Pittwater Online News

 COTA – NSW - http://cotansw.com.au/

ABOUT US

The Council on the Ageing NSW (COTA NSW) is the peak organisation for people over 50 in our state. We’re an independent, non-partisan, consumer-based non-government organisation. We work with politicians, policy makers, and service providers as well as media representatives to make sure your views are heard and your needs are met. COTA NSW works to empower and engage people over 50. For decades, we’ve shaped the policies and programs that change lives.

COTA NSW, through constant contact with consumers and consumer groups across the state, through the research it conducts and through partnerships with other NGOs, research bodies and universities, is also an important source of information and advice on issues and decisions that people will navigate through as they live long, healthy, and productive lives. We have always made this information and advice available publically through telephone advice and over eighty Fact Sheets. Browse through our website or contact us and help COTA NSW continue its work in advancing the interests of people over 50.

HAVE YOUR SAY! - 8th of May 2013

We have launched our 2013 COTA NSW Survey. We want to know what you think about important issues. Your input helps to determine the policies and positions we communicate to Government. Everyone who completes the survey goes into a draw to win one of five $50 gift cards. Click the link to access the survey.

Click here to complete the COTA NSW 2013 Survey.

 DEEMING RATES SHOULD BE ADJUSTED - 7th of May, 2013

The Reserve Bank’s decision to cut interest rates today spells bad news for retirees living off their investments, say the consumer lobby for older Australians. The decision to lower the cash rate by 25 basis points to 2.75 per cent was announced this afternoon.

“Today’s decision means the low, fixed incomes of many retirees are set to fall,” said National Seniors chief executive Michael O’Neill. “This rate cut will come as a blow for seniors living off simple investments such as term deposits,” he said. 

“Official deeming rates, used to determine age pension levels, have not kept pace with falling interest rates. This, while essentials such as electricity and gas continue to soar around the country. After six official interest rate cuts, the federal government lowered the deeming rates for the first time in three years in February 2013. They didn’t go far enough; it’s time to drop the deeming rates again.” said O’Neill.

Your Money research conducted in November 2012 showed returns from term deposits and online savings accounts had slumped 15 to 30 per cent.

 The Benevolent Society has turned 200 this week - First Old Age Pension in the world approved after Benevolent Society campaign - 1901

Benevolent Society President Arthur Renwick led a five year campaign resulting in the introduction of an Old Age Pension in New South Wales in 1901. This was the first of its kind in the world. Renwick was also the president of the Old Age Pensions League and he fought hard with his colleagues for over five years to secure this pension for the elderly.  In 1898, the Benevolent Society appreciated that the level of aid currently able to be offered to the elderly was insufficient and a survey was conducted of people over the age of 65 who were receiving assistance. It was quite clear that people preferred to live at home with the limited aid the Benevolent Society could provide, no matter how 'humble or wretched' than live in a government insitution which was regarded as 'totally repugnant.'

When it was finally approved by the NSW State Government, the Old Age Pension initially provided a payment of ten shillings per week for men over 65 and women over 60. This was considerably more than The Benevolent Society could afford to give in handouts.  Pensioners had to satisfy certain conditions before they received their payment - each recipient needed to be of good character and to have lived in the colony for at least 25 years.  A strict means test was also applied. The Benevolent Society still supports and campaigns for older people today. 

Health Papers Published this week:

Missing Link in Signals Contributes to Neurodegeneration

May 8, 2013 — In many neurodegenerative diseases the neurons of the brain are over-stimulated and this leads to their destruction. After many failed attempts and much scepticism this process was finally shown last year to be a possible basis for treatment in some patients with stroke. But very few targets for drugs to block this process are known.

