of their community, and thus among the last to heed the changing winds of knowledge and priority. This present stage, in which researchers are now interested and supportive but lacking in sources of funding that will allow them to actually work on the problem at hand, is a natural, albeit frustrating, part of the process. It is a considerable step up from the previous era in which few researchers had any interest in working on the biotechnologies of engineered human longevity, and even talking about it in public was discouraged.

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

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

FIGHT AGING! NEWSLETTER
September 3rd 2012

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!

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CONTENT

- A Perspective on Progress in Longevity Science
- What’s Really Delaying the Defeat of Aging?
- Absent Optimism
- Everyone Has a Plan to Save Medicare
- Discussion
- Latest Headlines from Fight Aging!
    - SIRT6 Overexpression Reverses DNA Repair Decline in Aging Mice
    - A Good Lifestyle Makes a Difference Even Late in Life
    - Impact of Mid-Life Fitness on Later Risk of Age-Related Disease
    - No Extension of Average Lifespan in Primate Study of Calorie Restriction
    - A View of Diet and Aging
    - Work on Blocking Damage in Brain Injury
    - More on DNA Methylation and Human Longevity
    - Cytomegalovirus and Type 2 Diabetes Risk
    - How Long Do You Want to Live?
    - Wiring Up Engineered Tissue

A PERSPECTIVE ON PROGRESS IN LONGEVITY SCIENCE

Here is an overview of some of what I see when looking out on the world of research and development relating to engineered longevity, spurred by someone who asked whether it was plausible for aging to be defeated by 2029:

http://www.fightaging.org/archives/2012/08/an-outline-of-progress-in-longevity-science.php

“The bottom line is that the research community and state of the field today is very different from that of even a mere ten years ago. This is a time of rapid change and progress: far more is known and far more impressive feats of medicine can be performed in the lab and the clinic. There is every reason to believe that ten years from now we’ll be able to say the same thing. Costs in biotechnology and life science research are falling rapidly, and with that trend more research can be accomplished in each new year.

“That said, however, the only way that we’ll see significant inroads into the defeat of aging by 2029 is for the SENS Foundation and its attendant research community to undergo the same sort of growth over the next decade as has been exhibited in recent years by regenerative medicine, calorie restriction research, or study of the genetics of longevity. A growth to billions in funding and thousands of researchers, in other words. It will require at least that and a decade of time in order to have a 50/50 shot at reversing aging in old mice in the lab – which is to say something that can make them live at least twice as long as they otherwise would have done.

“Of all the items covered in this post, only SENS provides a path towards achieving this end. Even regenerative medicine and complete control over stem cells can’t offer the possibility of reversing aging in and of itself – it is only the way to reverse one component of aging, the decline of tissue maintenance and frailty that results from stem cells shutting down. You will still get nailed by your own mitochondria and the build up of metabolic byproducts even if your stem cells are perfectly restored.

“[So], no, there is no plausible road to the defeat of aging by 2029. But there is a plausible road to the first laboratory demonstrations of real, meaningful, but partial age reversal by then, ways to actually repair the root biological causes of aging rather than just slow it down. Whether that happens or not depends absolutely on funding – there are more than enough scientists and research groups out there who would work on the SENS vision for rejuvenation biotechnology if given a budget, but as of yet not enough funding sources to make it a reality.”

WHAT’S REALLY DELAYING THE DEFEAT OF AGING?

Aubrey de Grey of the SENS Foundation answers this question in an open access editorial from the Rejuvenation Research journal:

http://www.fightaging.org/archives/2012/08/whats-really-delaying-the-defeat-of-aging.php

“In the mid-1990s, when I decided to switch from computer science to gerontology, I recognized that the creation of a credible assault on aging would require solving three basic problems: (1) Creating a credible plan; (2) getting the people best placed to implement it to be interested in doing so; and (3) giving them the financial resources to get on with the job.

“I broke the back of the first problem in mid-2000, when I realized that regenerative medicine – repairing the accumulating damage of aging – will probably be far simpler and easier to implement than the alternative followed by most biogerontologists, namely slowing the creation of that damage. By that time, I had also done most of the heavy lifting of item 2 (as I continued to do thereafter), by connecting with leading researchers worldwide, mostly face to face at conferences, and improving their understanding of how their expertise could be productively applied to aging. By way of illustration, quite a few of the most prestigious such people are named on the front cover of this journal as associate editors, and they accepted such a position for that reason. But what about item 3?

“Unfortunately, I cannot tell so positive a story with respect to financial resources. Nearly a decade ago, I began to make public predictions of how soon we would achieve success in our crusade. I did so, as I still do, in the manner that (for better or worse) preoccupies the general public, namely in terms of longevity, but I have always been careful to incorporate two key caveats: (1) The level of uncertainty of the time frames, even if only scientific uncertainty is considered, and (2) the reliance of such estimates on adequate funding.

“The first of these caveats is often elided, but it is simple: I estimate that we have a 50% chance of achieving the milestone of “robust human rejuvenation” (essentially, the rejuvenation of 60 year olds comprehensively enough that they won’t be biologically 60 again until they’re chronologically 90) within 25 years, but I also estimate that we have at least a 10% chance of not getting there in 100 years. But…that is all subject to the second caveat, namely funding.

“Tragically, the level of funding that has been forthcoming during the past decade is only a few percent (at most) of what is necessary. The rate of progress in research to defeat aging has been quite amazing in view of that, but nonetheless, I estimate that it has been only about one-third of what could have been achieved with 10-20 times more money.”

ABSENT OPTIMISM

Our culture is far too short-sighted, focused on what is, and pessimistic, and that harms the prospects for progress:

http://www.fightaging.org/archives/2012/08/absent-optimism.php

“For a society in the midst of accelerating, rapid, and evident technological progress, public discussion and attitudes show a surprising lack of optimism for the future. Optimism of course exists, but nowhere near as widely as it should. It seems self-evident at this point that a golden era lies ahead in which we defeat disease and aging, colonize the solar system, and expand the limits of what it means to be human. We and our descendants will discard pain and suffering along the way, just as we have already discarded so much of the pain and suffering that our ancestors bore. … The upward ramp of the necessary underlying technology is within our grasp. But you wouldn’t think this from listening to the public. Much of the world seems convinced that nothing but collapse and catastrophe lies ahead: their view of the future is the ever-mistaken Malthusian collection of beliefs revolving around static resources that are exhausted. They fail to see the dynamism of resource generation and progress that proved past Mathusians just as wrong as the present crop.”

