10 Questions to Ask About Nutrition and Aging


Good nutrition is the cornerstone of healthy aging. Yet as we age, our dietary requirements change. We usually don’t need as many calories. But we have to be sure we get enough of certain key nutrients, like calcium, vitamin B12, and vitamin D.

Getting proper nutrition often becomes harder with age because of things like loss of appetite or problems with chewing or swallowing food. That’s why it’s so important to talk to your doctor about nutrition. Here are questions you may want to ask.

How do I know if I’m getting all the nutrition I need?

Surveys show that many Americans, especially older Americans, aren’t getting all the nutrition they need.

Even many people who are overweight fall short on vitamins, minerals, and other nutrients. They get plenty of calories, but they may not be getting enough nutrition. Unfortunately, a long-term lack of nutrients may happen before symptoms show up.

Early signs of this may include:

A physical exam may alert your doctor to poor nutrition. Blood tests can show whether you get enough of some key nutrients, such as iron or vitamin D.

Do any of my meds affect my appetite or how food tastes?

A range of medicines, including many often used by older adults, can interfere with good nutrition.

Some pain relievers and arthritis meds irritate the stomach, for example. Some antibiotics, stool softeners, and chemotherapy drugs can affect how food tastes. Antidepressants, diuretics, pain medications, and some heart drugs can lower your appetite.

Does anything I’m taking get in the way of nutrients I need?

A variety of treatments can stifle the body’s ability to absorb vitamins, minerals, and other nutrients. These include chemotherapy, radiation therapy, and medications.

I’m not very hungry when I know it’s time to eat. Is that normal for someone my age?

There are many reasons why older adults often don’t have a big appetite. Because they are usually less active than younger people, they need fewer calories. And less ability to taste may mean that food just doesn’t have as much appeal as it once did.

However, a big loss of appetite or weight loss can also be a sign of depression or other serious health problems. Tell your doctor if you see a change in your appetite or lose weight without trying.

Should I take a multivitamin?

Experts disagree about whether older Americans should take multivitamins. Most nutritionists agree that the best way to get your nutrients is from food, not pills.

If you have trouble eating a balanced diet, ask your doctor whether you should take a multivitamin. Be sure to let your doctor know about all pills you take, including supplements.

What about taking other supplements?

Some people may need to take additional supplements of certain nutrients.

For example, if you don’t eat foods rich in calcium, like dairy products, you may need a supplement. Talk to your doctor before taking any pills.

Should I cut back on salt?

If you have high blood pressure, or even if your blood pressure is at the high end of normal, try cutting back on salt.

The American Heart Association recommends everyone have less than 1,500 milligrams of sodium a day. They estimate that if people did this, it would result in a 25% drop in high blood pressure across the country.

Up to three-quarters of the salt we eat comes in packaged foods, so reading labels is particularly helpful.

How much alcohol is safe to drink?

Moderate amounts of alcohol reduce the risk of heart disease.

This doesn’t mean you should start drinking. But if you already drink alcohol, talk to your doctor about a safe level for you. Drinking too much can lead to serious health problems.

Could I cut back on some of my medications by following a healthier lifestyle?

Many older people can cut back on blood pressure, cholesterol, or other medications if they eat a healthier diet and get more exercise. Some discover they can go off certain prescription drugs completely.

Talk to your doctor about whether a healthier lifestyle could mean taking fewer pills. Don’t stop taking medicines on your own.

Should I see a registered dietitian?

Even though doctors understand the importance of a healthy diet, they often don’t have time to provide complete dietary counseling. If you have more questions than your doctor has time to answer, ask him to recommend a registered dietitian. Medicare and private insurers often cover nutrition consultations.

Sleep and Aging


Is your sleep different than it used to be when you were younger? It happens to a lot of people.

Nearly half of men and women over the age of 65 say they have at least one sleep problem. With age, many people get insomnia or have other sleep disorders.

It’s true that as we get older, our sleep patterns change. In general, older people sleep less, wake up and go back to sleep more often, and spend less time in deep sleep or dreaming than younger people.

But at any age, you still need quality rest to be healthy.

What Causes Sleep Problems With Age?

Some common reasons include:

Poor sleep habits: If you don’t keep a steady schedule for going to bed and waking up, it can affect your body’s internal clock and make it even harder to get good sleep. Also, at any age, it’s a minus if you drink alcohol before bedtime, nap too much, or stay in bed when you’re not sleeping.

