StemCell Therapy

Updated January 23, 2020 20:22:47

One in five middle-aged Australians are finding it difficult to read road signs while driving, according to a new survey of the nation's visual health.

The 2020 Vision Index Report survey of 1,000 people, commissioned by Optometry Australia and released today, reveals 19 per cent of respondents aged 35 to 54 admit they struggle with signs behind the wheel.

One in three people surveyed had also never heard of myopia despite a global epidemic that experts say will leave half the world myopic by 2050.

Peter van Wijngaarden, a principal investigator for the Centre for Eye Research Australia, said the findings on driver behaviour had "significant safety implications".

"The vast majority of that sort of difficulty is easily corrected with glasses or an update to existing glasses, so it's something I'd strongly encourage people, that if they are feeling that they're having trouble seeing road signs, that that's a bit of a red flag for going and seeking out an eye check," he said.

Optometrist Sophie Koh from Optometry Australia said the survey's findings backed a view that many people were "in denial" about the state of their vision, or simply avoided conditions that made it most difficult, such as driving at night.

Indeed, 22 per cent of all people surveyed indicated they squinted at night "to see better while driving", while 15 per cent of people admitted to squinting behind the wheel during the day.

Ms Koh said everyone needed regular eye tests, regardless of symptoms.

Two-thirds of parents in the survey said they had taken their children to an optometrist, yet vision experts said it was critical for all children to have their eyes tested before starting school.

"Before they start school we recommend that they get an eye exam with or without symptoms," Ms Koh said.

"A lot of children, for example, are happy with the way they see and don't know they have a vision problem because that's the way they've always seen.

"We know a lot of eye problems are undetected. But most eye diseases 75 to 90 per cent are preventable."

But they need to be caught early. Ms Koh said waiting for symptoms to arrive was leaving it too late.

Associate Professor van Wijngaarden said having children's eyes checked was particularly critical.

"Often it's hard to notice when kids aren't seeing as well as they should and we know there's a critical period in childhood where correcting vision impairment, the need for glasses for instance, is really important for development of the sense of vision," he said.

"We are actually born with quite poor vision and it's visual experience that leads to the development of our eyes and our brain together.

"Good eye checks in childhood are really important to make sure your child's going to develop the best possible vision."

Ms Koh said the rapid rise of myopia made eye testing even more critical for children.

"Ninety to 95 per cent of kids in countries like South Korea and Singapore are now myopic, and it's a direct relation to more indoor activity versus outdoor and sedentary behaviour," she said.

"The message of two hours outside play per day is most important.

"It doesn't matter if you want to read a lot and be on screens, but you need to have a protective balance, which is outdoor [time]."

Associate Professor van Wijngaarden said the myopia epidemic still was not fully understood.

"In part it's environmental risk and in part it's genetic risk," he said.

"There's certainly an evidence base building for the need for outdoor activity, some sunlight exposure and reducing your work-screen time, extended periods of close focusing work."

Australians were also ignorant of the UV-induced eye disease known as pterygium, with three-quarters of survey respondents saying they had never heard of the problem.

Yet one in 100 Australians are affected, and Queensland has the highest prevalence of the condition in the world.

The National Eye Health Survey in 2016 estimated more than 450,000 Australians had some form of vision impairment, and that figure was expected to grow rapidly with the nation's ageing population.

Topics:health-policy,occupational-health-and-safety,travel-health-and-safety,womens-health,mens-health,driver-education,education,road-transport,road,doctors-and-medical-professionals,australia,brisbane-4000,qld

First posted January 23, 2020 06:44:46

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Driver eyesight and myopia awareness key concerns from national vision survey - ABC News

January is Glaucoma Awareness Month and Brownwood Regional Medical Center along with local Ophthalmologists, Dr. Carol Boren and Dr. Larry Wood want to remind you that early detection of Glaucoma requires a comprehensive eye exam and is recommended for those ages 40 and over. Early detection and treatment combined with lifestyle choices can help protect your sight.

Unfortunately, Glaucoma affects about 3 million people in the United States according SafeVisionTexas.org. It is one of the leading causes of vision loss, because there are no symptoms early on. Once vision is lost to glaucoma, it cannot be regained. Sadly, about half of the people with this disease do not know they have it.

Glaucoma damages the optic nerve, which transmits visual information from the retina to the brain. Typically, the disease progresses slowly, gradually destroying peripheral vision. Because people are unaware of early peripheral vision loss, a patient can lose most of it before they even know they have glaucoma.

Thats why SafeVisoinTexas.org and the American Academy of Ophthalmology recommends that everyone have acomprehensive eye exam at age 40. This exam provides ophthalmologists physicians who specialize in medical and surgical eye care an opportunity to carefully examine the eye including the optic nerve for signs of damage and other possible problems that may affect vision. Individuals at greater risk for developing glaucoma include people:

over age 40;

of African, Asian or Hispanic heritage;

who havehigh eye pressuredetected during an eye exam;

who arefarsightedornearsighted;

who have experienced eye trauma or eye injury;

whosecorneasare thin in the center;

or who have health problems such asdiabetes,migraines,high blood pressureor poor blood circulation.

Appropriate treatment for glaucoma depends on the specific type and severity of the disease. Medicatedeye dropsor laser treatments are the most common initial approach. These treatments lower eye pressure to reduce the amount offluid in the eye.

Brownwood Regional Medical Center reminds you, if you are ages 40 or above or have been experiencing eye discomfort, make that appointment now. Early detection of eye diseases may help save your eyesight.

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Early detection of Glaucoma may save your sight - Brownwood Bulletin

Posted: Jan 22, 2020 / 08:24 PM HST / Updated: Jan 22, 2020 / 08:24 PM HST

HONOLULU (KHON2) Lions clubs worldwidewill be performing community service projects as part of theLions In Sightinitiative to raise public awareness of the vital role Lions clubs play in their communities.

As Spring cleaning gets underway, theHawaii Lionsare asking people to look through dresser drawers and closets for used eyeglasses and hearing aids and donate them to theLions Recycle For Sightprogram.