EVERYONE HAS A PLAN TO SAVE MEDICARE

There are any number of people out there putting forward their proposals:

http://www.fightaging.org/archives/2012/08/everyone-has-a-plan-to-save-medicare.php

“Having a plan to save Medicare is somewhat like wearing a tie or cufflinks, in that it is somewhat de reigueur in some parts of society – but ultimately a cultural signal of belonging, of little value otherwise. The economic future of the US is somewhat grim; the decline of an empire is inevitable as its increasingly unaccountable elite class debauch the currency, centralize power, and regulate all aspects of a citizen’s life. They tax and waste ever more of the flow of resources whilst destroying the freedom and competition needed for the creation of those resources – in much the same way as a cancer is parasitic to its host but ultimately destroys both host and itself. This is an inexorable progression of society, built upon the foundation of human nature and the individual actions and interactions of millions of people. It has happened over and again and is just about as likely as the tide to be turned aside.

“So having a plan to save Medicare is rather like having a plan to save a part of your cancer. That portion in the lower left, perhaps. Medicare is but one part of the network of regulation, perverse incentives, and regulatory capture that causes medicine in the US to be ever more expensive, wasteful, and poor in quality. It’s large enough to be considered in the context of the more general economic decline across the board, which occurs for roughly the same set of reasons, and is just as hard to turn back. Medicine is in a more advanced state of socialist decrepitude than most other US industries, but the same process operates throughout society.

“From there let me segue into a discussion of responses to shortage. Regulation inevitably creates shortage and rationing: we see this in the provision of medicine in countries like Canada and the UK, where regulators set up waiting systems or simply forbid treatment, especially to the old. Much of the public discussion that results from this state of affairs looks at what to do about the shortages – though of course without a great deal of reflection on how they came to exist in the first place, sad to say. There are two broad lines of thinking here: firstly, use less of whatever is rationed; secondly try to create more of whatever is in short supply.

“One of the defining and frankly rather sorry aspects of our age is that public debates veer towards cutting back on use far more often than towards creating abundance. See the bulk of the environmentalist or other Malthusian movements for example – they have little to say about building more of whatever it is they think is in short supply.

“When it comes to Medicare, and given that very few people are calling to get rid of the whole system and let freedom and free markets rule the day, the two sides of the coin look much like (a) a call for increased rationing of services to ensure that people use less in the way of medicine, and (b) a call for ways to create greater health such that people use less in the way of medicine. There are of course many different approaches to either of these paths, but both ultimately sidestep the real issue, the real cause of the problem – and this again is absolutely characteristic of debate over societal organization and politics in our age.”

DISCUSSION

The highlights and headlines from the past week follow below. Remember – if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!

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LATEST HEADLINES FROM FIGHT AGING!

SIRT6 OVEREXPRESSION REVERSES DNA REPAIR DECLINE IN AGING MICE
Friday, August 31, 2012
http://www.fightaging.org/archives/2012/08/sirt6-overexpression-reverses-dna-repair-decline-in-aging-mice.php
This interesting research result adds a little more to the debate over whether nuclear DNA damage is relevant to aging beyond its effects on cancer risk – though I think it’s still a bit early to point to differences in DNA repair as the definitive cause of SIRT6-related longevity in mice: researchers “found that the decline in a cell’s ability to repair DNA during aging coincided with a global reduction in the levels of proteins involved in the repair process. [They] tried to reverse the age-related decline in DNA repair efficiency by restoring the proteins to their original levels and found only one protein, SIRT6, did the trick. … [Other research results have shown] that overexpressing the SIRT6 protein extended the lifespans of mice. Our research looked at DNA repair and found a reason for the increased longevity, and that is SIRT6′s role in promoting more efficient DNA repair. … The next step [is] to study the factors that regulate SIRT6, in an effort to learn more about the early stages of the DNA repair process. … multiple groups are trying to develop drugs that activate SIRT6, and [researchers hope] that this research will one day lead to therapies that help extend a person’s lifespan and treat cancer. … SIRT6 plays a critical role in repairing the most dangerous type of DNA damage: double-strand breaks. DNA is a two-stranded molecule, and breaks can occur to one strand of the molecule or to both. In the case of single-strand breaks, the unbroken strand guides the repair process and the DNA molecule is typically restored to its original state. However, double-strand breaks, in which both strands are severed, are particularly hazardous because they are more difficult to repair and can lead to a rearrangement of the cell’s genetic material.”

A GOOD LIFESTYLE MAKES A DIFFERENCE EVEN LATE IN LIFE
Friday, August 31, 2012
http://www.fightaging.org/archives/2012/08/a-good-lifestyle-makes-a-difference-even-late-in-life.php
Keeping up on the health basics makes a difference even in the last years of life: “It is well known that lifestyle factors, like being overweight, smoking and heavy drinking, predict death among elderly people. But is it uncertain whether these associations are applicable to people aged 75 years or more. So a team of researchers based in Sweden measured the differences in survival among adults aged 75 and older based on modifiable factors such as lifestyle behaviours, leisure activities, and social networks. The study involved just over 1,800 individuals who were followed for 18 years (1987-2005). Data on age, sex, occupation, education, lifestyle behaviours, social network and leisure activities were recorded. During the follow-up period 92% of participants died. Half of the participants lived longer than 90 years. Survivors were more likely to be women, be highly educated, have healthy lifestyle behaviours, have a better social network, and participate in more leisure activities than non-survivors. The results show that smokers died one year earlier than non-smokers. Former smokers had a similar pattern of survival to never smokers, suggesting that quitting smoking in middle age reduces the effect on mortality. Of the leisure activities, physical activity was most strongly associated with survival. The average age at death of participants who regularly swam, walked or did gymnastics was two years greater than those who did not. Overall, the average survival of people with a low risk profile (healthy lifestyle behaviours, participation in at least one leisure activity, and a rich or moderate social network) was 5.4 years longer than those with a high risk profile (unhealthy lifestyle behaviours, no participation in leisure activities, and a limited or poor social network). Even among those aged 85 years or older and people with chronic conditions, the average age at death was four years higher for those with a low risk profile compared with those with a high risk profile. In summary, the associations between leisure activity, not smoking, and increased survival still existed in those aged 75 years or more, with women’s lives prolonged by five years and men’s by six years, say the authors. These associations, although attenuated, were still present among people aged 85 or more and in those with chronic conditions.”

IMPACT OF MID-LIFE FITNESS ON LATER RISK OF AGE-RELATED DISEASE
Thursday, August 30, 2012
http://www.fightaging.org/archives/2012/08/impact-of-mid-life-fitness-on-later-risk-of-age-related-disease.php
How you manage your health in earlier parts of your life will have an effect further down the line: “To examine the association between midlife fitness and chronic disease outcomes in later life, participant data from the Cooper Center Longitudinal Study were linked with Medicare claims. We studied 18,670 healthy participants (21.1% women; median age, 49 years) who survived to receive Medicare coverage from January 1, 1999, to December 31, 2009. Fitness estimated by Balke treadmill time was analyzed [according] to age- and sex-specific quintiles. Eight common chronic conditions were defined [and] associations between midlife fitness and the number of conditions were assessed. … After 120,780 person-years of Medicare exposure with a median follow-up of 26 years, the highest quintile of fitness [was] associated with a lower incidence of chronic conditions [in men and women]. After multivariate adjustment, higher fitness [was] associated with a lower risk of developing chronic conditions in [men and women]. … In this cohort of healthy middle-aged adults, fitness was significantly associated with a lower risk of developing chronic disease outcomes during 26 years of follow-up. These findings suggest that higher midlife fitness may be associated with the compression of morbidity in older age.”