Medications: Some drugs make it harder to fall or stay asleep, or even stimulate you to stay awake. If you think that might be true for you, ask your doctor to check.

Worry, stress, or grief. Aging brings many life changes. Some are positive. Others are really hard. When you lose someone you love, move from your family home, or have a condition that changes your life, that can cause stress, which can hamper your sleep.

If changes like these affect you or an aging loved one, talk with your doctor or a counselor. It could help ease your mind so you can sleep better.

Sleep disorders: Besides insomnia, these include apnea, restless legs syndromeperiodic limb movement disorder, and REM behavior disorder. Your doctor can see if you have one of these conditions.

Too much downtime. Many people stay active well into their golden years. But if your days are too idle, you may find it harder to get good sleep.

Do You Get Enough Sleep?

Everyone is different. If you sleep less than when you were younger but still feel rested and energetic during the day, it might be that you now need less sleep.

But if you have noticed that your lack of sleep affects you during the day, tell your doctor. There are steps you can take to get better rest. Many are simple tweaks to your daily routine, like setting a regular bedtime, being more active, and taking steps to ease your mind before you hit the hay.

Tips for More Energy, Better Mood With Age


With aging comes wisdom, perspective, and yes, changes that may sap your energy. Even if you’re not dancing quite as fast as you once did, there are ways you can keep that bounce in your step.

Focus on:

  • Diet
  • Exercise
  • Sleep

Manage Your Menu

If you’ve been eating the same things for a while, take a fresh look at what’s on your plate. The right types of food can raise your energy and make you feel better.

As you age, your body’s ability to turn food into energy slows down. As a result, many put on weight. Still, you can help yourself stay fit and energetic.

Sugar levels play a big role. Some experts say “low-glycemic” foods, like beans, non-starchy veggies, nuts, and whole-grain products, can help keep your blood sugar in balance.

“High-glycemic” foods, like white rice, white bread, and sugar-sweetened drinks, can cause fast spikes in your blood sugar. You may feel a brief energy jolt, but when the dip comes, you may feel more drained than before.

Quantity Matters, Too

Too few calories can leave your body starved for energy. Too many can make you gain weight, which can make you feel sluggish.

How much you should eat each day depends on several things, especially how active you are. Talk to your doctor or a dietitian about how many calories you need.

Get Moving

You may notice you’re working out less than you were when you were younger. Perhaps training for 5Ks has given way to after-dinner strolls.

The more active you are, the more energetic you’ll feel. Exercise and physical activity are great ways to help your mood, too. If you have issues that stop you from doing the things you once enjoyed, feel free to get creative. If arthritis in your knees keeps you from running or playing basketball, swimming or cycling might work for you.

You shouldn’t stop moving as you get older. Just move in a different way. Look for fitness programs at local senior centers or find a partner so you can motivate each other. If you have trouble finding time to be active, maybe a workout first thing in the morning, before you do anything else, can do the trick. Just make sure you eat some breakfast first.

Talk to your doctor before you begin a new routine.

Get Some Rest

For some of us, it’s one of life’s little jokes: When you retire and don’t have to get up for work, you can’t seem to sleep in anymore.

But getting enough shut-eye is important. Most people need about 7 hours a night. If you’re not getting that much, for whatever reason, look for ways to adjust your nighttime routine.

Try not to drink alcohol right before bedtime. While it might make you drowsy for a little while, it actually makes it harder to get a full night’s sleep.

You should also:

  • Finish all your caffeine by midafternoon.
  • Turn off your computer, smartphone, and TV well before bedtime.
  • Keep your bedroom as cool, dark, and quiet as possible.
  • Go to bed and wake up at the same time as often as you can.

If you still can’t get enough sleep, talk with your doctor.

Try These Other Tips, Too

For a few more ways to improve energy and mood as you age, you might:

Cut back on alcohol in general. As you age, its effects stay with you longer.

Drink more water . If you’re even a little dehydrated, it can sap your energy and affect your mood.

Cut stress where you can. For example, try to scale back your to-do list if you feel like you are spread too thin. Turn off the TV and take a walk if the news is making you anxious.

If you’re tired or depressed, talk to your doctor. Those things are not a normal part of aging. Another health problem may be to blame, like depression, heart disease, or sleep apnea.