The glasses will be distributed to those in need within developing countries where eye care is often unaffordable and inaccessible.

The glasses will be cleaned, categorized by prescription and prepared for distribution by Lions, Leos, and other groups. According to the World Health Organization, the eyesight of approximately one-fourth of the worlds population can be improved through the use of a corrective lens.

Hawaii Lions collect eyeglasses year-round and the Lions members will be out in force receiving your unwanted eyewear at Walmart and other locations throughout the state.

You may also place them in specially markedLions Recycle For Sightcollection boxes.Locations are also posted on the website, visithawaiilions.organd click on Eyeglasses.

In addition to the eyeglasses,hearing aidswill be also collected, cleaned and tested for local distribution.

As part of the 11th Annual State-Wide Lions in Sight project, January 25, 2020, the Lions stationed at Kahala Mall from 10:00 a.m. 2:00 pm. will be offering free vision screening between Macys and The Walking Store.

For more information, contactKelvin Moniz(808) 652-4737 for Kauai Island, and for other islands, contact Alice Kudo456-7278 or emailpback@hawaiiantel.net

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Lions In Sight initiative helps those who struggle to see, hear - KHON2

Centuries of domestic breeding have resulted in cats and dogs that come in a wide variety of shapes, sizes, and colors. If you have a favorite breed, theres a good chance that you like it to some degree because of the way it looks. But what do our pets see when they look back at us?

Lets clear up the most common misconception first. Dogs do not see in black and white. They do, however, see a different color spectrum. This is because their retinasthe light-detecting membranes at the back of the eyesare built differently. Human retinas have three types of light-sensitive cells called cones, each of which is tuned to a single color: red, blue, or green. Dogs have only red and blue cones, which makes their vision similar to that of a person with red-green color blindness.

Like humans, cats have three types of cones, but they still dont see color all that well. This is because cats and dogs have another problem with color vision: Regardless of which cones they have, they dont have very many of them. Instead, their retinas are packed with a different kind of light-sensing cells, called rods, that dont detect color at all. Rods are better suited to seeing in dim light than they are to parsing the hues of rainbow. People have fewer rods than cones, so while we get to see the daytime world in bright color, we are fated to stub our toes searching for the toilet at night.

But all those rods arent the only reason why cats and dogs can see so well in the dark. Youve likely noticed your pets eyes glow bright green at night. This is courtesy of the tapetum lucidum, a reflective layer behind the retina. Any light that slips through the retina bounces off this secondary layer for another pass through the animals retina, effectively doubling its sensitivity.

Theres more to vision than color and brightness, however. Compared to people, dogs and cats have limited visual acuity. Dogs have roughly the equivalent of 20/75 vision, meaning they need to be 20 feet away from something to see it as well as a normal person could at 75 feet. And you may be surprised to hear that cats fare even worse! Those sleek and gorgeous eyes seem built for precision, but cats are close to legally blind with vision somewhere around 20/150!

Making matters worse, dogs and cats have trouble adjusting their vision to different distances. This is because their lenses cant adjust shape as readily as ours can. If youre over 40, youre familiar with what happens when your lenses start to become inflexible. It gets harder and harder to focus on anything close to your face. Welcome to life as a dog.

The short of it is that cats and dogs see better at night than we do, but those adaptations come at the cost of clarity. But poor vision doesnt slow them down any. They dont need to drive cars or read the fine print. And what they lack in eyesight, they make up with magnificently superior senses of smell and hearing. Even animals that lose their vision due to degenerative diseases do incredible job of navigating their homes, because their vision was never that great to begin with.

Dr. Mike Fietz is a small animal veterinarian at Georgetown Veterinary Hospital. He moved to Charlottesville in 2003, the same year he received his veterinary degree from Cornell University.

Continued here:
The vision thing: What do cats and dogs actually see? - C-VILLE Weekly

Libby Clegg, 29, has represented both Scotland and Great Britain at international sporting events. She won a silver medal at the 2008 Summer Paralympics and won gold at the 2016 Paralympic Games. Clearly up for any challenge, the sprinter is now competing in ITVs Dancing On Ice.

But why exactly is the star registered as blind? The sporting star has a deteriorating eye condition known as Stargardts Macular Dystrophy which gives her only slight peripheral vision in her left eye.

Libby has described her eyesight as being like looking at a pixelated computer screen or a scrunched-up firework, when speaking to The Daily mail.

She added: I have some peripheral sight - barely any - and with what little sight I do have I was able to use to use to follow the lines on the track.

Libby wasnt born blind, and started losing her eyesight at the age of 9.

But theres currently no treatment for Stargardt, and eventually, the mother-of-one will lose her entire sight.

She continued: Im at the age where my sight should be stabilising but its still deteriorating.

Things will never go black, but I dont know yet exactly what I will be able to see.

Speaking to The Radio Times about her learning process on the ice rink, Live explained: Its been a learning process.

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On the track I run with a guide runner and were attached all the time, but basically its like learning a different vocabulary to communicate.

Myself and my partner Mark Hanretty use touch and verbal communication.

Im not as bad as I thought I was going to be, but its not as easy as it looks.

Its a lot harder than I thought itd be, its very technical."

Moorfields Eye Hospital, part of the NHS Foundation Trust, says Stargardt disease is a rare inherited condition affecting one in 8,000 to 10,000 people.

It explains: In Stargardts the light-sensitive layer of cells in the macular region of the eye degenerate.

The macular is the area at the back of the eye which is responsible for the fine detailed vision necessary for activities such as watching TV and reading.

Symptoms of the condition include:

Moorfields Eye Hospital says UV blocking sunglasses can offer some protection for remaining vision, but the condition is currently untreatable.

It adds: A number of novel interventions are currently under investigation, including stem cell therapies. Stem cells are a special type of cell which, when put under the right conditions, can develop into many other types of cell including those found in the macular. It is hoped that new cells derived from stem cells can be grown in a laboratory to be transplanted into the eye to replace areas of dead or non-functioning cells. Stem cells can be sourced from a number of places including blood, bone marrow, umbilical cord and fertilized egg cells.

