Look, something shiny! How color images can influence consumers


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

When it comes to buying things, our brains can’t see the big, black-and-white forest for all the tiny, colorful trees.

That’s the conclusion of a study at The Ohio State University, which found that people who were shown product images in color were more likely to focus on small product details — even superfluous ones — instead of practical concerns such as cost and functionality.

The findings, published in the Journal of Consumer Research, mesh well with notions of how vision evolved in the brain, and suggest that viewing objects in black and white helps our brains focus on what’s most important.

“Color images help us notice details,” said Xiaoyan Deng, an author of the study and assistant professor of marketing at Ohio State. “But black-and-white images let us see the ‘big picture’ without getting bogged down by those details.”

The findings also suggest how marketers can strategically use color — or its absence — to change how we feel about a product.

“Marketers may take it for granted that color is always the best presentation format for advertising,” Deng added. “This study shows that while color is desirable in most situations, it’s not desirable in all situations.”

If a product has broad features that set it apart from the competition, then black-and-white images will help customers cast aside minor details and focus on those key features, the researchers found. If a product’s details are what set it apart, color images will make those details stand out.

In one part of the study, 94 college students were asked to imagine that they were traveling to a remote campsite where they could receive only one radio station. There, the campsite manager offered two radios for rent: a basic analog radio for $10 a day, or a fancy digital radio with many station preset buttons for $18 a day. Not only was the digital radio more expensive, but its preset buttons would be useless at the campsite.

Students who saw pictures of the radios in black and white tended to make the practical choice — the analog radio. Only 25 percent chose the digital radio.

But among students who saw the radios in color, twice as many chose the digital radio. In that scenario, 50 percent of students were willing to pay a higher price for a radio with features that they could not use.

“Color drew their focus away from the most important features to the less important features, and their choice shifted to the more expensive radio,” Deng said. “I think that’s surprising — that just by manipulating whether the product presentation is in color or black and white, we can affect people’s choice.”

Color also proved to be a distraction when study participants were asked to sort objects into groups. The researchers recruited people through Amazon Mechanical Turk, a service that provides online study participants.

The 287 participants were shown pictures of shoes and asked to sort them. Each grouping contained two types of shoes that differed greatly in form and function, such as open-toe high heels and rain boots. In that particular example, half of the high heels and the boots were a solid red color, and the other half were red with white polka dots.

When people viewed the shoes in black and white, they sorted the high heels into one group and the rain boots into another 97 percent of the time. But when they saw the shoes in color, that number dropped to 89 percent, with 11 percent sorting the solid-color high heels and boots into one group and the polka-dot heels and boots into another.

The polka dots were clearly visible in black and white, but they had more impact on participants’ decision-making when they were seen in color.

Study co-author Kentaro Fujita, associate professor of psychology at Ohio State, has an idea why. It has to do with the origin of our visual systems, and how our brains process night vision.

Of the light-sensitive rod and cone structures in the retina, it’s the cones that detect color and the rods that give us night vision, peripheral vision and motion detection. Rods outnumber cones in the eye 20 to 1, and at night, when the cones don’t receive enough light to let us distinguish colors properly, we rely on the rods to see what’s happening around us — in black and white.

This would have been especially true for early humans, who didn’t have sources of artificial light. At night, being able to tell the difference between objects by shape would have been key to survival.

“Our visual systems evolved to work in both optimal and suboptimal conditions,” Fujita explained. “Optimal conditions might be during the day, when I want to distinguish a red apple from a not-so-red apple. The form of the object tells me it’s an apple, but I can focus on the color because that’s what’s important to me. Suboptimal conditions might be at night, when I have to tell whether that object that’s moving toward me is my friend or a hungry lion. Then the form of the object is critical.”

He suspects that when our eyes see black-and-white images, our brains interpret them in ways similar to night vision: We focus on form and function, and tend to ignore details.

Deng pointed out another circumstance in which people “see” in black and white: when we imagine the distant future. Other studies have shown that people who are asked to think of an event from the near or distant future and then presented with a series of photographs tend to pick less colorful photos as most closely matching their vision.