Exercise an Antidote for Aging


If you want to counter the physical costs of getting old, regular exercise might be your best option, researchers report.

The findings “debunk the assumption that aging automatically makes us more frail,” said researcher Janet Lord. She is director of the Institute of Inflammation and Ageing at the University of Birmingham in England.

In the study, the team assessed 84 male and 41 female cyclists, aged 55 to 79. The men had to be able to cycle 62 miles in under 6.5 hours, while the women had to be able to cycle 37 miles in 5.5 hours.

Unlike a “control group” of adults who did not get regular exercise, the cyclists did not have loss of muscle mass or strength, did not have age-related increases in body fat or cholesterol levels, and their immune systems were as robust as much younger people.

Male cyclists also had higher testosterone levels than men in the control group, according to the study authors.

“Our research means we now have strong evidence that encouraging people to commit to regular exercise throughout their lives is a viable solution to the problem that we are living longer but not healthier,” Lord added in a university news release.

The findings were published March 8 in the journal Aging Cell.

Researcher Niharika Arora Duggal, also from the University of Birmingham, said, “We hope these findings prevent the danger that, as a society, we accept that old age and disease are normal bedfellows, and that the third age of man is something to be endured and not enjoyed.”

International Longevity and Cryopreservation Summit Spain


It is always good to see the increasing interest internationally in treating age-related diseases for healthier lives through the development of new medicines. Members of the Spanish scientific and cryonics communities have organized three conferences to be held in Barcelona, Madrid and Seville later this year. The conferences will cover topics relating to biotechnology, longevity, aging research and cryopreservation and are the first of their kind in Spain.

Spain will host the first International Longevity and Cryopreservation Summit during May 26-28, 2017. Fundacion VidaPluswill be the main organizer of this world congress, with the help of other leading associations and organizations working on longevity, indefinite lifespans, cryopreservation, and other biomedical areas.

The show includes a great selection of researchers and futurists all working on bringing cutting edge technology to the world.

Jose Luis Cordeiro of Fundacion VidaPlus is an influential futurist and President Emeritus of the Future World Society (Venezuela). He is a professor, founder and researcher at NASA created Singularity University in Silicon Valley. The goal of the research centre is to tackle problems such as health, nutrition, poverty and education using the medium of technology. He is also on the board of directors for the Lifeboat Foundation and He has written more than 10 books and co-written over 20 more in five languages, including sections of the State of the Future by the Millennium Project. His extensive associations and achievements are far too numerous to list here in this short article, and we invite you to read more about Jose here.

Dr. Aubrey de Grey is the Chief Science Officer and co-founder of the SENS Research Foundation. He is considered one of the original proponents of the repair strategy to treat age-related disease and is the author of the book Ending Aging co-written with Michael Rae also from the SENS Research Foundation. Aubrey spends much of his time travelling and advocating about aging and how we can use the tools of the emerging rejuvenation biotechnology industry to treat age-related diseases. Aubrey would like to see a world where we reimagine aging.

João Pedro de Magalhães is a Senior Lecturer in aging at the University of Liverpool in the UK and he is one of the driving forces behind the Human Aging Genomic Resources (HAGR) database. In 2015 João sequenced and analyzed the genome of the bowhead whale[1] and he has also helped with the analysis of the genome of the naked mole rat[2]. João is also active in advocating for rejuvenation biotechnology and has given many talks about the possibilities of science in the field of aging.

David Wood is a futurist and pioneer of the smartphone industry which includes him co-founding Symbian back in 1998. He is chair of the London Futurists, a non-profit organisation with over 5,500 members, who hold regular meetings to discuss technoprogressive issues. David is author of six books including the recent “The Abolition of Aging: The forthcoming radical extension of healthy human longevity” which explores the future of rejuvenation biotechnology.

These are only a few of the great speakers that will be there and to do them all justice is beyond the scope of this small article. If you can make it to the show it should be a memorable experience.

Seeing the increasing amount of discussion about finding new ways to treat age-related diseases is extremely good news, and shows the rising interest in these technologies as they draw ever closer.

This rising interest by the wider public is matched in academia. Frequently the question is no longer, can we do anything about the aging process? And more often, what is the best way to address it?