What is this missing link? We have known for years that over-stimulated neurons produce nitric oxide molecules. Although this can activate a signal for destruction of cells, the small amount of nitric oxide produced cannot alone explain the damage to the brain. The team now show that a protein called NOS1AP links the nitric oxide that is produced to the damage that results.. NOS1AP binds an initiator of cell destruction called MKK3 and also moves within the cell to the source of nitric oxide when cells are over-activated.. The location of these proteins in cells causes them to convert the over-stimulation signal into a cell destruction response. The team designed a chemical that prevents NOS1AP from binding the source of nitric oxide. This reduces the cell destruction response in cells of the brain and as a result it limits brain lesions in rodents.

This translational research was funded mainly by the Academy of Finland, the European Union and the University of Eastern Finland and used the recently developed high-throughput imaging facilities at the A. I. Virtanen Institute. The researchers hope that continuation of their work could lead to improved treatments for diseases such as stroke, epilepsy and chronic conditions like Alzheimer's disease. As NOS1AP is associated with schizophrenia, diabetes and sudden cardiac death, future research in this area may assist the treatment of a wider range of diseases.

L.-L. Li, V. Ginet, X. Liu, O. Vergun, M. Tuittila, M. Mathieu, C. Bonny, J. Puyal, A. C. Truttmann, M. J. Courtney. The nNOS-p38MAPK Pathway Is Mediated by NOS1AP during Neuronal Death. Journal of Neuroscience, 2013; 33 (19): 8185 DOI: 10.1523/JNEUROSCI.4578-12.2013

Dynamic Behavior of Progenitor Cells in Brain Discovered

May 9, 2013 — By monitoring the behavior of a class of cells in the brains of living mice, neuroscientists at Johns Hopkins discovered that these cells remain highly dynamic in the adult brain, where they transform into cells that insulate nerve fibers and help form scars that aid in tissue repair.

Published online April 28 in the journal Nature Neuroscience, their work sheds light on how these multipurpose cells communicate with each other to maintain a highly regular, grid-like distribution throughout the brain and spinal cord. The disappearance of one of these so-called progenitor cells causes a neighbor to quickly divide to form a replacement, ensuring that cell loss and cell addition are kept in balance.

"There is a widely held misconception that the adult nervous system is static or fixed, and has a limited capacity for repair and regeneration," says Dwight Bergles, Ph.D., professor of neuroscience and otolaryngology at the Johns Hopkins University School of Medicine. "But we found that these progenitor cells, called oligodendrocyte precursor cells (OPCs), are remarkably dynamic. Unlike most other adult brain cells, they are able to respond to the repair needs around them while maintaining their numbers."

OPCs can mature to become oligodendrocytes - support cells in the brain and spinal cord responsible for wrapping nerve fibers to create insulation known as myelin. Without myelin, the electrical signals sent by neurons travel poorly and some cells die due to the lack of metabolic support from oligodendrocytes. It is the death of oligodendrocytes and the subsequent loss of myelin that leads to neurological disability in diseases such as multiple sclerosis.

During brain development, OPCs spread throughout the central nervous system and make large numbers of oligodendrocytes. Scientists know that few new oligodendrocytes are born in the healthy adult brain, yet the brain is flush with OPCs. However, the function of OPCs in the adult brain wasn't clear.

To find out, Bergles and his team genetically modified mice so that their OPCs contained a fluorescent protein along their edges, giving crisp definition to their many fine branches that extend in every direction. Using special microscopes that allow imaging deep inside the brain, the team watched the activity of individual cells in living mice for over a month.

The researchers discovered that, far from being static, the OPCs were continuously moving through the brain tissue, extending their "tentacles" and repositioning themselves. Even though these progenitors are dynamic, each cell maintains its own area by repelling other OPCs when they come in contact.

"The cells seem to sense each other's presence and know how to control the number of cells in their population," says Bergles. "It looks like this process goes wrong in multiple sclerosis lesions, where there are reduced numbers of OPCs, a loss that may impair the cells' ability to sense whether demyelination has occurred. We don't yet know what molecules are involved in this process, but it's something we're actively working on. Scar cells are not oligodendrocytes, so the term 'oligodendrocyte precursor cell' may now be outdated," says Bergles. "These cells are likely to have a broader role in tissue regeneration and repair than we thought. Because traumatic brain injuries, multiple sclerosis and other neurodegenerative diseases require tissue regeneration, we are eager to learn more about the functions of these enigmatic cells."