Researchers are involved in Europes first ongoing stem cell trial for Stargardts. More research will need to be undertaken in the future to determine to what extent stem cell therapy might help improve vision for people with Stargardts.

Read more:
Libby Clegg health: Dancing On Ice star is registered blind - what is her condition? - Express

Driving with poor eyesight could be a danger to other road users and data from the DVLA shows thousands lose their licence due to eye-related problems. The DVLA data, requested by car insurance prover DirectLine, found 19,644 motorists had their licence revoked between January 2017 and September 2019 for inadequate eyesight.

The data equated to over 7,000 per year or a staggering 134 per week in a devastating blow for sufferers.

The survey of 2,000 had users found 21 percent of motorists had not got their eyes tested over the last two years.

If applied to all licence holders in the UK, almost nine million have not been checked for possible poor vision.

The data revealed Brighton had the highest percentage of motorists who had not had an eye test in the last two years.

READ MORE:DVLA: Driving licences are revoked for this medical reason

A total of 33 percent said they had not had their eyes checked, closely followed by Glasgow and Leeds where 30 percent of those surveyed admitted to not having a test.

It is against the Highway Code to drive with bad eyesight as this could put you and other road users at risk of having a car crash.

Ian McIntosh, CEO of RED Driving School toldExpress.co.uk: Impaired vision may mean drivers are not able to accurately judge stopping distances or identify hazards in sufficient time.

Road signs and signals are key to ensuring road safety is adhered to those with poor eyesight can often end up reading these too late or missing them completely, putting themselves and other drivers in danger.

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Impaired vision can often slow down reaction times, which are imperative for safe driving practices.

Police officers can identify motorists who may not be able to see through simple warning signs such as direction changes and late braking.

Law enforcement can then conduct a simple roadside test to see if motorists have enough vision to legally drive.

This will usually involve reading a number plate from a minimum distance of 20.5 metres or five car lengths.

Failure to pass the test could result in your licence being revoked and could potentially lead to fines.

Driving with bad eyesight could be considered careless or dangerous driving which can see penalties dramatically rise.

In severe cases, motorists could be prosecuted and sent to court where fines could be up to 5,000.

Failing to inform the DVLA of a medical condition which affects their driving ability could also land road users with a 1,000 bill.

Those with bad eyesight may need to wear glasses to ensure they are road legal and can read road signs and identify hazards correctly.

Car insurance providers may refuse to pay out for repair bills in the event of an accident caused by bad eyesight if they believe a road user failed to take precautions.

Nor wearing your glasses could be considered an at-fault claim as you did not do everything in your power to prevent the crash.

Research from GEM Motoring Assist claims poor eyesight can be linked to more than 3,000 fatal or serious accidents each year.

Data from the Royal Society for the Prevention of Accidents (RoSPA) says around 1.8 million motorists use Britains roads below the minimum legal eye standard.

Ian McIntosh adds: If you notice a change in your eyesight, whether that be struggling to read road signs or difficulty driving at night, you should visit your opticians.

Eyesight deteriorates over time and can happen at any age, so its recommended all drivers have an eye test at least every two years.

Any issues with eyesight must be addressed straight away, as not to endanger any other drivers or cause road incidents.

Read more:
DVLA shock: Your driving licence could be revoked for driving with this condition - Express

Researchers have found that the majority of Swedish 70-year-olds could boost their vision either by getting glasses or changing the prescription of their spectacles.

The study, which was published in Acta Ophthalmologica, reported on findings from a survey of 1200 Gothenburg residents.

The participants were asked how they perceived their eyesight and whether they thought their daily life was affected by vision problems.

Around half of participants (560) also had their central vision, peripheral vision and contrast sensitivity examined.

Scientists found that 61.5% of those surveyed could improve their sight either by getting glasses or changing the prescription of their current spectacles.

PhD student at the University of Gothenburg, Lena Havstam Johansson, shared that visual impairment can creep up on patients, making it difficult for them to notice when their eyes are getting worse.

Its a good idea to visit an optician regularly when you get older, even if you dont feel your sight is deteriorating, Ms Havstam Johansson said.

Image credit: Pixabay/Free-Photos

Read more:
Six out of 10 Swedish 70-year-olds could improve vision by getting new spectacles - AOP

For the around 300,000 people in Australia who have glaucoma, about half dont even know they have it, Professor MacGregor said.

By the time they go and get their eyes checked, theyve got irreversible damage, because all the treatments we have are to prevent the condition getting worse, they cant resurrect the nerve cells that have died.

Glaucoma is the catch-all term for a group of related diseases of the eye that damage the optic nerve, usually because of high pressure inside the eyeball.

It causes a gradual loss of vision, usually starting with peripheral vision, often so gradually the sufferers arent aware there is a problem until they have lost a significant portion of their sight.

It is the leading cause of irreversible blindness worldwide and is predicted to affect 76 million people by the end of this year.

Paul Neumann was 49 when he was diagnosed with glaucoma about 20 years ago, except no one bothered to tell him.

I went in for a new pair of glasses and the optometrist sent me to an ophthalmologistwho gave me some drops to take, Mr Neumann said.

That was 20 years ago.

Paul Neumann is one of the first wave of what researchers hope will be a 20,000-strong cohort to investigate glaucoma risk.

More recently I asked the opthamologist, 'Do I actually have glaucoma?' and she said, 'Yes, you do'."

Mr Neumann is now taking part in the second phase of the research.

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Professor MacGregor said they wanted 20,000 people either with glaucoma or with a family history of glaucoma to take part, to help them make their test more accurate.

Theres a group of people especially who have a sort of intermediate level of risk, so we can offer them generic testing, but its not accurate enough yet to know exactly what their risk is, it might be lower or higher, he said.

If its higher, then those people need to be going to screening more regularly.

Anyone wishing to take part in the study can find a link at this website or email glaucoma_genetics@qimrberghofer.edu.au.

The research was published on Tuesday in the journal Nature Genetics.

Stuart Layt covers health, science and technology for the Brisbane Times. He was formerly the Queensland political reporter for AAP.