 

Literature

[1] Keane, M., Semeiks, J., Webb, A. E., Li, Y. I., Quesada, V., Craig, T., … & Michalak, P. (2015). Insights into the evolution of longevity from the bowhead whale genome. Cell reports, 10(1), 112-122.
[2] Keane, M., Craig, T., Alföldi, J., Berlin, A. M., Johnson, J., Seluanov, A., … & de Magalhães, J. P. (2014). The Naked Mole Rat Genome Resource: facilitating analyses of cancer and longevity-related adaptations. Bioinformatics, 30(24), 3558-3560.

Source:leafscience.org

Scientists Reverse DNA Damage in Mice. Human Trials are Next. 


DNA is a critical part of the cell, it is the instruction manual for building cells. Whilst DNA is well protected within the cell nucleus damage does occur, therefore DNA repair is absolutely essential for cell function, cell survival and the prevention of cancer. The good news is cells are able to repair damaged DNA but the bad news is that this ability declines with aging for reasons as yet to be fully understood.

An exciting new study by researchers led by Dr. David Sinclair at Harvard Medical School shows a part of the process that enables cells to repair damaged DNA involving the signalling molecule NAD. This offers insight into how the body repairs DNA and why that repair system declines as we age. Before we get into the new research study let’s take a look at how DNA damage relates to aging and what NAD is.

Genomic instability a driver of aging?

The stability and integrity of our DNA is challenged on a daily basis by various external physical, chemical and biological agents as well as by internal threats such as replication errors, reactive oxygen species and other factors.

Some aging theories such as the Hallmarks of aging implicate DNA damage as one of the primary driving processes of aging contributing to genomic instability[1]. Various premature aging diseases such as progeria are the consequence of accumulated DNA damage, however the relationship between progeria and normal aging is as yet unresolved. This is partly due to the fact that the different progeroid syndromes only manifest certain aspects of aging seen in normally aging people.

This means that this new study is very important in helping us to understand the relationship between DNA damage and aging.

What is NAD?

Nicotinamide adenine dinucleotide (NAD) is a dinucleotide, meaning that it consists of two nucleotides joined by their phosphate groups. One nucleotide contains an adenine base and the other contains nicotinamide. NAD is found in two forms, an oxidized and reduced form abbreviated as NAD+ and NADH respectively. As part of its role in metabolism, nicotinamide adenine dinucleotide supports redox reactions, the moving of electrons from one reaction to another. The transfer of electrons is the primary function of NAD but it has other roles too.

Found in every cell in our body, NAD helps to suppress genes that accelerate the aging process and is a fundamental part of our metabolic system. NAD is associated with the sirtuins, which are closely linked to longevity in mammals and other organisms. Its control over cell damaging oxidation is also well documented. NAD declines during the aging process due to being actively destroyed by inflammatory signalling as shown in a 2013 study by Schultz and Sinclair[2].

So what’s the big news?

This new study demonstrates a previously unknown role for the NAD signalling molecule as a master regulator of protein to protein interaction during DNA repair. It also gives us valuable insight into why the body’s ability to repair DNA damage begins to fail as we age[3].

These experiments conducted in mice demonstrate that treatment with a NAD precursor known as nicotinamide mononucleotide (NMN) can mitigate and resist age-related DNA damage as well as the damage resulting from exposure to radiation. Whilst there is no guarantee that these results will translate from mice to humans due to differences in biology, if they do it is of great interest.

Building on previous research

David Sinclair and his team already demonstrated that NMN can extend the lifespan of mice in a previous study[4] and reverses loss of mitochondrial function with age[5]. The team began this new study by examining the various proteins and molecules they believed were involved in the aging process.

They knew that NAD, whose levels fall with age, increases the activity of the SIRT1 protein (one of the Sirtuin family) and can delay some aspects of aging, extending the lifespan in yeast, flies and mice. They also knew that SIRT1 and PARP1, a protein that is involved in DNA repair, both consume NAD during their activation.

The team also looked at a protein called DBC1, a common protein found in humans and many other organisms from bacteria upwards. Studies had shown that DBC1 was able to inhibit the activity of SIRT1, so they believed it might also influence PARP1 given their similar roles, and wanted to see if it was connected to NAD. It turns out they were correct and the study revealed this link.

The research group tested the relationship between the three proteins by measuring protein-to-proteins interaction within human kidney cells. They discovered that PARP1 and DBC1 actually bond strongly to each other but, when NAD levels increase that bonding is reduced. Simply put, the more NAD in a cell the fewer bonds DCB1 and PARP1 can form, freeing up PARP1 so it can repair damaged DNA. They also took this further, inhibited NAD and noted the number of DBC1 to PARP1 bonds increased. This shows that reduced levels of NAD strongly influence the ability of cells to repair DNA damage.

