Posts tagged retina
Articles and news from the latest research reports.
Cells from the eye are inkjet printed for the first time
A group of researchers from the UK have used inkjet printing technology to successfully print cells taken from the eye for the very first time.
The breakthrough, which has been detailed in a paper published today, 18 December, in IOP Publishing’s journal Biofabrication, could lead to the production of artificial tissue grafts made from the variety of cells found in the human retina and may aid in the search to cure blindness.
At the moment the results are preliminary and provide proof-of-principle that an inkjet printer can be used to print two types of cells from the retina of adult rats―ganglion cells and glial cells. This is the first time the technology has been used successfully to print mature central nervous system cells and the results showed that printed cells remained healthy and retained their ability to survive and grow in culture.
Co-authors of the study Professor Keith Martin and Dr Barbara Lorber, from the John van Geest Centre for Brain Repair, University of Cambridge, said: “The loss of nerve cells in the retina is a feature of many blinding eye diseases. The retina is an exquisitely organised structure where the precise arrangement of cells in relation to one another is critical for effective visual function”.
“Our study has shown, for the first time, that cells derived from the mature central nervous system, the eye, can be printed using a piezoelectric inkjet printer. Although our results are preliminary and much more work is still required, the aim is to develop this technology for use in retinal repair in the future.”
The ability to arrange cells into highly defined patterns and structures has recently elevated the use of 3D printing in the biomedical sciences to create cell-based structures for use in regenerative medicine.
In their study, the researchers used a piezoelectric inkjet printer device that ejected the cells through a sub-millimetre diameter nozzle when a specific electrical pulse was applied. They also used high speed video technology to record the printing process with high resolution and optimised their procedures accordingly.
“In order for a fluid to print well from an inkjet print head, its properties, such as viscosity and surface tension, need to conform to a fairly narrow range of values. Adding cells to the fluid complicates its properties significantly,” commented Dr Wen-Kai Hsiao, another member of the team based at the Inkjet Research Centre in Cambridge.
Once printed, a number of tests were performed on each type of cell to see how many of the cells survived the process and how it affected their ability to survive and grow.
The cells derived from the retina of the rats were retinal ganglion cells, which transmit information from the eye to certain parts of the brain, and glial cells, which provide support and protection for neurons.
“We plan to extend this study to print other cells of the retina and to investigate if light-sensitive photoreceptors can be successfully printed using inkjet technology. In addition, we would like to further develop our printing process to be suitable for commercial, multi-nozzle print heads,” Professor Martin concluded.
Study Treats Alzheimer’s by Delivering Protein Across Blood-Brain Barrier
The body is structured to ensure that any invading organisms have a tough time reaching the brain, an organ obviously critical to survival. Known as the blood-brain barrier, cells that line the brain and spinal cord are tightly packed, making it difficult for anything besides very small molecules to cross from the bloodstream into the central nervous system. While beneficial, this blockade also stands in the way of delivering drugs intended to treat neurological disorders, such as Alzheimer’s.
In a new study published in the journal Molecular Therapy, University of Pennsylvania researchers have found a way of traversing the blood-brain barrier, as well as a similar physiological obstacle in the eye, the retinal-blood barrier. By pairing a receptor that targets neurons with a molecule that degrades the main component of Alzheimer’s plaques, the biologists were able to substantially dissolve these plaques in mice brains and human brain tissue, offering a potential mechanism for treating the debilitating disease, as well as other conditions that involve either the brain or the eyes.
The work was led by Henry Daniell, a professor in Penn’s School of Dental Medicine’s departments of biochemistry and pathology and director of translational research. The research team included Penn Dental Medicine’s Neha Kohli, Donevan R. Westerveld, Alexandra C. Ayache and Sich L. Chan. Co-authors at the University of Florida College of Medicine, including Amrisha Verma, Pollob Shil, Tuhina Prasad, Ping Zhu and Quihong Li, analyzed retinal tissues.
The researchers began their work by considering how they might breach the blood-brain barrier. Daniell hypothesized that a molecule might be permitted to cross if it was attached to a carrier that is able to pass over, as a sort of molecular crossing guard. The protein cholera toxin B, or CTB, a non-toxic carrier currently approved for use in humans by the Food and Drug Administration, is used in this study to traverse the blood-brain barrier.