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Now you see it: Test spots risk of eye disease before vision is lost - The Age

All things digital rule, and most people these days are glued to a screen for several hours a day, slowly eroding away their precious eyesight. Whether at home, at the office, or even while travelling, it is almost hard to imagine life without mobile screens, computer screens and the television! For corporate professionals, both their professional and social life often involves staring intently at a screen. For these reasons, a lot of computer users today are developing digital eye strain or computer vision syndrome and experience symptoms such as eye strain, headaches, dry eyes and blurred vision, says Dr. Mahmood Husein, Head of the Ophthalmic Department, Saifee Hospital. If you spend a lot of time looking at a screen and have started to experience any of these symptoms, the first thing to do is to reduce your screen time. He further shares a few tips to take better care of your eyes:

1Place the screen at least 20 inches away from you. Ideally, the computer screen should be between 20-40 inches away. If it is too close or too distant, it may cause you to sit in an awkward position.

2Ensure that the screen is not too bright. When your screen is very bright, you are exposed to more blue light. This type of light can harm the eyes and affect vision. Instead, ensure that the room is well lit. Reduce the brightness of your screen and add a glare filter if possible. Also, reduce the colour temperature of your display in order to reduce the amount of blue light emitted by the monitor.

3Use a separate pair of computer glasses if necessary. Some people who do not need glasses for everyday use may benefit from using glasses specifically prescribed for computer use.

4Take a break and look away from your screen. Follow the 20:20:20 rule to reduce eye strain: every 20 minutes, look at an object about 20 feet away for 20 seconds. This change in focus helps relax the eye muscles.

5Keep your eyes refreshed. When you stare at a screen, you tend to blink less, which tires and dries the eyes. This, coupled with the air-conditioning, may result in the eyes becoming very dry. To avoid this, take a break every couple of hours to splash some cold water on the eyes. Remember to blink more often to keep the eyes lubricated. Cooling drops also help. If you still experience any vision troubles, visit an ophthalmologist at the earliest. IANS

Link:
Words of wisdom, for the digital junkies - The Tribune

New research by Dorothy P. Schafer, PhD, at the University of Massachusetts Medical School, reveals the molecular process in which synaptic connections in the brain are damaged in multiple sclerosis and how this contributes to neurodegenerative symptoms. The paper, published in Immunity, also shows how gene therapy may be used to preserve neural circuits and protect against vision loss in the disease.

These findings suggest a path for developing therapies that may protect synapses from the damaging effects of MS and could be broadly applicable to other neurodegenerative disorders, according to Dr. Schafer, assistant professor of neurobiology, and Sebastian Werneburg, PhD, a postdoctoral fellow in the Schafer lab.

"Most MS research and FDA-approved treatments focus on demyelination and axon death," said Schafer. "Far less is known about what happens to the synaptic connections between neurons, which has proven to be a key aspect of neurodegeneration likely leading to cognitive decline in other diseases such as Alzheimer's disease."

Multiple sclerosis is a neurological disease of the central nervous system affecting more than 2 million people worldwide. The disease involves an abnormal response of the body's peripheral immune system against the brain, spinal cord and optic nerves, which damages the fatty substance surrounding nerve fibers called myelin. Recurrent episodes of inflammation result in demyelination. As the myelin is stripped away, the nerve fibers are exposed to inflammatory attacks from the immune system and the transmission of nerve signals within the central nervous system are altered or stopped completely. A small subset of MS patients experience chronic progressive neurodegenerative symptoms accompanied by significant synaptic loss and central nervous system atrophy. This version of the disease is called progressive MS.

FDA-approved medications for treating MS have been developed to limit and reduce the number of relapses, which delay progression of the disease and minimize demyelination, but there is no cure for the disease and patients are still left with disability. Current therapies work to inhibit peripheral immune attack of the central nervous system and inflammatory demyelination, but the neurodegenerative aspects of the disease have proven harder to decelerate, particularly for patients with progressive MS.

Vison loss is one of the most common symptoms of MS and is often one of the first that patients notice. Problems with vision result from damage to the optic nerve that connects the eye to the brain or from lack of coordination in the eye muscle.

"The retinogeniculate system, which comprises neurons that extend their axons via the optic nerve to the thalamus in the brain, is an ideal model for investigating MS because it's easy to access for therapeutic intervention, subtle changes can be readily detected and the visional pathway is affected in almost half of all patients with the disease," said Dr. Werneburg.

Profound synaptic loss was observed in animal models as microglia engulfed and eliminated presynaptic connections. Microglia are the immune cells of the central nervous system and are emerging as key players in regulating neural circuit structure in health and disease. One of the vast number of functions microglia perform in the brain is similar to the role macrophages perform in the immune system: clearing cellular decay and dead neurons from tissue.

"We found the protein C3 in abundance at synapses," said Werneburg.

C3 is not normally found in adult brain tissue. C3 protein usually only shows up in neural tissue during the developmental stages of the brain when synapses are being pruned. Synaptic pruning eliminates weak or unused synapsis as the brain matures to help efficiency and conserve energy.

In the case of demyelinating disease, it is not known why C3 is being produced and activated. This complement protein binds to synapses, sending the signal to microglia that the otherwise healthy-seeming synapse should be eliminated. This leads microglia to attack synapses.

Schafer, in collaboration with Guangping Gao, PhD, the Penelope Booth Rockwell Professor in Biomedical Research, professor of microbiology & physiological systems, director of the UMMS Horae Gene Therapy Center and Viral Vector Core, and co-director of the Li Weibo Institute of Rare Disease, used a gene therapy approach and adeno-associated virus to deliver Crry, an inhibitor of C3, specifically to synapses in the visual system while leaving the rest of the brain untouched, to see if synapses could be spared and vision preserved. Crry is a natural inhibitor of complement proteins such as C3. These regulators help protect cells or tissue from unwanted attack by the immune system.

After injection of the AAV into the circuit, Crry localized to synapses and successfully preserved them by binding to C3 so microglia couldn't damage them.

"As a result of this inhibition, we saw improved visional function in mice," said Werneburg.