These findings suggest that as NAD falls during the aging process the less NAD there is to prevent DBC1 and PARP1 bonding, which is harmful to DNA repair. The result of this ultimately causes DNA damage to go unrepaired and accumulate over time, leading to cell damage, mutations, loss of tissue, cell function, and organ failure.

Getting down to the nitty gritty

That in itself was interesting enough to have discovered this previously unknown function of NAD, but the researchers wanted to understand exactly how NAD was doing this. To find out how NAD prevents DBC1 from bonding with PARP1 they examined a region of DBC1 known as NHD. NHD is a pocket shaped structure common to around 80,000 different proteins in a huge number of species, and its function has been a mystery to scientists. The team showed that this NHD region is a NAD binding site and in DBC1, NAD binds to this region and prevents DBC1 from bonding with PARP1 to prevent DNA repair.

Interestingly NHD is so common in across species it suggests that this NAD binding may play a similar role preventing harmful protein interactions in many species including humans.

Moving to mice

Next the researchers treated old mice with NMN, but before they did they checked the protein levels in the mice. As predicted the old mice had lower levels of NAD in their livers, as well as lower PARP1 levels and a larger number of bonded PARP1 and DBC1 proteins. However once given NMN in their drinking water for just one week, the old mice showed significant improvement in NAD and PARP1 levels. Tests showed the NAD levels in the livers of the old mice increased similar to those observed in younger mice. PARP1 levels were a similar story and PARP1 and DBC1 bonded proteins were reduced. The researchers also recorded a reduction in biomarkers for DNA damage suggesting that DNA repair had been improved.

Finally the researchers exposed mice to radiation to damage their DNA. They discovered that mice treated with NMN before radiation exposure showed lower levels of DNA damage. The mice also did not display the characteristic changes to blood counts, such as changes to lymphocyte and hemoglobin levels typically seen after radiation exposure. Interestingly, mice treated post radiation also enjoyed similar protective effects from NMN treatment.

Of mice and men

Human trials with NMN are anticipated to begin within the next six months according to researchers and the potential discoveries are significant for our understanding of the biology of aging.

In conclusion the results show the mechanism behind DNA repair and cell death caused by DNA damage. Should further animal studies and human clinical results confirm the findings, this may pave the way for therapies that repair DNA damage due to radiation exposure from sources such as radiotherapy and environment and of course, for treating age-related decline.

 

Literature

[1] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.
[2] Schultz, M. B., & Sinclair, D. A. (2016). Why NAD+ Declines during Aging: It’s Destroyed. Cell metabolism, 23(6), 965-966.
[3] Li, J., Bonkowski, M. S., Moniot, S., Zhang, D., Hubbard, B. P., Ling, A. J., … & Aravind, L. (2017). A conserved NAD+ binding pocket that regulates protein-protein interactions during aging. Science, 355(6331), 1312-1317.
[4] North, B. J., Rosenberg, M. A., Jeganathan, K. B., Hafner, A. V., Michan, S., Dai, J., … & van Deursen, J. M. (2014). SIRT2 induces the checkpoint kinase BubR1 to increase lifespan. The EMBO journal, e201386907.
[5] Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., … & Mercken, E. M. (2013). Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624-1638.

Source:http://www.leafscience.org/

Stem Cell Technique Could Regenerate Any Human Tissue Damaged By Aging or Disease


Stem Cells: They Keys To Human Health

Stem cells are, in may ways, our lifeblood, and understanding them could utterly transform human biology. While stem cells have already worked wonders in medicinal research, showing signs of curing everything from spinal cord injuries to blindness, they’ve always had their shortcomings—mostly tied to our own lacking understanding.

However, each year brings us closer to truly understanding these cells, how they function, and how they can be manipulated for a variety of health purposes. For example, we know that stem cells are tied to aging, and we know that understanding exactly how they are tied to aging is critical to combating age-associated degeneration. As work published in the National Center for Biotechnology Information outlines:

“Aging tissues experience a progressive decline in homeostatic and regenerative capacities, which has been attributed to degenerative changes in tissue-specific stem cells, stem cell niches and systemic cues that regulate stem cell activity.”