Picture: Montage of three images collected at one-week intervals showing an oligodendrocyte precursor cell migrating towards a lesion (white). (Credit: Ethan Hughes and Dwight Bergles)

Ethan G Hughes, Shin H Kang, Masahiro Fukaya, Dwight E Bergles. Oligodendrocyte progenitors balance growth with self-repulsion to achieve homeostasis in the adult brain. Nature Neuroscience, 2013; DOI: 10.1038/nn.3390

Social Connections Drive the 'Upward Spiral' of Positive Emotions and Health

May 9, 2013 — People who experience warmer, more upbeat emotions may have better physical health because they make more social connections, according to a new study published in Psychological Science, a journal of the Association for Psychological Science.

The research, led by Barbara Fredrickson of the University of North Carolina at Chapel Hill and Bethany Kok of the Max Planck Institute for Human Cognitive and Brain Sciences also found it is possible for a person to self-generate positive emotions in ways that make him or her physically healthier.

"People tend to liken their emotions to the weather, viewing them as uncontrollable," says Fredrickson. "This research shows not only that our emotions are controllable, but also that we can take the reins of our daily emotions and steer ourselves toward better physical health."

To study the bodily effects of up-regulating positive emotions, the researchers zeroed in on vagal tone, an indicator of how a person's vagus nerve is functioning. The vagus nerve helps regulate heart rate and is also a central component of a person's social-engagement system.

Because people who have higher vagal tone tend to be better at regulating their emotions, the researchers speculated that having higher vagal tone might lead people to experience more positive emotions, which would then boost perceived positive social connections. Having more social connections would in turn increase vagal tone, thereby improving physical health and creating an "upward spiral."

To see whether people might be able to harness this upward spiral to steer themselves toward better health, Kok, Fredrickson, and their colleagues conducted a longitudinal field experiment.

Half of the study participants were randomly assigned to attend a 6-week loving-kindness meditation (LKM) course in which they learned how to cultivate positive feelings of love, compassion, and goodwill toward themselves and others. They were asked to practice meditation at home, but how often they meditated was up to them. The other half of the participants remained on a waiting list for the course.

Each day, for 61 consecutive days, participants in both groups reported their "meditation, prayer, or solo spiritual activity," their emotional experiences, and their social interactions within the last day. Their vagal tone was assessed twice, once at the beginning and once at the end of the study.

The data provided clear evidence to support the hypothesized upward spiral, with perceived social connections serving as the link between positive emotions and health.

Participants in the LKM group who entered the study with higher vagal tone showed steeper increases in positive emotions over the course of the study. As participants' positive emotions increased, so did their reported social connections. And, as social connections increased, so did vagal tone. In contrast, participants in the wait-list group showed virtually no change in vagal tone over the course of the study.

"The daily moments of connection that people feel with others emerge as the tiny engines that drive the upward spiral between positivity and health," Fredrickson explains.

These findings add another piece to the physical health puzzle, suggesting that positive emotions may be an essential psychological nutrient that builds health, just like getting enough exercise and eating leafy greens.

"Given that costly chronic diseases limit people's lives and overburden healthcare systems worldwide, this is a message that applies to nearly everyone, citizens, educators, health care providers, and policy-makers alike," Fredrickson observes.

B. E. Kok, K. A. Coffey, M. A. Cohn, L. I. Catalino, T. Vacharkulksemsuk, S. B. Algoe, M. Brantley, B. L. Fredrickson. How Positive Emotions Build Physical Health: Perceived Positive Social Connections Account for the Upward Spiral Between Positive Emotions and Vagal Tone. Psychological Science, 2013; DOI: 10.1177/0956797612470827

Boosting 'Cellular Garbage Disposal' Can Delay the Aging Process

May 6, 2013 — UCLA life scientists have identified a gene previously implicated in Parkinson's disease that can delay the onset of aging and extend the healthy life span of fruit flies. The research, they say, could have important implications for aging and disease in humans.