They next identified a protein that could clear the plaques that are found in the brains of Alzheimer’s patients. These plaques, which are believed to cause the dementia associated with the disease, are made up of tangles of amyloid beta (Aβ), a protein that is found in soluble form in healthy individuals. Noting that myelin basic protein (MBP) has been shown to degrade Aβ chains, the team decided to couple it with CTB to see if MBP would be permitted to cross.
“These tangles of beta amyloid are known to be the problem in Alzheimer’s,” says Daniell. “So our idea was to chop the protein back to their normal size so they wouldn’t form these tangles.”
To test this idea, the Penn-led team first exposed healthy mice to the CTB-MBP compound by feeding them capsules of freeze-dried leaves that had been genetically engineered to express the fused proteins, a method developed and perfected by Daniell over many years as a means of orally administering various drugs and vaccines. Adding a green-fluorescent protein to the CTB carrier, the researchers tracked the “glow” to see where the mice took up the protein. They found the glowing protein in both the brain and retina.
“When we found the glowing protein in the brain and the retina we were quite thrilled,” said Daniell. “If the protein could cross the barrier in healthy mice, we thought it was likely that it could cross in Alzheimer’s patients brains, because their barrier is somewhat impaired.”
When CTB was not part of the fused protein, they did not see this expression, suggesting that their carrier protein, the crossing guard, was an essential part of delivering their protein of interest.
To then see what MBP would do once it got to the brain, Daniell and colleagues exposed the CTB-MBP protein to the brains of mice bred to have an Alzheimer’s disease. They used a stain that binds to the brain plaques and found that exposure to the CTB-MBP compound resulted in reductions of staining up to 60 percent, indicating that the plaques were dissolving.
Gaining confidence that their compound was appropriately targeting the plaques, the researchers worked with the National Institutes of Health to obtain brain tissue from people who died of Alzheimer’s and performed the same type of staining. Their results showed a 47 percent decrease in staining in the inferior parietal cortex, a portion of the brain found to play an important role in the development of Alzheimer’s-associated dementia.
As a final step, the researchers fed the CTB-MBP-containing capsules to 15-month-old mice, the equivalent of 80 or more human years, bred to develop Alzheimer’s disease. After three months of feeding, the mice had reductions in Aβ plaques of up to 70 percent in the hippocampus and up to 40 percent in the cortex, whereas mice fed capsules that contained lettuce leaves without CTB-MBP added and mice that were not fed any capsules did not have any reduction in evidence of brain plaques.
Because Alzheimer’s patients have also been found to have plaques in their eyes, the researchers examined the eyes of the mice fed the protein. They found that, indeed, the Alzheimer’s-mice did have retinal plaques, but those fed the CBP-MBP compound had undetectable Aβ plaques in their retinae.
“Really no one knows whether the memory problems that people who have Alzheimer’s disease are due to the dementia or problems with their eyes,” Daniell said. “Here we show it may be both, and that we can dissolve the plaques through an oral route.”
Daniell hopes that this technique of delivering proteins across the blood-brain and blood-retina barriers could serve to treat a variety of diseases beyond Alzheimer’s. Several current clinical trials have failed because of an inability to deliver drugs to the brain. Currently, treatments of some eye conditions must physically penetrate the retina with an injection, an approach that requires anesthesia and risks retinal detachment. Treatment with an ingestible capsule would be safer, easier, and more cost-effective.
As a next step, Daniell hopes to collaborate with Alzheimer’s experts at Penn to advance these studies and add a behavioral component to determine whether the CBP-MBP compound not only removes plaques but also improves the memory and functioning of mice with the Alzheimer’s disease.
Critical Gene in Retinal Development and Motion Sensing Identified
Our vision depends on exquisitely organized layers of cells within the eye’s retina, each with a distinct role in perception. Johns Hopkins researchers say they have taken an important step toward understanding how those cells are organized to produce what the brain “sees.” Specifically, they report identification of a gene that guides the separation of two types of motion-sensing cells, offering insight into how cellular layering develops in the retina, with possible implications for the brain’s cerebral cortex. A report on the discovery is published in the Nov. 1 issue of the journal Science.