NO EXTENSION OF AVERAGE LIFESPAN IN PRIMATE STUDY OF CALORIE RESTRICTION
Thursday, August 30, 2012
http://www.fightaging.org/archives/2012/08/no-extension-of-average-lifespan-in-primate-study-of-calorie-restriction.php
A discussion on published results from this primate study suggest that both it and a comparison study are different in ways that make it harder to pull rigorous conclusions from the data – beyond the fact that diet clearly has influence, and the effects of calorie restriction on life span (average and maximum) are expected to be smaller in longer-lived species versus shorter-lived speces: “Scientists have found that calorie restriction – a diet composed of approximately 30 percent fewer calories but with the same nutrients of a standard diet – does not extend years of life or reduce age-related deaths in a 23-year study of rhesus monkeys. However, calorie restriction did extend certain aspects of health. … The survival results in the study reported [by] NIA researchers differ from those published in 2009 by NIA-supported investigators at the University of Wisconsin-Madison. The Wisconsin study followed two groups of rhesus monkeys for 20 years and found that monkeys on a calorie-restricted diet lived longer than those on a standard diet. Beyond longevity, the parallel NIA and Wisconsin studies have reported similar beneficial health effects of calorie-restriction. Both studies found that certain age-related diseases – including diabetes, arthritis, diverticulosis and cardiovascular problems – occurred at an earlier age in monkeys on the standard diet compared to those on calorie restriction. However, this observation was not statistically significant in the NIA study. NIA researchers did find that monkeys started on calorie restriction at an early age had a statistically significant reduction in cancer incidence. NIA researchers also found that while calorie restriction had a beneficial effect on several measures of metabolic health and function in monkeys who were started on the special diet regimen during old age (at 16 to 23 years), it did not have the same positive outcome for monkeys started on calorie restriction at a young age (less than 14 years). In the Wisconsin study, all the monkeys were 7 to 14 years when started on calorie restriction. … Differences in the monkeys’ meal and other nutritional factors were cited as possible explanations for NIA’s and Wisconsin’s different outcomes. Both studies used a similar percentage of calorie restriction with their intervention groups; however, the Wisconsin monkeys in both the calorie restricted and control groups were eating more and weighed more than the matched NIA monkeys. … NIA researchers cited genetics as another possible reason for their differing results. NIA monkeys had a greater genetic diversity, originating from China and India. Wisconsin’s monkeys came only from an Indian colony.”

A VIEW OF DIET AND AGING
Wednesday, August 29, 2012
http://www.fightaging.org/archives/2012/08/a-view-of-diet-and-aging.php
A review paper: “Nutrition has important long-term consequences for health that are not only limited to the individual but can be passed on to the next generation. It can contribute to the development and progression of chronic diseases thus effecting life span. Caloric restriction (CR) can extend the average and maximum life span and delay the onset of age-associated changes in many organisms. CR elicits coordinated and adaptive stress responses at the cellular and whole-organism level by modulating epigenetic mechanisms (e.g., DNA methylation, posttranslational histone modifications), signaling pathways that regulate cell growth and aging (e.g., TOR, AMPK, p53, and FOXO), and cell-to-cell signaling molecules (e.g., adiponectin). The overall effect of these adaptive stress responses is an increased resistance to subsequent stress, thus delaying age-related changes and promoting longevity. In human, CR could delay many diseases associated with aging including cancer, diabetes, atherosclerosis, cardiovascular disease, and neurodegenerative diseases.”

WORK ON BLOCKING DAMAGE IN BRAIN INJURY
Wednesday, August 29, 2012
http://www.fightaging.org/archives/2012/08/work-on-blocking-damage-in-brain-injury.php
Some of the damage that occurs in brain injury is secondary to the initial trauma and takes place at the level of cellular components. Researchers here demonstrate a possible way to stop that from happening: “Treatment with an agent that blocks the oxidation of an important component of the mitochondrial membrane prevented the secondary damage of severe traumatic brain injury (TBI) and preserved function that would otherwise have been impaired. … For the study, the research team conducted a global assessment of all the phospholipids in rat brain cells. This revealed that damage from TBI was nonrandom and mostly involved cardiolipin, a phospholipid that is found in the membranes that form mitochondria, the cell’s powerhouse. They noted that in the healthy animal, only 10 of the 190 cardiolipin species were modified by oxygen, but after a brain injury, the number of oxidized species rose many-fold. The researchers then developed an agent, called XJB-5-131, which can cross the blood-brain barrier and prevent the oxidation of cardiolipin. Using an established research model of severe TBI, the agent or a placebo was injected into the bloodstream of rats five minutes and again 24 hours after head injury. In the weeks that followed, treated animals performed akin to normal on tests of balance, agility and motor coordination, learning, and object recognition, while placebo-treated animals showed significant impairment. The results indicate that blocking cardiolipin oxidation by XJB-5-131 protected the brain from cell death. … a targeted oxidation-blocker might also be beneficial in the treatment of other neurological disorders, such as Parkinson’s disease, amyotrophic lateral sclerosis, or ALS, and stroke.”

MORE ON DNA METHYLATION AND HUMAN LONGEVITY
Tuesday, August 28, 2012
http://www.fightaging.org/archives/2012/08/more-on-dna-methylation-and-human-longevity.php
A great deal of data is being generated on patterns of DNA methylation, aging, and variations in human longevity: “(1) we evaluated the DNA methylation from peripheral leukocytes of 21 female centenarians, their 21 female offspring, 21 offspring of both non-long-lived parents, and 21 young women … (2) we compared the DNA methylation profiles of these populations … We observed an age-related decrease in global DNA methylation and a delay of this process in centenarians’ offspring. Interestingly, literature data suggest a link between the loss of DNA methylation observed during aging and the development of age-associated diseases. Genome-wide methylation analysis evidenced DNA methylation profiles specific for aging and longevity: (1) aging-associated DNA hypermethylation occurs predominantly in genes involved in the development of anatomical structures, organs, and multicellular organisms and in the regulation of transcription; (2) genes involved in nucleotide biosynthesis, metabolism, and control of signal transmission are differently methylated between centenarians’ offspring and offspring of both non-long-lived parents, hypothesizing a role for these genes in human longevity. Our results suggest that a better preservation of DNA methylation status, a slower cell growing/metabolism, and a better control in signal transmission through epigenetic mechanisms may be involved in the process of human longevity. These data fit well with the observations related to the beneficial effects of mild hypothyroidism and insulin-like growth factor I system impairment on the modulation of human lifespan.”