“It’s almost like seeing in black and white is a vehicle for time travel,” she said. “When you need to visualize ambiguous, uncertain future events, you want to get away from all those details, to construct that future event in your mind in a meaningful way. Seeing in black and white allows you to construct that event.”

Marketers can take advantage of our ability to time travel, too. Deng said that black-and-white images would probably work well in ads for products that will be used in the distant future, such as retirement plans, investments or insurance.

Co-authors on the paper included marketing doctoral student Hyojin Lee, who performed this research for her dissertation, and H. Rao Unnava, senior associate dean and W. Arthur Cullman Professor of Marketing in Ohio State’s Fisher College of Business.

Boosting older adults’ vision through training


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

Just a weeks’ worth of training can improve vision in older adults, according to new research in Psychological Science, a journal of the Association for Psychological Science. The findings show that training boosted older adults’ sensitivity to contrast and also their ability to see things clearly at close distances.

“Our research indicates that the visual system of older adults maintains a high degree of plasticity and demonstrates that training methods can be used to improve visual function,” explains psychological scientist G. John Andersen of the University of California, Riverside who co-authored the study with graduate student Denton DeLoss and colleague Takeo Watanabe of Brown University.

Age-related declines in vision and visual processing are common and they can have serious negative consequences for the health and well-being of older adults. Older adults are particularly likely to show declines in their ability to process low-contrast visual stimuli — for example, images that are grainy or not clearly defined. This decline hampers their ability to see visual detail, and can hinder their ability to process information that is important for both balance and driving.

While some age-related declines in vision can be traced to the eye itself, research suggests that decline in other aspects of vision are the result of changes in brain function, and DeLoss and colleagues wondered whether a training program that involved repeated exposure to specific stimuli might counteract these changes in brain function.

The researchers recruited 16 young adults (on average, about 22 years old) and 16 older adults (on average, about 71 years old) to participate in the study, all of whom were screened to ensure that they didn’t show signs of cognitive decline or eye disease.

The participants came to the lab for 1.5-hour sessions over the course of 7 days. In general, each trial of the experiment involved looking at a striped visual stimulus and determining whether it was rotated clockwise or counterclockwise from its original orientation. The researchers varied the contrast of the stimulus across trials, altering how grainy or clear the image was.

Each day, the contrast threshold of the trials was calibrated to the participants’ previous performance so that they were training near the limit of what they could reliably detect. Participants were exposed to 750 trials on each training day, for a total of 3,750 training trials over the course of the study.

The data showed that visual training effectively eliminated the age deficit in contrast sensitivity. At the beginning of the experiment, younger adults outperformed older adults on the task; but the older adults improved with training, showing performance similar to that of their younger peers by the end of the 7 days.

Further analyses confirmed that these improvements stemmed from changes in visual processing in the brain and not changes in the eye.

“We found that the training effect was not due to factors such as dilating the pupils to let in more light to the retina,” explains Andersen.

Even more remarkable, both younger and older adults showed improvements in visual acuity when they were tested using an eye chart similar to the one at your doctor’s office. At the end of training, older adults showed improvement in near acuity, or the ability to see things clearly when they are near; younger adults, on the other hand, showed improved ability to see things clearly when they are far.

“Given the short training period, the degree of improvement is quite impressive, particularly in the cases of near and far acuity, in which subjects were able to read an average of two to three additional letters on acuity charts after training,” the researchers write.

It’s important to note that these findings don’t shed light on visual function among adults suffering from age-related eye diseases, such as glaucoma or macular degeneration. Nonetheless, the findings could have broad relevance for the many millions of adults who experience age-related decline in visual processing.

The researchers hope to further explore the mechanisms involved in perceptual learning and whether the effects of visual training carry over to real-world tasks, such as driving.

Stem cell injection may soon reverse vision loss caused by age-related macular degeneration


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

An injection of stem cells into the eye may soon slow or reverse the effects of early-stage age-related macular degeneration, according to new research from scientists at Cedars-Sinai. Currently, there is no treatment that slows the progression of the disease, which is the leading cause of vision loss in people over 65.