Schafer said the protective effects of the AAV-delivered inhibitor were specific to the visual circuit. "It's possible that therapies targeting different circuits of the brain can be used to protect against synaptic damage in other neurodegenerative diseases such as Alzheimer's."

The next step for Schafer and colleagues will be to determine how the C3 protein is being activated and produced during MS and other neurodegenerative diseases.

Reference: Werneburg, S., Jung, J., Kunjamma, R. B., Ha, S.-K., Luciano, N. J., Willis, C. M., Gao, G., Biscola, N. P., Havton, L. A., Crocker, S. J., Popko, B., Reich, D. S., & Schafer, D. P. (2020). Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease. Immunity, 52(1), 167-182.e7. https://doi.org/10.1016/j.immuni.2019.12.004

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Gene Therapy Protects Eyesight in Models of Multiple Sclerosis - Technology Networks

Early research in animal models and human samples reveals how loss of communication between nerve cells contributes to the symptoms of multiple sclerosis (MS), and shows how gene therapy could be used to preserve such connections and protect againstvision loss.

Researchers say their work identifies a new approach for developing MS therapies that target nerve cell communication, rather than myelin loss, and could be applicable to other neurodegenerative disorders.

The study, Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease, was published in the journal Immunity.

MS is a neurological disease marked by inflammation and a self-attack of the immune system against a persons brain, spinal cord, and optic nerves.

This attack damages the protective fatty substance covering nerve fibers (axons), which are necessary for proper transmission of nerve signals called myelin. As the myelin sheath is lost (demyelination), the communication between nerve cells is damaged or even interrupted, and nerve cell death occurs, leading to a range of disease symptoms.

Some MS patients experience a version of the disease called progressive MS, in which symptoms continuously worsen over time while their central nervous system (brain and spinal cord) shrinks (atrophies), and the junctions at which nerve cell terminals meet to communicate with each other, called synapses, are lost.

The majority of MS medications work to inhibit the self-attacking immune responses and inflammatory demyelination, but the neurodegenerative aspects of the disease have been more difficult to stop, particularly for patients with progressive MS.

Most MS research and FDA-approved treatments focus on demyelination and axon death, Dorothy P. Schafer, PhD, professor at the University of Massachusetts Medical School, said in a press release.

Far less is known about what happens to the synaptic connections between neurons, which has proven to be a key aspect of neurodegeneration likely leading to cognitive decline in other diseases such as Alzheimers disease, Schafer said.

Using tissue samples from deceased MS patients, a primate model of MS, and mice models of demyelinating disease, Schafer and colleagues investigated how synapses change during MS.They specifically looked at synapses involved in transmitting visual information from the eye to the brain via the optic nerve.

According to the studys first author, Sebastian Werneburg, PhD, a postdoctoral researcher at Schafers lab, the visual system is an ideal model for investigating MS because its easy to access for therapeutic intervention, subtle changes can be readily detected, and the visional pathway is affected in almost half of all patients with the disease.

Most MS patients experience vision problems at some point, which result from damage to the optic nerve or from lack of coordination in the eye muscle. These problems can be the first indication of the disease.

Similar to other neurodegenerative diseases, researchers found a profound synaptic loss in patient samples as a consequence of immune cells called microgliaeating nerve cell connections.

Microglia are cells that serve as one of the first and main forms of immune defense in the central nervous system, acting to clear cellular debris and dead neurons via phagocytosis a process by which some cells engulf other cells or particles.

In mice, synapse loss occurred independently of local demyelination and neuronal degeneration, but coincided with a rise in a specific immune factor called C3. C3 is part of the complement system, and is normally not present in the brains of adults. It is produced and activated during demyelinating diseases, but it is not clear why.

As C3 was seen to bind to synapses in models of MS, researchers reasoned this complement protein might be involved with the ongoing destruction of synapses in mice with MS-like disease.

To test this hypothesis, they specifically neutralized C3 at synapses of the visual pathway using gene therapy in mice. The strategy basically worked by delivering genetic material to synapses that provided instructions for the production of a C3 inhibitor.

After injection of the therapy, the inhibitor successfully blocked C3, reduced microglia engulfment, and preserved nerve cell connections, which improved eyesight in mice.

As a result of this inhibition, we saw improved visional function in mice, Werneburg said.

Overall, based on the results, the team believes that C3 probably is sending a signal to microglia telling them to eliminate synapses.

The next step will be to determine how C3 turns active during MS and other neurodegenerative diseases.

Its possible that therapies targeting different circuits of the brain can be used to protect against synaptic damage in other neurodegenerative diseases such as Alzheimers, Schafer said.

Ana is a molecular biologist with a passion for discovery and communication. As a science writer she looks for connecting the public, in particular patient and healthcare communities, with clear and quality information about the latest medical advances. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she specialized in genetics, molecular biology, and infectious diseases

Total Posts: 1,053

Patrcia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.

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Gene Therapy Recovers Vision in Mice Models of MS, Uncovers How... - Multiple Sclerosis News Today

Glaucoma is a serious and lifetime eye disease that can cause permanent vision loss if not controlled before time. The Australian researchers have studied 107 genes that are involved in increasing the risk of eye disease glaucoma and identified a genetic test for those who are at the risk of getting blind.

The researchers are in search of many other genes that cause eye disease. The research conducted by the QIMR Berghofer Medical Research Institute and FlinUniversity finds that glaucoma-related blindness happens due to optic nerve degeneration and it is the most important cause of blindness in the whole world and researchers predicts that 76 million people will be affected by it in 2020. Possible cure for glaucoma is not found yet and fifty percent of people dont know that they are living with glaucoma.

This research was published in the journal Nature Genetics.

Stuart MacGregor, an associate professor of QIMR Berghofers Statistical Genetics Group explains that with the help of newly identified genes the people with eye disease can be identified with the help of a glaucoma polygenic risk score (PRS).

MacGregor finds that the only way to stop the loss of eyesight from genetic disease glaucoma is the discovery and the treatment of disease before time.

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It can be determined which person has eye disease or who will have in the future and need early treatment by analyzing the DNA taken from blood or saliva. If the people came to know before the time that in the future they will get glaucoma, they can take basic precautions that can prevent them from getting glaucoma.