CYTOMEGALOVIRUS AND TYPE 2 DIABETES RISK
Tuesday, August 28, 2012
http://www.fightaging.org/archives/2012/08/cytomegalovirus-and-type-2-diabetes-risk.php
Cytomegalovirus (CMV) is a persistent and very common herpesvirus that is thought to be a major contributor to the age-related decline of the immune system, due to an ever increasing portion of its limited number of cells becoming specialized to CMV and thus unavailable for other duties. Various past studies have linked CMV with forms of age-related frailty, but here the researchers find an association with type 2 diabetes – which is interesting and perhaps somewhat unexpected, given that type 2 diabetes is essentially a lifestyle disease: “Cytomegalovirus (CMV) infection has been reported to contribute to the pathogenesis of type 1 diabetes and post-transplantation diabetes. However, CMV infection has not been evaluated as a possible risk factor for type 2 diabetes. Our aim was to investigate potential associations between CMV seropositivity, CMV IgG antibody level and glucose regulation in the oldest old. … CMV seropositive subjects were more likely to have type 2 diabetes (17.2% vs 7.9%), had a higher level of HbA1c and higher non-fasting glucose in the oldest olds. These associations remained significant after adjustment for possible confounders. CMV IgG antibody level was not significantly associated with glucose regulation … In the oldest old, CMV seropositivity is significantly associated with various indicators of glucose regulation. This finding suggests that CMV infection might be a risk factor for the development of type 2 diabetes in the elderly.”

HOW LONG DO YOU WANT TO LIVE?
Monday, August 27, 2012
http://www.fightaging.org/archives/2012/08/how-long-do-you-want-to-live.php
Here is an example to show that the urge to conform is somewhat stronger than the urge to live, and never mind the urge to think critically. People will tend to say that they want to be in the majority position now, no matter what that might be, and depending on how you phrase the question, the vast majority will tell you that they want to age to death and have a life that is no longer than that of their parents. Yet if longer lives were already common, those very same people would answer that they wanted to live those longer lives. It is frustrating, to say the least, the degree to which people live in the moment and blind themselves to what might be created: “How many years might be added to a life? A few longevity enthusiasts suggest a possible increase of decades. Most others believe in more modest gains. And when will they come? Are we a decade away? Twenty years? Fifty years? Even without a new high-tech ‘fix’ for aging, the United Nations estimates that life expectancy over the next century will approach 100 years for women in the developed world and over 90 years for women in the developing world. (Men lag behind by three or four years.) Whatever actually happens, this seems like a good time to ask a very basic question: How long do you want to live? Over the past three years I have posed this query to nearly 30,000 people at the start of talks and lectures on future trends in bioscience, taking an informal poll as a show of hands. To make it easier to tabulate responses I provided four possible answers: 80 years, currently the average life span in the West; 120 years, close to the maximum anyone has lived; 150 years, which would require a biotech breakthrough; and forever, which rejects the idea that life span has to have any limit at all. I made it clear that participants should not assume that science will come up with dramatic new anti-aging technologies, though people were free to imagine that breakthroughs might occur – or not. The results: some 60 percent opted for a life span of 80 years. Another 30 percent chose 120 years, and almost 10 percent chose 150 years. Less than 1 percent embraced the idea that people might avoid death altogether. These percentages have held up as I’ve spoken to people from many walks of life in libraries and bookstores; teenagers in high schools; physicians in medical centers; and investors and entrepreneurs at business conferences. I’ve popped the question at meetings of futurists and techno-optimists and gotten perhaps a doubling of people who want to live to 150 – less than I would have thought for these groups. Rarely, however, does anyone want to live forever, although abolishing disease and death from biological causes is a fervent hope for a small scattering of would-be immortals.”

WIRING UP ENGINEERED TISSUE
Monday, August 27, 2012
http://www.fightaging.org/archives/2012/08/wiring-up-engineered-tissue.php
This is interesting, the early stirrings of something that may change the tenor of future tissue engineering if carried through to its logical conclusions. Why build a plain heart if you can build a sensor-laden heart with its own embedded network for monitoring and medical intervention? From the release: “A multi-institutional research team has developed a method for embedding networks of biocompatible nanoscale wires within engineered tissues. These networks – which mark the first time that electronics and tissue have been truly merged in 3D – allow direct tissue sensing and potentially stimulation, a potential boon for development of engineered tissues that incorporate capabilities for monitoring and stimulation, and of devices for screening new drugs. … One of the major challenges in developing bioengineered tissues is creating systems to sense what is going on (e.g., chemically, electrically) within a tissue after it has been grown and/or implanted. Similarly, researchers have struggled to develop methods to directly stimulate engineered tissues and measure cellular reactions. … In the body, the autonomic nervous system keeps track of pH, chemistry, oxygen and other factors, and triggers responses as needed. We need to be able to mimic the kind of intrinsic feedback loops the body has evolved in order to maintain fine control at the cellular and tissue level. … With the autonomic nervous system as inspiration, [scientists] built mesh-like networks of nanoscale silicon wires – about 80 nm in diameter – shaped like flat planes or in a ‘cotton-candy’-like reticular conformation. The networks were porous enough to allow the team to seed them with cells and encourage those cells to grow in 3D cultures. … Previous efforts to create bioengineered sensing networks have focused on 2D layouts, where culture cells grow on top of electronic components, or on conformal layouts where probes are placed on tissue surfaces. It is desirable to have an accurate picture of cellular behavior within the 3D structure of a tissue, and it is also important to have nanoscale probes to avoid disruption of either cellular or tissue architecture.”

______________________________

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SEOUL, South Korea, Sept. 8, 2012 /PRNewswire/ — Dr. Jeong-Chan Ra, founder and largest shareholder of RNL Bio (www.rnl.co.kr),an international biotechnology research and development firm, has pledged to give away 90% of his personal wealth over the next 10 years to promote social causes consistent with the values of human life. Dr. Ra will donate 90% privately owned equity, equity-related bonds, warrants and other assets of RNL Bio Co. and RNL Bio affiliates to the following four non-profit organizations: Bethesda Life Foundation, Yesung Medical Corporation, Academia Christiana of Korea, and Central Christian Academy.

Since 2009, Dr. Ra, based on the value of respect for human life, has supported various causes that promote social justice, access to health care, and wellness across the lifespan. A donation of $1M from Dr. Ra established the Bethesda Life Foundation (http://www.bethesdalife.org/index.php/donate), a nonprofit organization for social welfare, committed to providing patients with chronic rare diseases with access to medical care and life-saving therapies.