“This is the first study to show preservation of vision after a single injection of adult-derived human cells into a rat model with age-related macular degeneration,” said Shaomei Wang, MD, PhD, lead author of the study published in the journal STEM CELLS and a research scientist in the Eye Program at the Cedars-Sinai Board of Governors Regenerative Medicine Institute.

The stem cell injection resulted in 130 days of preserved vision in laboratory rats, which roughly equates to 16 years in humans.

Age-related macular degeneration affects upward of 15 million Americans. It occurs when the small central portion of the retina, known as the macula, deteriorates. The retina is the light-sensing nerve tissue at the back of the eye. Macular degeneration may also be caused by environmental factors, aging and a genetic predisposition.

When animal models with macular degeneration were injected with induced neural progenitor stem cells, which derive from the more commonly known induced pluripotent stem cells, healthy cells began to migrate around the retina and formed a protective layer. This protective layer prevented ongoing degeneration of the vital retinal cells responsible for vision.

Cedars-Sinai researchers in the Induced Pluripotent Stem Cell (iPSC) Core, directed by Dhruv Sareen, PhD, with support from the David and Janet Polak Foundation Stem Cell Core Laboratory, first converted adult human skin cells into powerful induced pluripotent stem cells (iPSC), which can be expanded indefinitely and then made into any cell of the human body. In this study, these induced pluripotent stem cells were then directed toward a neural progenitor cell fate, known as induced neural progenitor stem cells, or iNPCs.

“These induced neural progenitor stem cells are a novel source of adult-derived cells which should have powerful effects on slowing down vision loss associated with macular degeneration,” said Clive Svendsen, PhD, director of the Board of Governors Regenerative Medicine Institute and contributing author to the study. “Though additional pre-clinical data is needed, our institute is close to a time when we can offer adult stem cells as a promising source for personalized therapies for this and other human diseases.”

Next steps include testing the efficacy and safety of the stem cell injection in preclinical animal studies to provide information for applying for an investigational new drug. From there, clinical trials will be designed to test potential benefit in patients with later-stage age-related macular degeneration.

Advancements in retinal detachment research pave the road to better visual recovery


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

Retinal detachment occurs when layers of the light sensitive retina peel away from the back wall of the eye. The condition can be caused by age, injury or disease, and currently, the only available treatment is surgery to manually reattach the retina.

However, even with surgery, as many as ten percent of people will ultimately suffer permanent vision loss due to a problem that has puzzled researchers for decades.

“Despite having the detachment repaired, some people will develop a severe condition called proliferative vitreoretinopathy, or PVR, which causes scar tissue to grow on the retina,” said surgeon Colleen Cebulla, MD, PhD Assistant Director of the Retina Division at The Ohio State University Havener Eye Institute. “The brain depends on the retina to transform light into electrical pulses. PVR interrupts that process, causing vison problems ranging from distorted images to total blindness.”

Though there are many theories regarding PVR formation and prevention, it is still considered somewhat of a mystery. Fueled by a desire to offer her patients better post-surgery outcomes, Cebulla and a team of scientists at Ohio State have been studying how retinal scar tissue develops in the hopes of stopping it before it can start. Supported by several KL2 grants from Ohio State’s Center for Clinical and Translational Science (CCTS), Cebulla’s research is starting to reveal some answers.

“We found more than 500 proteins that are produced following retinal detachment, many of which trigger the kind of inflammation that starts the scarring process,” said Cebulla. “By identifying those proteins that are the most active, we can begin developing experimental therapeutics that alter those proteins and hopefully either help promote tissue regeneration or inhibit scarring.”

An estimated 57,000 people in the United States experience retinal detachment each year. The lifetime risk of developing a retinal detachment is about 1/300 and it remains a significant cause of legal blindness in the US, particularly if the macula has been damaged or if PVR develops, underscoring the need for better alternatives.