“The separation of different types of cells into layers is critical to their ability to form the precise sets of connections with each other — the circuitry — that lets us process visual information,” says Alex Kolodkin, Ph.D., a professor in the Johns Hopkins University School of Medicine’s Solomon H. Snyder Department of Neuroscience and an investigator at the Howard Hughes Medical Institute. “There is still much to learn about how that separation happens during development, but we’ve identified for the first time proteins that enable two very similar types of cells to segregate into their own distinct neuronal layers.”
Kolodkin’s research group specializes in studying how circuitry forms among neurons (brain and nerve cells). Past experiments revealed that two types of proteins, called semaphorins and plexins, help guide this process. In the current study, Lu Sun, a graduate student in Kolodkin’s laboratory, focused on the genes that carry the blueprint for these proteins in two of the 10 layers of cells in the mammalian retina.
Those two layers are made up of so-called starburst amacrine cells (SACs). One type of SAC, known as “Off,” detects motion by sensing decreases in the amount of light hitting the retina, while the other type, “On,” detects increases in light. Sun examined the amounts of several semaphorin and plexin proteins being made by each type of cell, and found that only the “On” SACs were making a semaphorin called Sema6A. Sema6A can only work in the retina by interacting with its receptor, a plexin called PlexA2, but Sun found both types of SAC were churning out roughly equal amounts of PlexA2.
Reasoning that Sema6A might be the key difference that enabled the “On” and “Off” SACs to segregate from one another, Kolodkin’s team analyzed mice in which the genes for either Sema6A, PlexA2 or both could be switched off, and looked at the effects of this manipulation on their retinas. “Knocking out” either gene during development led the “On” and “Off” layers to run together, the team found, and caused abnormalities in the “On” SACs’ tree-like extensions. However, the “Off” SACs, which hadn’t been using their Sema6A gene in the first place, still looked and functioned normally.
“When signaling between Sema6A and PlexA2 was lost, not only was layering compromised, but the ‘On’ SACs lost both their distinctive symmetrical appearance, and, importantly, their motion-detecting ability,” Sun says. “This is evidence that the beautiful symmetric shape that gives starburst amacrine cells their name is necessary for their function.”
Adds Kolodkin, “We hope that learning how layering occurs in these very specific cell types will help us begin sorting out how connections are made not just in the retina, but also in neurons throughout the nervous system. Layering also occurs in the cerebral cortex, for example, which is responsible for thought and consciousness, and we really want to know how this is organized during neural development.”
(Source: newswise.com)
Scientists shed light on brain computations
University of Queensland (UQ) scientists have made a fundamental breakthrough into how the brain decodes the visual world.
Using advanced electrical recording techniques, researchers at UQ’s Queensland Brain Institute (QBI) have discovered how output cells of the eye’ balls retina compute the direction of a moving object.
QBI’s Dr Ben Sivyer and Associate Professor Stephen Williams have found that dendrites – the branching process of a neuron that conducts impulses toward the cell – play a critical role in decoding images.
“In the past decade our research shows that dendrites provide neurons with powerful processing capabilities,” Associate Professor Williams said.
“However the function of dendritic processing in the real-time operation of neuronal networks has remained elusive.”
To gain further insight, the group measured electrical activity from multiple sites in retinal ganglion cells when visual stimuli moved through space.
“The retina, a thin neuronal network at the posterior part of the eyeball, is ideal for investigating the role of active dendritic integration in neuronal circuit function,” he said.
“This is because this network can be maintained intact in a dish and retains its responsiveness to natural stimuli.”
He said while it had long been known that the retinal network extracted and signalled specific aspects of visual stimuli, the new work has discovered how such responses are computed.
“We found that retinal ganglion cells compute the direction of light stimuli through exquisitely controlled local integration compartments in the dendritic tree, a finding which highlights the key function that dendrites play in brain computations,” said Associate Professor Williams.
QBI Director Professor Perry Bartlett said this new insight was vital to brain research.
“Discovering how nerve cells process information is fundamental to understanding how we learn, and to developing new strategies to enhance learning in education and in disease processes in the brain,” he said.
Queensland Minister for Science and Innovation Ian Walker congratulated Dr Sivyer and Associate Professor Williams on their internationally significant findings.
“This is another example of Queensland leading the world in health and medical research,” he said.
“Dendrite research also has flow-on implications for brain-function studies in a range of areas.