Through his donation, Dr. Ra wants to continue his healthcare support for those with retractable diseases as well as support for educating children of underprivileged patients with such diseases. Dr. Ra “hoped that this donation becomes the turning point for RNL Bio to fulfill its responsibility as a society helping enterprise.” He also explained that while he continues to serve as a stem cell scientist at RNL Stem Cell Technology Institute he plans to focus his efforts upon the research on finding cure of rare chronic diseases.

Dr. Ra’s gift is made in the spirit of other major corporate leaders worldwide who have become instrumental philanthropists by converting their personal fortune into a foundation for good, including Bill Gates, Warren Buffett and Bill Clinton. Dr. Ra is mirroring Mr. Buffet and Mr. Gates’ contributions that were made in late 2010 for the wealthy to donate at least 50% of their personal wealth.

A Commitment to Healing and Social Justice

Bethesda Life Foundation supports patients of rare and chronic disease in the socially and economically underprivileged class with various medical help. The mission of Bethesda Life Foundation is, based on the value life-respect, for all mankind to enjoy a healthy and happy life.

Yesung Medical Corporation operates the Bethesda General Hospital, located in Yangsan, Korea and the hospital has advanced in specializing theregenerative medicine using adult stem cell research and technology. With the realization of 100-year longevity utilizing stem cells as the mission, the corporation is enhancing the medical technology of respect for life.

Academia Christiana was established in order to contribute to establish the mental discipline of the country and people by Christian studies to meet the growth and development of the Church in Korea. Academia Christiana of Korea has been organizing academic seminars and public lectures, publishing academic research papers and operating Ulaanbaatar University in Mongol.

Founder Pastor Billy Kim and his wife were sent out to return to Korea in 1959 as missionaries from the Christian Service Center, an international mission organization, based in Ohio, USA and appointed to Suwon Central Baptist Church. After establishing Central Kindergarten in 1978, he obtained the lot in Woncheon-dong, Paldal-gu, Suwon, Korea, received the approval of School Corporation to open the Central Christian School to achieve the goal of nurturing Christians to become the world’s salt and light through cooperation of homes, schools and churches.

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Posted on: 7:20 pm, August 31, 2012, by Kelley Hoskins, updated on: 07:14pm, August 31, 2012

ST. LOUIS (KPLR)-A diagnosis of multiple sclerosis doesnt happen to just one person, it affects the whole family. Its a life long disease , and an unpredictable We take a closer look a two ordinary people dealing with life and the ups and downs of the disease. Two very different people with two very different life styles. MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively

One is aprominent St. Louis Pastor the other a local nurse . But what they do have is in common they both are battling multiple sclerosis. Pastor Charles Roach is very active at Trinity Mount Carmel Baptist Church in St. Louis County .He also served his country in the United States Air Force as Staff Sergeant.

Each and every Sunday he delivers a powerful message to his congregation. Pastor Roach says multiple sclerosis runs in his family and he wants to empower , equip and educate others about the disease. Its important that all of us to share an experience of some types of difficulty . It may not be physical as mine but it could be mental or emotional . But one has to learn how to conquer that. We have enough tenacity in us to conquer any difficut situation, said Pastor Roach.

Now we take a look a Michelle Keating a health care provider. a phenomenal women and volunteer with the St. Louis Gateway Area Chapter of Multiple Sclerosis. Keating says the diagnosis changed his life forever. Together they both have learned to adjust in different ways as MS affects what they can do .My first reaction was of denial and worry , what would my future be like?But my future has been very beautiful. I have two children I have raised and I continue my career as a nurse and wife.

Multiple sclerosis (MS) is a potentially debilitating disease in which your bodys immune system eats away at the protective sheath that covers your nerves. This interferes with the communication between your brain and the rest of your body. Ultimately, this may result in deterioration of the nerves themselves, a process thats not reversible.

Symptoms vary widely, depending on the amount of damage and which nerves are affected. People with severe cases of multiple sclerosis may lose the ability to walk or speak. Multiple sclerosis can be difficult to diagnose early in the course of the disease because symptoms often come and go sometimes disappearing for months.

Like anyone else in the MS movement, they actively volunteer and seek effective means to move closer to a world free of MS.

At this point theres no cure for multiple sclerosis. If you would like to join the movement with over 3,000 other cyclists riding towards a world free of MS, you can team up for the Bike MS Gateway Getaway Ride September 8&9 2012 in Columbia Missouri.

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Fighting Back -Ordinary People Battling The Everyday Effects Of MS

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PHILADELPHIA Researchers at the Perelman School of Medicine will receive $11.9 million over the next five years from the National Institute of Neurological Disorders and Stroke (NINDS) for the Penn Udall Center for Parkinsons Disease (PD) research. This grant is a renewal of an NINDS funded PD center that successfully completed its research program over the last five years.

Parkinsons is one of the most common neurodegenerative diseases, second only to Alzheimer’s disease in the number of people affected. Estimates suggest that approximately 1,000,000 Americans have PD.

Cognitive impairment, executive dysfunction and dementia add to the burden of PD and increase mortality, but the underlying basis of dementia in PD is unclear. There are no effective disease modifying therapies. Despite important research advances, the exact causes of PD, Parkinsons with dementia (PDD), and dementia with Lewy Bodies (DLB) are unknown. To address this, a NINDS Morris K. Udall Parkinsons Disease Research Center of Excellence was launched at Penn in 2007.

This renewal for years six through ten of the Penn Udall Center builds on recent progress advancing researchers understanding of the progression of PDD from normal cognition to cognitive impairment, executive dysfunction and dementia in PDD, and disease progression in DLB, in addition to central nervous system degeneration mediated by progressive accumulations of pathological alpha-synuclein.

Recent Penn Udall Center studies raise the provocative, but highly plausible possibility that the progression of PD/PDD/DLB is linked to the cell-to-cell spread of pathological alpha-synuclein. Therefore, the overarching goals of the Penn Udall Center are to explore mechanisms of disease progression and alpha-synuclein transmission through collaborations between basic and translational research projects that work with each of the cores to implement the mission of the Penn Udall Center in the renewal period.

“The Penn Udall Center will elucidate mechanisms of cognitive impairment, executive dysfunction and dementia in Parkinsons Disease as well as mechanisms of neurodegeneration that are mediated by the transmission of alpha-synuclein pathologies, said Center Director John Trojanowski, MD, PhD, director of Penn’s Institute on Aging and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine. By using new approaches and model systems to achieve its goals, the Penn Udall Center will investigate novel disease mechanisms in Parkinsons and advance efforts to develop new interventions and better diagnostics for this disorder.