“What we are learning here not only applies to retinal detachment caused by trauma, but also people who have diseases like diabetes or macular degeneration. Having a non-surgical way to prevent retinal damage or help regenerate damaged tissue would impact millions of lives,” said Cebulla.


Cebulla’s identification of protein targets has been advanced significantly through the development of two novel animal models of retinal detachment.

In order to identify the target proteins, Cebulla developed a mouse model to conduct a proteomic study of how protein levels changed in response to retinal detachment. Using a technology called iTRAQ, Cebulla’s team were able to measure and monitor each individual protein to see how quantities changed over time, and then compare those to a control group.

With the target proteins identified, Cebulla then collaborated with neuroscientist Andy Fischer, PhD, at Ohio State’s College of Medicine, to develop the first ever chick model of retinal detachment. Chicks have a larger eye, making it easier for scientists to study the process of retinal detachment as well as the efficacy of experimental therapeutics versus smaller mammalian models. Unlike common mammalian models, chicks have good color vision, making their retinas rich in the type of cells found in a human eye.

“The development of new therapies for retinal detachment has been somewhat slowed by the high costs and difficulty of using smaller mammalian models,” said Cebulla. “The study of chicks offers several advantages that ultimately can help make our findings more applicable humans.”


Recently, Cebulla has started studying what happens inside the human eye after retinal detachment to supplement her observations from the animal models. During retinal detachment surgery, vitreous fluid is being collected from participating patients. Cebulla’s team will use the fluid sample, along with the patient’s blood to see how different proteins are being expressed.

Currently, Cebulla’s team has zeroed in on one protein in particular, and is testing a pharmacological agent that inhibits that protein to see if it can stop or slow the development of PVR and damage to the retina. She expects that she will have enough data to publish her next round of findings in just a few months.

“I’m hopeful that what we learn in our studies will identify a treatment that we can bring into clinical trials in the next five years, and that I’ll be able to tell my patients that I have something new that can help preserve their vision,” said Cebulla.

Brain development suffers from lack of fish oil fatty acids, study finds


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

While recent reports question whether fish oil supplements support heart health, UC Irvine scientists have found that the fatty acids they contain are vitally important to the developing brain.

In a study appearing in The Journal of Neuroscience, UCI neurobiologists report that dietary deficiencies in the type of fatty acids found in fish and other foods can limit brain growth during fetal development and early in life. The findings suggest that women maintain a balanced diet rich in these fatty acids for themselves during pregnancy and for their babies after birth.

Susana Cohen-Cory, professor of neurobiology & behavior, and colleagues identified for the first time how deficits in what are known as n-3 polyunsaturated fatty acids cause molecular changes in the developing brain that result in constrained growth of neurons and the synapses that connect them.

These fatty acids are precursors of docosahexaenoic acid, or DHA, which plays a key role in the healthy creation of the central nervous system. In their study, which used female frogs and tadpoles, the UCI researchers were able to see how DHA-deficient brain tissue fostered poorly developed neurons and limited numbers of synapses, the vital conduits that allow neurons to communicate with each other.

“Additionally, when we changed the diets of DHA-deficient mothers to include a proper level of this dietary fatty acid, neuronal and synaptic growth flourished and returned to normal in the following generation of tadpoles,” Cohen-Cory said.

DHA is essential for the development of a fetus’s eyes and brain, especially during the last three months of pregnancy. It makes up 10 to 15 percent of the total lipid amount of the cerebral cortex. DHA is also concentrated in the light-sensitive cells at the back of the eyes, where it accounts for as much as 50 percent of the total lipid amount of each retina.

Dietary DHA is mainly found in animal products: fish, eggs and meat. Oily fish — mackerel, herring, salmon, trout and sardines — are the richest dietary source, containing 10 to 100 times more DHA than nonmarine foods such as nuts, seeds, whole grains and dark green, leafy vegetables.

DHA is also found naturally in breast milk. Possibly because of this, the fatty acid is used as a supplement for premature babies and as an ingredient in baby formula during the first four months of life to promote better mental development.