“While all of these areas are important, I will be particularly interested to see its application to dementia research, which has been a major focus for recent Queensland Government support.”
The paper, Direction selectivity is computed by active dendritic integration in retinal ganglion cells, is published in the prestigious journal Nature Neuroscience.
The eyes have it: Scientists reveal how organic mercury can interfere with vision
More than one billion people worldwide rely on fish as an important source of animal protein, states the United Nations Food and Agriculture Organization. And while fish provide slightly over 7 per cent of animal protein in North America, in Asia they represent about 23 per cent of consumption.
Humans consume low levels of methylmercury by eating fish and seafood. Methylmercury compounds specifically target the central nervous system, and among the many effects of their exposure are visual disturbances, which were previously thought to be solely due to methylmercury-induced damage to the brain visual cortex. However, after combining powerful synchrotron X-rays and methylmercury-poisoned zebrafish larvae, scientists have found that methylmercury may also directly affect vision by accumulating in the retinal photoreceptors, i.e. the cells that respond to light in our eyes.
(Image: A cross section of a zebrafish eye shows the localization of mercury in the outer segments of photoreceptor cells.)
Dr. Gosia Korbas, BioXAS staff scientist at the Canadian Light Source (CLS), says the results of this experiment show quite clearly that methylmercury localizes in the part of the photoreceptor cell called the outer segment, where the visual pigments that absorb light reside.
“There are many reports of people affected by methylmercury claiming a constricted field of vision or abnormal colour vision,” said Korbas. “Now we know that one of the reasons for their symptoms may be that methylmercury directly targets photoreceptors in the retina.”
Korbas and the team of researchers from the University of Saskatchewan including Profs. Graham George, Patrick Krone and Ingrid Pickering conducted their experiments using three X-ray fluorescence imaging beamlines (2-ID-D, 2-ID-E and 20-ID-B) at the Advanced Photon Source, Argonne National Laboratory near Chicago, US, as well as the scanning X-ray transmission beamline (STXM) at the Canadian Light Source in Saskatoon, Canada.
After exposing zebrafish larvae to methylmercury chloride in water, the team was able to obtain high-resolution maps of elemental distributions, and pinpoint the localization of mercury in the outer segments of photoreceptor cells in both the retina and pineal gland of zebrafish specimens. The results of the research were published in ACS Chemical Biology under the title “Methylmercury Targets Photoreceptor Outer Segments”.
Korbas said zebrafish are an excellent model for investigating the mechanisms of heavy metal toxicity in developing vertebrates. One of the reasons for that is their high degree of correlation with mammals. Recent studies have demonstrated that about 70 per cent of protein-coding human genes have their counterparts in zebrafish, and 84 per cent of genes linked to human diseases can be found in zebrafish.
“Researchers are studying the potential effects of low level chronic exposure to methylmercury, which is of global concern due to methylmercury presence in fish, but the message that I want to get across is that such exposures may negatively affect vision. Our study clearly shows that we need more research into the direct effects of methylmercury on the eye,” Korbas concluded.
(Source: lightsource.ca)
First to measure the concerted activity of a neuronal circuit
Neurobiologists from the Friedrich Miescher Institute for Biomedical Research have been the first to measure the concerted activity of a neuronal circuit in the retina as it extracts information about a moving object. With their novel and powerful approach they can now not only visualize networks of neurons but can also measure functional aspects. These insights are direly needed for a better understanding of the processes in the brain in health and disease.
For many decades electrophysiology and genetics have been the main tools in the toolbox of approaches to study individual neurons in the central nervous system to understand perception and behavior. In the last five years however, neurobiology has been riding a wave of technological advances that brought unprecedented insights: Optogenetics and genetically encoded activity sensors has allowed scientists to control and measure the activity of clearly defined neurons; the application of rabies viruses enabled the visualization of networks of interconnected nerve cells. What was still missing, was the link between neural circuit and monitoring of activity.
Scientists from the Friedrich Miescher Institute for Biomedical Research have now been the first to measure the concerted activity of a neuronal circuit in the retina as it extracts information about the movement of an object.
In a world defined through eyesight, it is crucial to be able to discern whether something moves towards us, moves away or moves next to us. It comes as no surprise then that in the retina several parallel neuronal circuits are reserved for the extraction of information about movement and that most of them are dedicated to the analysis of the direction of motion.