The Penn Udall Center is based on 20 years of basic research on neurodegenerative diseases within the Center for Neurodegenerative Disease Research and clinical programs at the Parkinsons Disease and Movement Disorders Center, both within Penn Medicine.

The Udall Centers of Excellence were developed in honor of former Congressman Morris K. Udall, who died in 1998 after a long battle with Parkinsons disease. The first center was named in 1997.

The Udall Center renewal grant (P50 NS053488) will include four core groups focusing on clinical care: neuropathology, biomarker and genetics; data management, biostatistics and bioinformatics; and administration. Planned projects will look for an immune therapy to block PD transmission in animal models, biomarkers to evaluate and predict cognitive decline in Lewy Body spectrum disorders, language and executive dysfunction in PD, and how transmission of alpha-synuclein occurs in neurons. The Penn Udall Center team includes John Trojanowski, MD, PhD, Howard Hurtig, MD, Dan Weintraub, MD, Vivianna Van Deerlin, MD, PhD, Edward B. Lee, MD, PhD, Sharon Xie, PhD, Li-San Wang, PhD, Alice Chen-Plotkin, MD, Murray Grossman, MD, PhD, Rachel Gross, MD, Kelvin Luk, PhD, and Virginia M-Y Lee, PhD, MBA.

The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report’s survey of research-oriented medical schools. The School is consistently among the nation’s top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 fiscal year.

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Perelman School of Medicine Granted $11.9 Million Renewal of NINDS Support for Morris K. Udall Parkinson's Disease …

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WEDNESDAY, Aug. 29 (HealthDay News) — Four indicators, or “biomarkers,” found in cerebrospinal fluid can help differentiate patients with Alzheimer’s disease from those with other forms of dementia, and a different biomarker can distinguish patients with Parkinson’s disease from those with parkinsonian disorders, researchers say.

Overlapping symptoms, especially in the early stages, can make it difficult to distinguish between regular Parkinson’s disease and atypical Parkinsonism, and also between Alzheimer’s disease and other forms of dementia, the study authors explained.

The investigators identified the five biomarkers by analyzing cerebrospinal fluid samples from 453 patients with Parkinson’s, Parkinson’s disease with dementia, Alzheimer’s and other forms of dementia.

“Together with earlier published data, our results indicate that these five [cerebrospinal fluid] biomarkers might have clinical value in the differential diagnosis of dementia and/or parkinsonism,” concluded Dr. Sara Hall, of Skane University Hospital in Sweden, and colleagues.

The study was published online Aug. 27 in the journal Archives of Neurology.

The findings represent “a significant step forward, demonstrating how a relatively modest panel of robust [cerebrospinal fluid] protein biomarkers can categorize dementias and parkinsonian syndromes on the basis of pathology rather than clinical/behavioral changes,” Dr. Richard Perrin, of the Washington University School of Medicine in St. Louis, wrote in an accompanying editorial.

The use of these indicators in cerebrospinal fluid could improve the efficiency of clinical trials and speed up the development and evaluation of new treatments for neurological diseases, Perrin concluded.

— Robert Preidt

Copyright 2012 HealthDay. All rights reserved.

SOURCE: Archives of Neurology, news release, Aug. 27, 2012

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Discovery May Improve Diagnosis of Alzheimer's, Parkinson's

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Re: Dementia case puts Senate on the spot, Aug. 29

Dementia to the point of being declared incompetent does not happen overnight? Didnt any of Joyce Fairbairns colleagues notice that something was not quite right? Then again, I guess that its all relative.

Claude Gannon, Markham

So a Senator declared mentally incompetent continued for four months to perform her duties, and none of her colleagues noticed? Or worse, perhaps, noticed but said or did nothing? Makes you wonder about their mental competence.

Stephen Whitzman, Toronto

I suspect Prime Minister Stephen Harpers promise of Senate reform has slipped his mind until the next election. Since our country is foolish enough to reduce corporate taxes for greedy banks, insurance and gas companies, I may still have a shot at becoming a senator.

Although I am not a good fighter, I could drink a lot at lunch and be abusive to my staff in the afternoon. Do not worry about how I vote on bills because I will not show up very often anyway. With the generous salary and quarter million dollar plus expense account, I could probably attract a wife over 40 years my junior and take her on government-paid business-class flights, but I promise not to fight with her until we land.

Although I was never in the NHL I did not get hit too often in peewee so I am sure I could be a wise member of the upper chamber well into my old age. I hear government pensions are very generous and it will take Mr. Harper a few more elections to make insignificant changes to the plan.

My main qualification as a Conservative senator would be that I would support all of their bills no matter how harmful they are to the environment or how much pressure it puts on the working class.

Jim Ypma, Georgina

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Multiple sclerosis (MS) is an autoimmune disease that affects approximately 400,000 people in the United States. Caused by damage to the myelin sheath the protective coating of the nerves in the brain MS is marked by an array of symptoms, including muscle spasms, loss of vision and difficulty moving arms and legs.

While there is no cure for MS, there are various treatments available for those suffering from the disease. Dr. Michael Devereaux, a neurologist for University Hospitals Case Medical Center, spoke with FoxNews.com about the many options for MS patients looking for symptom relief. According to him, there are two main goals when it comes to treating MS.

One is treating the acute attacks, Devereaux said. And then, what youre really interested in even more is reducing the frequency of attacks and reducing overall disability over time. Thats been a harder to question to answer from studies and the like, because all the drugs are promoting the idea that they can reduce frequency and overall disability, but theres been some debate about that.

Modifying the disease

During MS, white blood cells, called T-cells, become activated and cross the blood-brain barrier into the brain. While there, they cause an inflammatory response, ultimately damaging the myelin sheath and destroying the axons of the nerves.

Various drugs, called immunologeratory agents, have been developed to dampen the inflammatory response for those with relapsing-remitting MS. The main injectable drugs include beta interferons (Avonex, Betaseron, Extavia), glatiramer acetate (Copaxone), and the somewhat controversial drug, natalizumab (Tysabri)

Tysabri has been in the news a lot because it led to breakouts of another condition progressive multifocal encephalopathy (PML), Devereaux said. Its a very small percentage of cases. Its often given to people not doing well. Its highly effective, but it has this significant, but small, real risk.

The last agent is an oral agent called fingolimod (Gilenya), and is the most convenient for patients, according to Devereaux.

Treating MS attacks

MS is marked by periods of remission, alternating with periods of mild to severe exacerbations. While the agents are used to prevent these flare-ups, there are also treatment options for when exacerbations do occur. The main treatment is to give patients a high dose of glucocorticosteroids

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Current treatment options for multiple sclerosis

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County Hall, Norwich.

David Freezer Friday, August 31, 2012 5:52 PM

Dementia patients and their families have been reassured that every effort will be made to smooth their transition from a closing day centre in Blofield to a larger unit in Norwich.