And one study is promising a “game-changing” technique for stem cells.

Taking their cue from salamander regeneration, research led by the University of New South Wales says that a stem cell therapy capable of regenerating any human tissue damaged by injury, disease, or aging could be available within a few years, thanks to an innovative technique.

But first, a breakdown of what stem cells are and why they are so terribly important:

The Technique

The technique pioneered by the researchers at University of New South Wales involves reprogramming bone and fat cells into “induced multipotent stem cells” (iMS). These cells are special in that they can regenerate multiple tissue types.

The team notes the significance of these cells, stating that, “unlike primary mesenchymal stem cells, which are used with little objective evidence in clinical practice to promote tissue repair, iMS cells contribute directly to in vivo tissue regeneration in a context-dependent manner without forming tumors.”

There are two kinds of stem cells: embryonic stem cells that during embryonic development generate every type of cell in the human body, and adult stem cells that are tissue-specific, and unable to regenerate multiple tissue types.

This method has the potential to transform current approaches in regenerative medicine.

Embryonic stem cells would be preferable, save that they are prone to form teratomas (tumors composed of different tissue types), and their use is highly controversial.

In any case, the scientists are quick to note the utterly transformative nature of this technique, and it’s great potential in relation to the future of medicine: “This method can be applied to both mouse and human somatic cells to generate multipotent stem cells and has the potential to transform current approaches in regenerative medicine.”

How It Works

The method used by the researchers is, quite frankly, amazing. They took bone and fat cells in mice, switched off their memory, and transformed them into stem cells.

To be specific, the technique involves extracting adult human fat cells and treating them with the compound 5-Azacytidine (AZA), along with platelet-derived growth factor-AB (PDGF-AB) for approximately two days. The cells are then treated with the growth factor alone for a further two to three weeks.

The AZA relaxes the hard-wiring of the cells by inducing cell plasticity, and this is expanded by the growth factor. Release the iMS into damaged tissue, and they will multiply, healing the tissue. The technique is a huge step up from other stem-cell therapies, since embryonic stem cell therapies may form tumors, and others use viruses to transform cells into stem cells.

The technique is a huge step up from other stem-cell therapies, since embryonic stem cell therapies may form tumors, and others use viruses to transform cells into stem cells. The current trials use iMS from adult human fat cells inserted into mice. Human trials for this technique are expected by late 2017.

Impact of aging on brain connections mapped in major scan study


UNIVERSITY OF EDINBURGH — Brain connections that play a key role in complex thinking skills show the poorest health with advancing age, new research suggests.

Connections supporting functions such as movement and hearing are relatively well preserved in later life, the findings show.

Scientists carrying out the most comprehensive study to date on ageing and the brain’s connections charted subtle ways in which the brain’s connections weaken with age.

Knowing how and where connections between brain cells – so-called white matter – decline as we age is important in understanding why some people’s brains and thinking skills age better than others.

Worsening brain connections as we age contribute to a decline in thinking skills, such as reasoning, memory and speed of thinking.

Researchers from the University of Edinburgh analysed brain scans from more than 3,500 people aged between 45 and 75 taking part in the UK Biobank study.

Researchers say the data will provide more valuable insights into healthy brain and mental ageing, as well as making contributions to understanding a range of diseases and conditions.

The study was published in Nature Communications journal.

Dr Simon Cox, of the University of Edinburgh’s Centre for Cognitive Ageing and Cognitive Epidemiology (CCACE), who led the study, said: “By precisely mapping which connections of the brain are most sensitive to age, and comparing different ways of measuring them, we hope to provide a reference point for future brain research in health and disease.

“This is only one of the first of many exciting brain imaging results still to come from this important national health resource.”

Professor Ian Deary, Director of CCACE, said: “Until recently, studies of brain scans with this number of people were not possible. Day by day the UK Biobank sample grows, and this will make it possible to look carefully at the environmental and genetic factors that are associated with more or less healthy brains in older age.”

Professor Paul Matthews of Imperial College London, Chair of the UK Biobank Expert Working Group, who was not involved in the study, said: “This report provides an early example of the impact that early opening of the growing UK Biobank Imaging Enhancement database for access by researchers world-wide will have.

“The large numbers of subjects in the database has enabled the group to rapidly characterise the ways in which the brain changes with age – and to do so with the confidence that large numbers of observations allow.