The UCI team utilized Xenopus laevis (the African clawed frog) as a model for this study because it allowed them to follow the progression and impact of the maternal dietary deficit in the offspring. Because frog embryos develop outside the mother and are translucent, the researchers could see dynamic changes in neurons and their synaptic connections in the intact, live embryos, where development can be easily studied from the time of fertilization to well after functional neural circuits form.

They focused on the visual system because it’s an accessible and well-established system known to depend on fatty acids for proper growth and utility.

Epilepsy drug may preserve eyesight for people with multiple sclerosis


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

A drug commonly taken to prevent seizures in epilepsy may surprisingly protect the eyesight of people with multiple sclerosis (MS), according to a study released today that will be presented at the American Academy of Neurology’s 67th Annual Meeting in Washington, DC, April 18 to 25, 2015.

“About half of people with MS experience at some point in their life a condition called acute optic neuritis, in which the nerve carrying vision from the eye to the brain gets inflamed,” said study author Raj Kapoor, MD, with the National Hospital for Neurology and Neurosurgery in London, England. “The condition can cause sudden total or partial blindness, foggy or blackened vision and pain. Even though eyesight can recover eventually, each attack still damages the nerve and the eye.”

For the study, the researchers randomly selected 86 people with acute optic neuritis within two weeks of having symptoms to receive either the epilepsy drug phenytoin or a placebo for three months. The researchers then used medical imaging to measure the thickness of the retina, the light sensitive nerve layer at the back of the eye at the beginning of the study and then six months later. Each patient’s eyesight (including sharpness and color perception) was also tested.

The study found on average that the group who took phenytoin had 30 per cent less damage to the nerve fiber layer compared to those who received the placebo. The volume of the macula, the most light-sensitive part of the retina, was actually 34 percent higher in those who took phenytoin than those who received the placebo. As expected after a single attack, patients’ vision successfully recovered, and there weren’t any significant differences in visual outcomes over the long-term between the two treatment groups.

“Eyesight is key to many important aspects of life, such as working, driving and participating in social activities,” said Kapoor. “If this finding is confirmed by larger studies, it could lead to a treatment that may prevent nerve damage and blindness in MS, and could help other attacks of MS, serving a major unmet need.”

The study was supported by the National Multiple Sclerosis Society, Multiple Sclerosis Society of Great Britain and Northern Ireland, an unrestricted grant from Novartis, the National Institute for Health Research Clinical Research Network and University College London Hospitals Biomedical Research Center.

Caring for blindness: A new protein in sight?


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

Vasoproliferative ocular diseases are responsible for sight loss in millions of people in the industrialized countries. Many patients do not currently respond to the treatment offered, which targets a specific factor, VEGF. A team of Inserm researchers at the Vision Institute (Inserm/CNRS/Pierre and Marie Curie University), in association with a team from the Yale Cardiovascular Research Center, have demonstrated in an animal model that blocking another protein, Slit2, prevents the pathological blood vessel development that causes these diseases. This work is published in Nature Medicine.

Vasoproliferative ocular diseases are the main cause of blindness in the industrialized countries. Age-related macular degeneration (ARMD), diabetic retinopathy and retinopathy of prematurity (in newborns) are characterised by progressive involvement of the retina, the area of the eye that receives visual information and transmits it to the brain. This damage is caused by abnormal growth of the blood vessels in the retina. These weakened vessels allow leakage of serum–which causes a swelling that lifts the retina–and/or blood, which leads to retinal haemorrhage.

This process involves several proteins required for normal or pathological development of the blood vessels. The action of vascular endothelial growth factor (VEGF) is a particularly decisive factor in this ocular disorder. At present, the main treatments are aimed at blocking its action by injecting inhibitors into the eye. Some patients are or become resistant to these anti-VEGF therapies.

For this reason, the team led by Alain Ch├ędotal, in collaboration with a team led by Anne Eichmann , sought to identify new factors involved in the growth of new blood vessels, angiogenesis. They paid particular attention to Slit2.