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News that Stocks Lane Day Centre is to close has been confirmed by Norfolk County Council and been described as very bad news by one person involved with the Blofield day centre.

The person, who asked not to be named, said: The patients will be moved from a very small, intimate and secure nine-person unit, to a very large unit.

This is very bad news because people with dementia dont like crowds or noise.

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Norfolk dementia unit to close this autumn

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COA to host dementia caregivers event

SAGINAW Living with a diagnosis of dementia or Alzheimers Disease can be a defining moment in anyones life. On Thursday, Sept. 27, the Dementia Advisory Board, a program of the Saginaw County Commission on Aging, will host a conference for caregivers working with persons with dementia.

The program will take place at the Riverfront Grille, 128 N Front St. in Chesaning from 9 a.m. to 1 p.m. and includes lunch (with a $5 donation).

We have seen such an increase in cases with people caring for loved ones with Alzheimers Disease or some other form of dementia, said Nicole Wiesenauer, care manager at the Saginaw Commission on Aging. Caregiver stress is at an all-time high. We are hoping to educate the residents of Saginaw County about this disease and to invite them to take advantage of the resources and support that are available throughout our area.

Carol Waarala, LMSW from Avalon Hospice, will be the keynote speaker for the event, and several local agencies and memory care experts will be on hand to provide information and answer questions. Seating is limited and reservations can be made by calling Wiesenauer at 1-866-763-6336.

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A new study finds that babies of older fathers have increased health risks due to genetic mutations that increase with age.

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SALT LAKE CITY Older fathers are more likely to father a child with autism or schizophrenia, due to genetic mutations that increase with age, according to a new study published online Wednesday in the journal Nature.

Researchers examined 78 Icelandic families with children who had been diagnosed with autism or schizophrenia. They found that a 40-year-old passes 65 genetic mutations to his child, while a 20-year-old passes 25. Fathers transmitted two new mutations in their DNA each additional year, while mothers passed on 15 new mutations at every age.

The research corrected false assumptions that the risks lie in the older ages of women alone, the Los Angeles Times reported. “Although older mothers are more likely to have children with chromosomal disorders such as Down syndrome because of problems with older eggs, the study found that practically all of the novel mutations detected in children came from the father’s sperm.”

Experts said the finding might influence reproductive decisions, but was hardly reason to forgo fatherhood at an older age, The New York Times reported. There is a 2 percent overall risk to a man in his 40′s or older, as well as other contributing factors that remain unknown.

The study found that as many as 20 to 30 percent of cases of autism diagnoses were linked to an older average age in fathers.

“The findings also give us insight into how our gene pool is changing, and what, in modern times, is driving the genetic diversity that is critical to the survival of our species,” the Washington Post observed. “Every difference in our DNA that distinguishes each of us as individuals, or that separates Homo sapiens from other species, arguably got its start as a mutation. Some of these alterations in DNA occur by chance, during cell division, others are triggered by exposure to environmental factors, while still others are selected for when they happen to confer some survival advantage, such as an ability to ward off disease.”

The only important thing when it came to explaining the mutations was the age of the father, study author Kari Stefansson, the chief executive officer of deCode Genetics, told the Bloomberg News. Theres very little else to be accounted for. Thats a stunning observation.

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Autism and schizophrenia in kids linked to fathers' age

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By Claire OSullivan

Saturday, September 01, 2012

Children with autism are having their home tuition halted and instead are being ordered to attend new special needs units, according to one of the countrys leading autism support groups.

The Department of Education announced that 91 new classes for children with special needs are to be introduced at special needs units at the countrys schools.

Shine Ireland, the Irish Progressive Association for Autism, initially welcomed the investment but yesterday criticised it as “rash cost- cutting” saying they hadnt realised then that such units would be used to replace more costly home tuition.

The home tuition service is used by hundreds of children with autism, some as young as two, who need specific learning support, seen as a form of early one- on-one intervention.

Shine Ireland said families have been told in the past fortnight their home tuition will no longer be funded.

Its CEO Kieran Kennedy said: “The children are being sent wherever. There has been no consultation, no chance to talk to teachers or the principal at school.

“There has been no chance to see if the needs of child can be met. No parent of a regular child would be told that you have to put your child into a particular school at four years of age.”

A Department of Education spokesperson denied grants were being cut.

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(CBS News) NORTHPORT, N.Y. – It’s a story that makes you think, “What are the chances?” It started with a mystery at a nursing home we visited, “On the Road.”

John Angerame says when you love someone with advanced dementia — like his father has — you can’t help but wonder: Are they still in there?

John asks his dad Augie for even the littlest signs that he’s present, like a wink or blink.

Fortunately, although Augie can’t communicate, by all indications he is aware — beyond words.

Augie Angerame served in the Korean War, in an artillery unit. He was a medic, which may partly explain his recent behavior at his VA nursing home on Long Island.

A few months ago, Augie started going into the room of another veteran with dementia named Frank Dibella.

“And I was like, ‘What’s this man doing?’” recalled Frank’s daughter, Mary Rose Monroe. “He’d rub his back and then he’d walk away.”

“Just check on him,” John Angerame added, “like maybe a medic would do as he made rounds.”

The kids agreed: It seemed like Augie was trying to care for Frank — like he was back in the war. Frank didn’t seem to mind. The staff eventually moved the two men into the same room.

And that’s when John started putting the pieces together.

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Newswise UCLA researchers have discovered a type of cell that is the missing link between bone marrow stem cells and all the cells of the human immune system, a finding that will lead to a greater understanding of how a healthy immune system is produced and how disease can lead to poor immune function.

The studies were done using human bone marrow, which contains all the stem cells that produce blood during postnatal life.

We felt it was especially important to do these studies using human bone marrow as most research into the development of the immune system has used mouse bone marrow, said study senior author Dr. Gay Crooks, co-director of the Eli and Edythe Broad Center of Regenerative Medicine and a co-director of the Cancer and Stem Cell Biology program at UCLAs Jonsson Comprehensive Cancer Center. The few studies with human tissue have mostly used umbilical cord blood, which does not reflect the immune system of postnatal life.

The research team was intrigued to find this particular bone marrow cell because it opens up a lot of new possibilities in terms of understanding how human immunity is produced from stem cells throughout life, said Crooks, a professor of pathology and pediatrics.

Understanding the process of normal blood formation in human adults is a crucial step in shedding light on what goes wrong during the process that results in leukemias, or cancers of the blood.

The study appears Sept. 2 in the early online edition of Nature Immunology.

Before this study, researchers had a fairly good idea of how to find and study the blood stem cells of the bone marrow. The stem cells live forever, reproduce themselves and give rise to all the cells of the blood. In the process, the stem cells divide and produce intermediate stages of development called progenitors, which make various blood lineages like red blood cells or platelets. Crooks was most interested in the creation of the progenitors that form the entire immune system, which consists of many different cells called lymphocytes, each with a specialized function to fight infection.