“This study highlights the feasibility of defining what is typical, to inform the development of quantitative MRI measures for decision making in the clinic.”

The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology receives funding from the Medical Research Council (MRC) and the Biotechnology and Biological Sciences Research Council (BBSRC).

UK Biobank was established by the Wellcome Trust, MRC, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. UK Biobank is hosted by the University of Manchester and supported by the NHS.A video explanation of the research is available at: http://www.ccace.ed.ac.uk/news-events/latest

A video explanation of the research is available at: http://www.ccace.ed.ac.uk/news-events/latest

 

Scientists may have just unlocked a real ‘fountain of youth’


Scientists have reversed signs of aging in mice, increasing their lifespan by 30 percent -– a finding that researchers believe could one day increase the life expectancy of humans.

The Salk Institute for Biological Studies in California announced Friday that scientists there are literally “turning back time” through a process known as cellular reprogramming, ultimately extending the animal’s lifespan from 18 weeks to 24 weeks – and without accumulating typical hallmarks of aging.

Scientists may have just unlocked a real ‘fountain of youth’

“Our study shows that aging may not have to proceed in one single direction,” Juan Carlos Izpisua Belmonte, a senior author of the paper and a professor at Salk’s Gene Expression Laboratory, said in a news release. “It has plasticity and, with careful modulation, aging might be reversed.”

The findings, which Belmonte claims indicate aging may be something doctors will one day be able to manipulate, appeared Friday in the journal Cell. Researchers say it’s the first time cellular reprogramming – a process that allows scientists to convert any cell into what are known as induced pluripotent stem cells (iPSCs) – extended the lifespan of a live animal.

“What we discovered is that we can change the program of a cell in an animal and we can convert an old program into a young program,” said research associate Alejandro Ocampo. “In this study, we were able to slow down aging by introducing cellular reprogramming both in a dish and in vivo.”

 Compared to the untreated mice, researchers said the reprogrammed animals appeared younger, with improved cardiovascular and organ function while living 30 percent longer and not developing cancer. They also showed healthier tissues than the untreated mice and overall did not “accumulate the aging hallmarks,” according to research associate Pradeep Reddy.

The researchers believe the new technique that rejuvenated the organs of mice and extended their lifespan be the “most promising approach to achieve rejuvenation in humans,” according to the news release. But due to the complexities of aging, any clinical trial could be up to 10 years away, they warn.

“Obviously, mice are not humans and we know it will be much more complex to rejuvenate a person,” Belmonte said. “But this study shows that aging is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than what we previously thought.”

Watch the video discussion. URL:https://youtu.be/3r_p__9EHxU

Scientists May Have Identified the Protein That Controls Aging


IN BRIEF
  • Two biochemists have discovered a link between a protein called carbonic anhydrase and aging in the brains and muscle cells of mice.
  • While still in the early stages of development, their research could lead to treatments for diseases such as Alzheimer’s and Parkinson’s.

A POWERFUL PROTEIN

In addition to being the “powerhouse of the cell,” the mitochondria could also be home to a certain protein that’s in charge of the body’s aging, according to a new study by two biochemists at Nottingham University.

Dr. Lisa Chakrabarti and PhD student Amelia Pollard examined the brain and muscle cells of both young and middle-aged mice and noted that high levels of a protein called carbonic anhydrase were found in those of the older mice. A high concentration of carbonic anhydrase was also reflected in samples from young brains suffering from early degeneration, suggesting that an increased concentration of the protein could be linked to the aging process.

To further test the theory, the scientists fed carbonic anhydrase to tiny nematode worms and found that their lifespans were shortened as well.

Credit: Pasieka/Science Photo Library

CLUES TO FURTHER RESEARCH

Knowing that carbonic anhydrase has this effect could help us unlock future treatments to slow general aging or mitigate such neurodegenerative diseases as Alzheimer’s and Parkinson’s Disease.

“This gives us a very promising start in working out how we can best target this protein within the mitochondria to slow the effects of aging in the body while limiting other unwanted side effects on the body,” said Chakrabarti. “It could potentially offer a significant new avenue in both tackling degenerative illnesses and the general effects of aging on the body.”

Though Chakrabarti and Pollard’s work is promising, we are still quite a long way from fully understanding the causes of cellular degeneration. There’s a big leap from mice to men, so further testing will need to be done before their research can be applied to human subjects.

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