Professor Jamie Craig, a clinical lead researcher and Academic Head of Ophthalmology at Flinders University, hopes that mass screening will be accessible for glaucoma in the next years.

Professor Craig finds that if the people are given a proper treatment earlier can be prevented from blindness. Many people come to know about glaucoma when visits the optometrist for a normal eye check-up or the loss of vision is felt by them. The early detection of glaucoma is necessary because the lost vision cant be restored even if the treatments are provided. The late detection is the main reason for blindness.

Most of the people are affected with glaucoma in older age but it can occur at any time of age. The researchers want to suggest blood tests to the older people that will help in the detection of glaucoma and will protect them from blindness.

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To identify the more genes the researchers want to sign up twenty thousand people with the record of disease in family or person to connect them with the Genetics of Glaucoma Study

This will benefit the researchers to approach all those people who are at high risk of disease or to those who are at lower risk and can be protected from getting blind by providing them the existing treatments. This study provides new insights for people with weak eyesight who are near to fifty to pay more attention to regularly visit the optometrist. It would protect their eyes and reduce the risk of permanent blindness in later years.

Link:
Early Detection And Prevention Of Blindness Associated With Glaucoma - TheHealthMania

A Mayo woman is raising funds for her niece who is losing her sight from three different eye conditions.

Magdalena Krawiec, originally from Poland, wants to help her goddaughter Zuzia Krawiec to get the best care possible.

Zuzia, four, was born with an eye disease called congenital nystagmus, which can be caused with the eye itself or by a problem with the visual pathway from the eye to the brain.

Around four months after she was born, Zuzia was then diagnosed with hyperopia astigmatism.

The condition affects Zuzias sight so that objects close to her are out of focus.

This along with her mcular hypoplasia, which she was only diagnosed with recently, make it impossible for her to see anything in detail.

Her aunt told Extra.ie: The macular hypoplasia is the worst because theres not much we can do about it.

It affects the vision clarity and because of it she will never be able to see clearly. She can only see as far as one metre and its basically shadows and lights

Were working on her sight so that she will eventually be able to see 10 or 15 metres in front of her but thats going to be over many years.

Zuzia has to take medication and do exercises to help her eyes improve but shes also had to have surgeries.

Shes had one of ten surgeries so far and the family are looking into stem cell treatment, which more people are interested in in recent years.

The family hope to schedule her second operation soon as the masses are really loose behind her eye and they need to tighten those muslces.

This operation will held Zuzias eyeball become more steady and so help her look straight because right now theyre all over the place.

Theyre kind of shaky, Magdalena continued. Thats the problem.

Zuzia is currently in play school but once a week she goes to a special school where she does two hours of different exercises for children with disabilities.

One hour she learns how to use her hands to recognise objects and another hour Zuzia uses an optical enlarger, something her family hopes to buy her so she can see things better.

It will be able to help her see better as it makes pictures at least 50 times larger, Magdalena said.

Zuzia needs constant care, her aunt tells Extra.ie, so that she doesnt hurt herself as she walks around.

Magdalena said: She needs help going to the toilet or going outside, anything where there may be obstacles in her way.

She cant see so she could walk into a wall or something, she could hurt herself.

Zuzia will never have the same sight the average person has, but with the operations she may gain better sight.

Magdalena revealed that she and her family dont know the root of the problem and hope genetic tests will help them get an idea of what is going on.

The genetic tests have to be done through the national health service and can take two to three years, but another huge hit is the cost of the tests.

Its around 2,500, Magdalena said. Its ridiculous because shes young, we need to do it as quick as possible.

The brain is getting used to the eyes not working, so the quicker we get it fixed the better. We want her to actually see something.

Despite her eyesight, Zuzia is a happy child and a big sister to her baby brother.

However, Zuzia has started asking about her brothers sight, wondering: How come he can see and I cant?

Its heartbreaking, Magdalena admitted. Its hard to explain to her that her eyes are sick.

To help her family, Magdalena set up a GoFundMe page to raise money for Zuzias operation and her care, which you can donate to here.

Magdalena has also has a collection point in The Breadski Brothers store in Westport to help raise funds.

She really needs specialised care, especially during these early years in her development, to improve her chances of avoiding total blindness and giving her the childhood she deserves.

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Mayo woman raising funds for niece, 4, who is losing her sight from three different eye conditions - Extra.ie

Dr Ezekiel Tallam with patients who have undergone surgery to treat trachoma, on January 14. [Mercy Kahenda, Standard]For a 70-year-old with impaired vision and no one to help him back up when he stumbles, life can be a punishment. Asman Chepochepunjo has been living alone inChemsarel village in Tiaty, Baringo County, after he was abandoned by his family when he became blind.He resorted to traditional herbs, but the condition worsened, making it hard for him to look after his livestock in the rocky locality.On the verge of becoming blind, Mr Chepochepunjo learnt he was suffering from trachoma, a neglected tropical disease in Baringo County.

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Hope in sight for locals as cases of punishing eye disease reduce - Standard Digital

A new study suggests its time you stopped worrying about cutting carbs or limiting the amount of fat in your diet. To live longer, its more important to focus on the quality of the foods than the quantity of carbs or fats they contain, according to a study from the JAMA Internal Medicine journal.

This means limiting processed carbohydrates, sugar, red meat and processed meats, and emphasizing whole grains, nuts, fruits and vegetables.

In the study, researchers asked more than 37,000 adults in the United States what they ate in the course of a 24-hour period in 1999 then followed them for 15 years.

At the end of the study the average age of the participants was 50 years old, and 4,866 of them had died around 13 percent of the group. Justless than half of those who died succumbed to heart disease (849 people) or cancer (1,068 people), certain types of which have been linked to diet.

Researchers found no difference in the risk of death between people on low-fat versus low-carb diets. Instead, the sources of those carbs or fats was what either risked or helped prevent an early death.

Low-fat diets full of unhealthy foods such as white bread, processed meats and sugary soda were associated with a 12 percent elevated risk of death, while similarly unhealthy low-carb diets made people 16 percent more likely to die.