Like the stem cells, the progenitor cells are also very rare, so before we can study them we needed to find the needle in the haystack. said Lisa Kohn, a member of the UCLA Medical Scientist Training Program and first author in the paper.

Previous work had found a fairly mature type of lymphocyte progenitor with a limited ability to differentiate, but the new work describes a more primitive type of progenitor primed to produce the entire immune system, Kohn said

Once the lymphoid primed progenitor had been identified, Crooks and her team studied how gene expression changed during the earliest stages of its production from stem cells.

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Children with Autism will soon have a new place to receive services in Siouxland.

The PierCenter for Autism, a non-profit organization, plans to open a center sometime this fall at 709 Iowa Street, according to founder Josh Cobbs.

Cobbs, whose 12-year-old son Noah has autism, said he formed the non-profit in hopes of filling a great and growing need in Sioux City.

According to a Centers for Disease Control and Prevention survey released in March, 1 in 88 children in the United States has autism. The prevalence of the condition has risen nearly 80 percent over the last decade, according to the CDC.

At the PierCenter, board certified behavior analysts will offer applied behavior analysis therapy to school-age children and certified teachers will also be on hand to provide tutoring support. From there, Cobbs said he only expects services to slowly grow.

“We really want to try to connect the spans as they go through life, so if an individual needs something at age 7, we want to provide that service for them,” Cobbs said. “If they need something at age 17, because those needs are different, we want to be able to provide that service.”

Many Sioux City area families, including his, Cobbs said, have driven long distances in order for their children to receive services.

“That’s common to a lot of families in this area. They drive to maybe Des Moines or Omaha or Sioux Falls or Iowa City,” he said. “We’re not going to be able to replace all of those services that families go out of town for, but we’re hoping to certainly supplement and cover some of those services.”

Although Cobbs said his group has talked about opening a center for children with autism for years, he said the idea took off in January. A seven-person board was formed and an agreement was reached to lease space from St. Joseph’s Catholic Church.

The center’s name, Cobbs said, plays off of the meaning of the word “pier” – a support for a bridge.

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Theres a saying: If you meet one person with autism, youve met one person with autism, Cathy Louden said.

Autism is a term used for complex disorders of brain development and symptoms tend to be very personal and different for each person.

These disorders are characterized, in varying degrees, by difficulties in social interaction, verbal and nonverbal communication and repetitive behaviors, the Autism Society of West Shore website said.

In Loudin’s home it rings true, she and her husband, Shawn Loudin and their two boys, Jason, 8, and Andrew, 11, are all have autism and they are all very different, she said, each with their own needs, their own quirks.

Andy is more withdrawn, Jason is the social butterfly, Cathy Loudin said. But it flips sometimes.

Andrew perfers to be left alone. Jason will pick on his brother.

Yet each has similarities too; they can focus for some time on electronic games.

Neither Cathy nor Shawn knew they had autism until they started noticing signs in their sons. They recognized things from their own childhoods, and it just made sense. The knowledge has strengthened their relationship and has given them a better understanding of each other, she said. They’ve learned to avoid situations that make them uncomfortable, such as large crowds.

As she learns the needs of her boys, Cathy found having a solid support system was a must. The family found that in the Autism Society of West Shore, the local chapter of the Autism Society of America.

ASWS has monthly coffee socials, Cathy said, where parents can just talk and share tips, tricks and ideas. They have a free speakers series with topics such as how to get through the individualized education plan, she said.

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Autism: It's personal

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Public release date: 23-Aug-2012 [ | E-mail | Share ]

Contact: Lisa Merkl lkmerkl@uh.edu 713-743-8192 University of Houston

HOUSTON, Aug. 23, 2012 Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson’s disease.

Affecting more than 500,000 people in the U.S., Parkinson’s disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.

“LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system,” said CNRCS director and professor Jan-ke Gustafsson, whose lab discovered LXRbeta in 1995. “The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders.”

To better understand the relationship between LXRbeta and Parkinson’s disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson’s in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.

The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.

“LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons,” Gustafsson said. “Microglia are the police of the brain, keeping things in order. In Parkinson’s disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson’s disease.”

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Gustafsson, professor Margaret Warner, research assistant professor Xin-Jie Tan, and postdoctoral fellows Wanfu Wu and Yubing Dai authored the PNAS study, which is available at http://www.pnas.org/content/early/2012/07/18/1210833109.abstract.

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Therapeutic avenues for Parkinson's investigated at UH

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Researchers have shown that people with Parkinson’s disease performed markedly better on a test of working memory after a night’s sleep, and sleep disorders can interfere with that benefit.

While the classic symptoms of Parkinson’s disease include tremors and slow movements, Parkinson’s can also affect someone’s memory, including “working memory.”

Working memory is defined as the ability to temporarily store and manipulate information, rather than simply repeat it. The use of working memory is important in planning, problem solving and independent living.

The findings underline the importance of addressing sleep disorders in the care of patients with Parkinson’s, and indicate that working memory capacity in patients with Parkinson’s potentially can be improved with training. The results also have implications for the biology of sleep and memory.

“It was known already that sleep is beneficial for memory, but here, we’ve been able to analyze what aspects of sleep are required for the improvements in working memory performance,” said postdoctoral fellow Michael Scullin, who is the first author of the paper.

The performance boost from sleep was linked with the amount of slow wave sleep, or the deepest stage of sleep. Several research groups have reported that slow wave sleep is important for synaptic plasticity, the ability of brain cells to reorganize and make new connections.

Sleep apnea, the disruption of sleep caused by obstruction of the airway, interfered with sleep’s effects on memory. Study participants who showed signs of sleep apnea, if it was severe enough to lower their blood oxygen levels for more than five minutes, did not see a working memory test boost.

54 study participants had Parkinson’s disease, and 10 had dementia with Lewy bodies: a more advanced condition, where patients may have hallucinations or fluctuating cognition as well as motor symptoms. Those who had dementia with Lewy bodies saw no working memory boost from the night’s rest. As expected, their baseline level of performance was lower than the Parkinson’s group.

Participants with Parkinson’s who were taking dopamine-enhancing medications saw their performance on the digit span test jump up between the fourth and fifth test. On average, they could remember one more number backwards. The ability to repeat numbers backward improved, even though the ability to repeat numbers forward did not.

Patients needed to be taking dopamine-enhancing medications to see the most performance benefit from sleep. Patients not taking dopamine medications, even though they had generally had Parkinson’s for less time, did not experience as much of a performance benefit. This may reflect a role for dopamine, an important neurotransmitter, in memory.

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Sleep improves memory in Parkinson's patients

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