Slit2 is a protein already known for its role in the development of neural connections. By acting on its receptors, Robo1 and Robo2, it is also involved in the development of many organs and certain cancers. The researchers therefore formulated the hypothesis that this factor might have a role in the abnormal vascularisation observed in vasoproliferative ocular diseases.

To test this postulate, the scientists inactivated Slit2 in a mouse model. They observed that ramification and growth of the retinal blood vessels were severely reduced, without any change in the stability of the pre-existing blood supply. Surprisingly, they discovered that without this protein, VEGF action was also partly reduced. By simultaneously blocking Robo1 and Robo2, they obtained the same results. They thus demonstrated that Slit2 is essential for angiogenesis in the retina.

“The success of these initial experiments led us to hope that controlling Slit2 might block the chaotic development of blood vessels in ocular diseases,” explains Alain Ch├ędotal, Inserm Research Director.

The team therefore repeated these tests in an animal model for retinopathy of prematurity. As they had suspected, the absence of Slit2 protein prevented abnormal vascularisation of the retina in these young mice.

This work suggests that therapies targeting Slit2 protein and its receptors, Robo1 and Robo2, might be beneficial for patients with vasoproliferative ocular disease, especially those who are resistant to conventional anti-VEGF therapies.

Moreover, it would be interesting to set up other studies to obtain a better understanding of the mechanism of action of Slit2 and its relationship with VEGF. This could open up new avenues for the treatment of tumours.

Nerve cells, blood vessels in eye ‘talk’ to prevent disease


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

A new study from scientists at The Scripps Research Institute (TSRI) shows that nerve cells and blood vessels in the eye constantly “talk” to each other to maintain healthy blood flow and prevent disease.

“It turns out these neurons produce a chemical critical for the survival of blood vessels and the survival and function of photoreceptors–the most important cells for maintaining sight,” said TSRI Professor Martin Friedlander, senior author of the new study.

The study, published online ahead of print in The Journal of Clinical Investigation, has implications for treating diseases such as diabetic retinopathy and age-related macular degeneration–the leading causes of vision loss in adults. Since the eye is often a good model for understanding the workings of the brain, the findings also provide clues to major neurological diseases such as Alzheimer’s.

Understanding the Eye

For such a small organ, the eye is extremely complex. Light enters through the pupil and passes through four layers in the retina before reaching the light-sensitive photoreceptors.

“The retina has a very sophisticated architecture,” said Friedlander. “If you have a little extra fluid, some swelling or a few dead cells, light isn’t going to come through correctly and vision can be impaired.”

The second, intermediate layer of the retinal blood vessels seems to activate during periods of low oxygen and acts as a “reserve” of blood vessels in the retina. When blood flow and oxygen levels are low, a transcription factor called hypoxia-inducible factor (HIF) triggers the production of a chemical called VEGF. The VEGF then prompts new blood vessel growth, bringing more oxygen to the area.

Unfortunately, these new blood vessels can leak blood and other fluids and obscure vision. This is the case with age-related macular degeneration–a “wet” version of which causes vision loss in the center of the eye–and diabetic retinopathy–in which some people with diabetes develop blurry or patchy vision.

A New Role for Neurons

In the new study, the team focused on neurons called amacrine cells and horizontal cells, which have a known role in “preprocessing”–or adjusting–electrical signals transmitted to the brain from the photoreceptors after they have been stimulated by light photons. These cells first caught the researchers’ attention because they appear to wrap themselves around the blood vessels (all together called the vasculature) of the intermediate layer.

“We wondered if these neurons were actually altering the way the vasculature forms and behaves,” said TSRI Research Associate Peter Westenskow, co-first author of the new paper with TSRI Research Associate Yoshihiko Usui.

To try to find out, in one experiment the researchers “knocked out” the production of VEGF in the amacrine and horizontal cells in mice before they were born. They found that these mice never developed normal blood vessels in the intermediate layer, leading to degeneration of the photoreceptors and severe vision impairment.

This was surprising since previous research had given no clues that these cells were an important source of VEGF.

Eye Spies

To track down more clues about the unexpected finding, the scientists set up further experiments to test whether amacrine and horizontal cells really did provide essential VEGF.