The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.

"Aging is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research. "We think that our findings shed light on the molecular mechanisms that connect these processes."

In the research, published today in the early online edition of the journal Proceedings of the National Academy of Sciences, Walker and his colleagues show that parkin can modulate the aging process in fruit flies, which typically live less than two months. The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 percent, compared with a control group that did not receive additional parkin.

"In the control group, the flies are all dead by Day 50," Walker said. "In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound."

"Just by increasing the levels of parkin, they live substantially longer while remaining healthy, active and fertile," said Anil Rana, a postdoctoral scholar in Walker's laboratory and lead author of the research. "That is what we want to achieve in aging research - not only to increase their life span but to increase their health span as well."

Treatments to increase parkin expression may delay the onset and progression of Parkinson's disease and other age-related diseases, the biologists believe. (If parkin sounds related to Parkinson's, it is. While the vast majority of people with the disease get it in older age, some who are born with a mutation in the parkin gene develop early-onset, Parkinson's-like symptoms.)

"Our research may be telling us that parkin could be an important therapeutic target for neurodegenerative diseases and perhaps other diseases of aging," Walker said. "Instead of studying the diseases of aging one by one - Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, diabetes - we believe it may be possible to intervene in the aging process and delay the onset of many of these diseases. We are not there yet, and it can, of course, take many years, but that is our goal."

'The garbage men in our cells go on strike'

To function properly, proteins must fold correctly, and they fold in complex ways. As we age, our cells accumulate damaged or misfolded proteins. When proteins fold incorrectly, the cellular machinery can sometimes repair them. When it cannot, parkin enables cells to discard the damaged proteins, said Walker, a member of UCLA's Molecular Biology Institute.

"If a protein is damaged beyond repair, the cell can recognize that and eliminate the protein before it becomes toxic," he said. "Think of it like a cellular garbage disposal. Parkin helps to mark damaged proteins for disposal. It's like parkin places a sticker on the damaged protein that says 'Degrade Me,' and then the cell gets rid of this protein. That process seems to decline with age. As we get older, the garbage men in our cells go on strike. Overexpressed parkin seems to tell them to get back to work."

Rana focused on the effects of increased parkin activity at the cellular and tissue levels. Do flies with increased parkin show fewer damaged proteins at an advanced age? "The remarkable finding is yes, indeed," Walker said.

Parkin has recently been shown to perform a similarly important function with regard to mitochondria, the tiny power generators in cells that control cell growth and tell cells when to live and die. Mitochandria become less efficient and less active as we age, and the loss of mitochondrial activity has been implicated in Alzheimer's, Parkinson's and other neurodegenerative diseases, as well as in the aging process, Walker said.

Parkin appears to degrade the damaged mitochondria, perhaps by marking or changing their outer membrane structure, in effect telling the cell, "This is damaged and potentially toxic. Get rid of it."

If parkin is good, is more parkin even better?

While the researchers found that increased parkin can extend the life of fruit flies, Rana also discovered that too much parkin can have the opposite effect - it becomes toxic to the flies. When he quadrupled the normal amount of parkin, the fruit flies lived substantially longer, but when he increased the amount by a factor of 30, the flies died sooner.

"If you bombard the cell with too much parkin, it could start eliminating healthy proteins," Rana said.

In the lower doses, however, the scientists found no adverse effects. Walker believes the fruit fly is a good model for studying aging in humans - who also have the parkin gene - because scientists know all of the fruit fly's genes and can switch individual genes on and off.

Previous research has shown that fruit flies die sooner when you remove parkin, Walker noted. Walker and Rana do not know what the optimal amount of parkin would be in humans.