People eating low-fat and low-carb diets composed of healthy foods including vegetables, fruits, legumes and whole grains lived longer, enjoying a 27 percent decreased risk of death.

Low-carb or low-fat diets can be good or bad depending on the foods that go into them, researcher Andrew Mente, who wasnt involved in the study, told Reuters.

Its more about selecting whole natural or minimally-processed foods, regardless of the amount of carbs or fat, Mente told Reuters. This would translate into a diet that may include a variety of whole foods in various combinations including fruit, vegetables, legumes, nuts and fish as well as whole fat dairy and unprocessed red meat and poultry.

Originally posted here:
New study says low-carb and low-fat diets don't boost longevity. Here's what does. - The Hill

(Editors note: This article is part of an editorial partnership between Next Avenue and The American Federation for Aging Research (AFAR), a national nonprofit whose mission is to support and advance healthy aging through biomedical research.)

Are you as old as you feel, as old as you look or as old as your birth certificate says? The best answer may be none of the above.

Actually, you may be as biologically old as your blood says you are.

For many years, aging researchers have sought markers of biological age, or biomarkers simple signals that reveal the expected length of your future health. The expected length of future health, after all, is the key biological difference between younger and older people.

Some people have called such markers biological clocks. I dont know about you, but I dont typically calculate my age by thinking of clocks. I think of calendars. So, I prefer to call these hypothetical signals biological calendars.

Plasma proteins may turn out to be just the type of biological calendar we are seeking.

The importance of these calendars is that they potentially allow researchers to quickly see whether a new drug, diet or other treatment that purports to slow, or even possibly reverse, aging is actually doing so.

Biological calendars of aging can also provide rapid feedback on how a lifestyle change, such as in diet or exercise habits, is affecting your biological age. This insight can motivate people to stick with that change.

Now, as a biological calendar, blood is a devilishly complex stew. Like a stew, it is liquid with lumps in it. We call the liquid plasma; the lumps, cells. Physicians for the past century have been using chemical analysis of plasma and counts of the various blood cell types to diagnose diseases. But we are now entering a brave new world of blood analysis.

Plasma contains not just the dozen or two chemicals that standard laboratory tests measure; it contains a constantly changing mixture of vitamins, nutrients, waste products, hormones and thousands of different proteins.

A hint that plasma might hold secrets about aging has come from research in which the plasma from young mice (or humans!) was found to rejuvenate the function of muscles, brain, heart and other organs of old mice. Dracula, it turns out, may have been onto something.

Recent advances in chemical analysis allow us to measure thousands of plasma chemicals at once, and advances in machine learning are helping make sense of that torrent of information. Plasma proteins may turn out to be just the type of biological calendar we are seeking.

I say this because a recent study of about 3,000 plasma proteins found that a specific combination of 373 of these proteins could accurately tell the age of the person from whom it was drawn. The study was conducted by AFAR Scientific Director Dr. Nir Barzilai with AFAR grantees David Gate of Stanford University and Dr. Sofiya Milman and Dr. Joe Verghese, both from the Albert Einstein College of Medicine in New York.

On top of that, people who were judged by their proteins to be younger than their real age scored better on a panel of physical and mental tests. We dont know yet how well these proteins might predict future health or life, but those studies will soon follow.

Blood cells, in addition to plasma, might have an even more promising aging tale to tell.

Your white blood cells (but not your red cells) contain your DNA, which provides the instruction manual for pretty much everything that goes on in your body. A few years ago, it was hoped that telomeres those protective DNA caps at the ends of your chromosomes from white blood cells might be a useful biological calendar. But telomeres as predictors of future health have not held up to scientific scrutiny.

However, we may have just been looking at the wrong part of our DNA.

Although we tend to think of DNA as little more than a long-coded sequence of DNA letters, there is a bit more to it. In particular, there are a number of small chemical tags that attach to DNA at specific sites to help turn off, or turn on, genes.

In recent years, combinations of particular tags called DNA methylation have, like plasma proteins, been shown to be good predictors of age and health in people and animals. These tags have even been shown to predict time to death and the development of later life diseases in people.

Perhaps even more exciting, a small, very preliminary study of 10 middle-aged men taking a hormone cocktail designed to stimulate the immune system showed a one-and-a-half-year regression in their DNA methylation calendar.

Lets not get too excited about this result yet. It is easy to overinterpret such very preliminary results, as some of the media have done. We have no idea at present what a small backward trend in DNA methylation age means, and this study has more than a few limitations. But it is without doubt provocative.

Stay tuned. Analysis of blood cells and blood plasma may hold secrets of aging that we are just beginning to discover.

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Originally posted here:
Does Our Blood Hold the Secrets of Our Longevity? - Next Avenue

SOPHIA Natural Health Center in Brookfield will be holding anupcoming FREE lecture, "The 6 Dynamics of Health and Longevity". This lecture willbe held exclusively at the Danbury Library.

Register online at the Danbury Library: https://bit.ly/30LIZyJ

Or RSVP at 203-797-4505

What is your health plan? Are you confused about all the different health information out there? Would you like to take charge of your health? This presentation will share the ancient secrets that you can apply TODAY that will help you take action. You will learn tools to start resolving your health issues naturally, regain energy, lose weight, balance hormones, restore health and regain vitality.

When: Thursday, February 13, 2020 - 5:30 PM 6:30 PM

Where: Danbury Library: 170 Main Street, Danbury, CT in the Farioly Program Room Cost: FREE

Visit our website: https://bit.ly/2vhaQLs

Read more from the original source:
Feb 13 | The 6 Dynamics of Health and Longevity Lecture | Brookfield - Patch.com

While we know that its important to watch exactly what were putting in our bodies, this study proves that when implemented correctly and nutritiously, a low-carb diet can boost longevity.

Just because someone is on a low-carb diet, however, does not mean that they are necessarily being healthy. According to the study, These findings suggest that the associations of low-carbohydrate and low-fat diets with mortality may depend on the quality and food sources of macronutrients.