Because HIF signals cells to produce VEGF, the researchers wondered whether deleting HIF in amacrine and horizontal cells would also stop the pipeline of VEGF and normal intermediate layer blood vessel development. Indeed, the researchers found that deleting the gene for one form of HIF, called Hif-1a, also led to a lack of blood vessels in this area and subsequent vision problems.

This provided further evidence that VEGF from the amacrine and horizontal cells really does make a difference in blood vessel growth.

For an even better understanding of VEGF production in those cells, the researchers investigated the role of a protein called VHL (von Hippel-Lindau), which normally keeps HIF levels low. After knocking out the gene to produce VHL in amacrine and horizontal cells, the researchers observed high HIF levels, overproduction of VEGF and dangerous blood vessel overgrowth typical of many eye diseases. Finally, they used a technique called genetic ablation to kill the amacrine cells and horizontal cells altogether and found this resulted in a lack of normal vessel growth in the intermediate layer.

Together, the experiments confirmed that neurons and blood vessels in the intermediate layer communicate to keep blood vessels growing normally–striking a balance between providing enough blood and avoiding blood vessel overgrowth.

“This is fascinating,” said Westenskow. “The signals from these cells are fine-tuning this layer of the vasculature.”

A Window into the Brain

Since the retina is a direct extension of the brain and the only place in the body where scientists can easily visualize neurons, blood vessels and other neurological players working together, the study not only has implications for treating vision loss, but also brain diseases such as Alzheimer’s, Parkinson’s and even amyotrophic lateral sclerosis (ALS).

“For example, patients with Alzheimer’s get protein deposits in the brain, and we can see similar deposits in the backs of the eyes of patients who have macular degeneration,” said Friedlander. “If we can better understand what leads to accumulations of these abnormal proteins in the eye, that will hopefully also give us insight into how the brain works.”

First embryonic stem cell therapy safety trial in Asian patients


Posted on 1st May 2015 by Pacific ClearVision Institute in Retina

A clinical trial in the Republic of Korea for patients with degenerative eye diseases is the first to test the safety of an embryonic stem cell therapy for people of Asian descent. The study, which followed four individuals for a year after they were treated with embryonic stem cell-derived retinal pigment epithelial cells for macular degeneration, observed no serious side effects (tumor growth or other unexpected effects) related to the therapy. The researchers report the results on April 30 in Stem Cell Reports, the journal of the International Society for Stem Cell Research.

“This is mainly a safety study, and the goal is to prevent the progress of disease. So we were pleasantly surprised to see an actual improvement in visual acuity in the patients,” says lead author Won Kyung Song of CHA University’s Department of Ophthalmology. “However, this is a preliminary result. The positive responses from the patients need to be interpreted cautiously until controlled phase II studies are carried out.”

The Korean trial was a collaborative effort between scientists at CHA University and stem cell pioneer Robert Lanza at Ocata Therapeutics (formerly known as Advanced Cell Technology). Lanza previously led a clinical trial in the United States–published November 2014 in the Lancet –that demonstrated embryonic stem cells could be used safely for patients with degenerative eye diseases, but the patient sample was Caucasian with the exception of one African-American.

The patients in both trials either had age-related macular degeneration or Stargardt’s macular dystrophy, the leading forms of adult and juvenile blindness in the developed world. Both are currently incurable. An embryonic stem cell-derived retinal cell therapy is an attractive option because they can be used to regrow the retina cells that are lost in both diseases.

“Embryonic stem cells are among the most complex/dynamic clinical therapies ever proposed,” Song says. “It is important that the clinical trials are carried out in a safe and responsible fashion.”

CHA Biotech Co., Ltd., the sponsor company of this clinical study, is planning to get approval from the Korean Ministry of Food and Drug Safety to carry out phase II clinical trials with Stargardt’s macular dystrophy this year and to continue dose escalation with the age-related macular degeneration trial. CHA Biotech Co., Ltd., hopes to get approval to commercialize the therapy in Korea within the next four years.