While the biologists increased parkin activity in every cell in the fruit fly, Rana also conducted an experiment in which he increased parkin expression only in the nervous system. That, too, was sufficient to make the flies live longer.

"This tells us that parkin is neuroprotective during aging," Walker said. "However, the beneficial effects of parkin are greater - twice as large - when we increased its expression everywhere."

"We were excited about this research from the beginning but did not know then that the life span increase would be this impressive," Rana said.

The image that accompanies this news release shows clumps or aggregates of damaged proteins in an aged brain from a normal fly (left panel) and an age-matched brain with increased neuronal parkin levels (right panel). As can be seen, increasing parkin levels in the aging brain reduces the accumulation of aggregated proteins.

Scientists have found that this kind of protein aggregation occurs in mammals as well, including humans, Rana said.

"Imagine the damage the accumulation of protein trash is doing to the cell," Walker said. "With increased Parkin, the trash has been collected. Without it, the garbage that should be discarded is accumulating in the cells."

Anil Rana, Michael Rera, and David W. Walker. Parkin overexpression during aging reduces proteotoxicity, alters mitochondrial dynamics, and extends lifespan. PNAS, May 6, 2013 DOI: 10.1073/pnas.1216197110

Disclaimer: These articles are not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of Pittwater Online News or its staff.

 National Seniors Literary Prize a catalyst for change

The 2014 National Seniors Literary Prize will have the theme 'reflections'. It will be open until 29 November 2013. 

National Seniors Australia and publishing powerhouse Random House Australia are working together to give one lucky writer, aged 50 years and over, the opportunity to make their mark in the world of publishing. 
The National Seniors Literary Prize 2014 will be awarded to a work of fiction based on the theme of 'reflections'. Random House and National Seniors are giving you the opportunity to be creative so this theme can be integrated into your storyline or your novel’s structure!

The winner of the National Seniors Literary Prize will receive:
$2,000 prize money
A three year membership to National Seniors Australia
A complete cover design for their manuscript
Professional editing by Random House Australia
E-book publication of their manuscript
12 printed copies of their novel
The opportunity for print-on-demand versions of their book

Submit your manuscript into the National Seniors Literary Prize 2014.

Got questions?  Read the National Seniors Literary Prize frequently asked questions here. Read the full terms and conditions of the prize here.

Media Releases concerning Seniors this week from National Seniors Australia

With around a quarter of a million members, National Seniors is Australia’s largest consumer organisation for the over 50s and fourth largest group of its kind in the world.

U3A Monthly Lectures Wednesday Afternoons at Newport -

First Wednesday of the month 2 – 4pm. All welcome - no need to book. Just come along hear interesting speakers and make new friends. Cost: $2 includes tea coffee and biscuits. Venue: Newport Community Centre, for more information contact Nancy Weir 8919 0243 or Mavis Bickerton 9970 7161 Website: www.sydneyu3a.org Website: www.sydneyu3a.org

Keep your Wits About You

A regular contributor suggests we all look at Lumosity to see if will suit keeping active mentally. Their website states: "improve Brain Health and performance. Designed by neuroscientists, Lumosity exercises improve core cognitive functions. Researchers have measured significant improvements in working memory and attention after Lumosity training. Dozens of research collaborations help improve the Lumosity training program and its effectiveness." You can visit their website to decide for yourself  at: www.lumosity.com/app/v4/personalization

The Senior Newspaper Online

Click on logo:

Super Seniors Directory

A massive directory for all northern beaches seniors is hitting the streets for Seniors Week. The Services, Activities & Housing Directory 2012-2013 is a one-stop-shop for all northern beaches seniors thanks to a successful partnership between Warringah, Pittwater and Manly Councils.

The directories can be found at Council's Customer Service; Libraries, Community Centres or online at the council websites.

If older people with mobility problems have difficulty assessing the directory - contact Aged Services and you will be sent a copy.

Copyright Pittwater Online News, 2013.