The study brings into conversation the important aspect of certain diets like these: the sources of carbs and fats arent well-enough defined to thrive off of only counting carbs or calories. Head researcher Zhilei Shan, Ph.D. says, The debate on the health consequences of low-fat or low-carbohydrate diets is largely moot unless the food sources of fats or carbohydrates are clearly defined.

This research may be especially relevant to those just starting on the keto dietwhile limiting your daily carb intake may keep you in ketosis, its also essential to make sure youre utilizing those few carbs to get nutrientsthings like fruits, veggies, nuts, and grains.

More here:
Low Carb Diets Can Boost Longevity, But Only If You Do This - mindbodygreen.com

Cara Santana opened up about how she made her romance with ex-fianc Jesse Metcalfework just a few hours before they split.

The Santa Clarita Diet alum, 35, told Us Weekly exclusively on January 4 that maintaining balance in her relationship with Metcalfe, 41, has allowed them to be successful after 13 years together. Its the thing that really, like, probably has given us such longevity in our relationship, she told Us at the Art of Elysiums 13th annual celebration, where she and Metcalfe made their last appearance as a couple.

We both have such fulfilling professional lives and were both so ambitious and Im really focused, she continued. So, I think thats something that we really respect in one another and that creates balance, because youre separate and then you really value the time that you have together. I think its all part and parcel of, like, what makes us work.

Us broke the newson Wednesday, January 22,that Metcalfe and Santana split on January 4andare not together. A source added,They are not even living together. He did not cheat on her.

On Wednesday, the Daily Mail posted photos of the Desperate Housewives alum cozying up with two different women weeks after Santanas comments to Us. He was photographed holding hands with model Livia Pillmann while dining at Gracias Madre in West Hollywood. Hours later, he was spotted getting close to another woman while visiting Attic bar in Sherman Oaks, California.

In August 2016, Us exclusively reported Metcalfe and Santana were engaged after dating for a decade. The John Tucker Must Die actor asked for his former longtime loves hand in marriage with a 5.5-carat diamond sparkler while aboard a sailboat on the Hudson River in New York. Metcalfe told Us at the time that their engagement was a long time coming and that they couldnt be happier.

More than two years into their engagement, Santana confirmed to Us exclusively in March 2019 that the exes were nowhere in their wedding planning process.

At this months Art of Elysium event, Santana talked about how she and Metcalfe have done their relationship on their own terms over the years. In a modern couple, its nice to be able to be like, Hes 41, Im 34 and were taking our time, the fashion blogger. And its just easy.

Santana added that it would be hard to imagine their lives without children in the picture. But she had no desire to start a family at the time.

Thats like the worst sound bite ever, but I have to have two amazing dogs. Were fostering a medically fragile French Bulldog right now and so those three dogs feel like my children, she continued. Jesse, hes like a grown man child. So, you know, theres that too.

With reporting by Carly Sloane

Go here to see the original:
Cara Santana Opened Up About the Longevity in Jesse Metcalfe Relationship Just Hours Before Split - Us Weekly

Its good to always be thinking however new research shows you may want to give your brain a break sometimes.

Healthy cognition is made possible by two opposing functions: neural excitation and neural inhibition. The former makes nerves more active while the latter achieves just the opposite.

Up until very recently the effects of this counter-balance were relatively unknown but a preliminary new report published in the journal Naturemotions an intriguing correlation.

The physiological activities that regulate metabolism also play a huge role in exciting our nervous system. According to the new paper prolonged hyper-activity bears the potential to shorten our lifespan.

This hypothesis began with an examination of brain tissue extracted from deceased humans. Subjects that evidenced increased neural activity died younger than those who did not. Because the disparity was upwards of ten years, the researchers set out to identify a primary effect.

From the report: Here we show that extended longevity in humans is associated with a distinct transcriptome signature in the cerebral cortex that is characterized by downregulation of genes related to neural excitation and synaptic function. Furthermore, longevity is dynamically regulated by the excitatory-inhibitory balance of neural circuits.

Depending on the objectivesome species are more conducive to human translation than others. Since the researchers wanted to examine the impact neural hyperactivity has on lifespan, worm models served the criteria well, given they do not live very long.

Following several follow-up trails, the Harvard researchers were confident about excitation being a crucial correlate of longevity.

As the worms aged their brain activity naturally increased, as is the case with humans. When administered a drug that inhibited neural activity the worms lived longer than the control group. When the researchers administered a drug that stimulated neural activity the inverse was demonstrated.

This meant excitation produced a profound effect on lifespan all on its own. To locate the specific protein that was at play, the researchers swapped the worms for mice models; animals frequently employed in the service of degenerative disease research. Mice and humans share many genetic similarities. Ninety-seven percent of our working DNA is identical to be more precise.

The deceased mice analyzed showcased a neurological journey parallel to the dead worm models. Moreover, after examining the genetic material of the living rodents with a complex computer algorithm an influencing CEO protein was successfully isolated.

The expression of a protein previously linked to the progression of dementia called REST, directly surged or diminished neural activity in the mouse models.

The transcription factor REST is upregulated in humans with extended longevity and represses excitation-related genes. Notably, REST-deficient mice exhibit increased cortical activity and neuronal excitability during aging, the report continued. These findings reveal a conserved mechanism of ageing that is mediated by neural circuit activity and regulated by REST.

Though pioneering, the data is leagues away from human application. The increased and decreased REST expression was engineered for the purpose of research but there are lifestyle changes you can make to pump the brakes on neural excitation. For more on these methods please refer to an article published by Ladders on the proven benefits of interception.

When we over-expressed or turned up, this protein in the worm, the worm now, interestingly, reduced the amount of nervous system excitation and lived longer. When we did the opposite, when we turned it down, we actually got more excitation and the worm lived a shorter lifespan, the studys co-author Dr. Bruce Yankner, a professor of genetics and neurology at Harvard Medical School explained toTime Magazine.

In the same press release the professor expressed interest in furnishing the ways in which a persons thoughts, personality and behavior affect their overall health and longevity.

Continue reading here:
Harvard scientists find people with more brain activity have shorter lives - Ladders