As they report online in Neuron, Keisuke Yonehara and Karl Farrow, two Postdoctoral Fellows in Botond Roska’s team at the FMI, have now been able to monitor the activity of all circuit elements in a motion sensitive retinal circuit at once, and pinpoint the site, at a subcellular level, where the information about the direction of the movement becomes encoded. To achieve this, they used genetically altered rabies viruses expressing calcium sensors developed by the laboratory of Klaus Conzelmann in Munich. The special property of rabies viruses is that they move across connected neurons and therefore are able to deliver the sensors to all circuit elements within a defined neuronal circuit. Simultaneous two-photon imaging allowed them then to monitor activity in every part of the neuronal circuit at once, even in subcellular compartments, such as axons, synapses and dendrites.
"We are extremely thrilled that with this new method, which combines the power of genetically altered rabies viruses with very powerful two-photon microscopy, we are now able to link circuit architecture with activity and ultimately function," comments Yonehara. "We have illustrated the power of the method for a better understanding of the perception of movement and are convinced that the method will allow us to reach a better understanding of many processes in the retina and in other parts of the brain."
(Source: medicalxpress.com)
Your eyes may hold clues to stroke risk
Your eyes may be a window to your stroke risk.
In a study reported in the American Heart Association journal Hypertension, researchers said retinal imaging may someday help assess if you’re more likely to develop a stroke — the nation’s No. 4 killer and a leading cause of disability.
“The retina provides information on the status of blood vessels in the brain,” said Mohammad Kamran Ikram, M.D., Ph.D., lead author of the study and assistant professor in the Singapore Eye Research Institute, the Department of Ophthalmology and Memory Aging & Cognition Centre, at the National University of Singapore. “Retinal imaging is a non-invasive and cheap way of examining the blood vessels of the retina.”
Worldwide, high blood pressure is the single most important risk factor for stroke. However, it’s still not possible to predict which high blood pressure patients are most likely to develop a stroke.
Researchers tracked stroke occurrence for an average 13 years in 2,907 patients with high blood pressure who had not previously experienced a stroke. At baseline, each had photographs taken of the retina, the light-sensitive layer of cells at the back of the eyeball. Damage to the retinal blood vessels attributed to hypertension — called hypertensive retinopathy — evident on the photographs was scored as none, mild or moderate/severe.
During the follow-up, 146 participants experienced a stroke caused by a blood clot and 15 by bleeding in the brain.
Researchers adjusted for several stroke risk factors such as age, sex, race, cholesterol levels, blood sugar, body mass index, smoking and blood pressure readings. They found the risk of stroke was 35 percent higher in those with mild hypertensive retinopathy and 137 percent higher in those with moderate or severe hypertensive retinopathy.
Even in patients on medication and achieving good blood pressure control, the risk of a blood clot was 96 percent higher in those with mild hypertensive retinopathy and 198 percent higher in those with moderate or severe hypertensive retinopathy.
“It is too early to recommend changes in clinical practice,” Ikram said. “Other studies need to confirm our findings and examine whether retinal imaging can be useful in providing additional information about stroke risk in people with high blood pressure.”
Lab team makes unique contributions to the first bionic eye
The Argus II will help people blinded by the rare hereditary disease retinitis pigmentosa or seniors suffering from severe macular degeneration.
As part of the multi-institutional Artificial Retina Project, Los Alamos researchers helped develop the first bionic eye. Recently approved by the U.S. Food and Drug Administration, the Argus II will help people blinded by the rare hereditary disease retinitis pigmentosa or seniors suffering from severe macular degeneration—diseases that destroy the light-sensing cell in the retina. Los Alamos scientists served as the Advanced Concepts team, focusing on fundamental issues and out-of the box ideas.
Significance of the research
The Argus II operates by using a miniature camera mounted in eyeglasses that captures images and wirelessly sends the information to a microprocessor (worn on a belt) that converts the data to an electronic signal. Pulses from an electrode array against the patient’s retina in the back of the eye stimulate the optic nerve and, ultimately, the brain, which perceives patterns of light corresponding to the electrodes stimulated. Blind individuals can learn to interpret these visual patterns.
Los Alamos research achievements
The Los Alamos team examined how visual information is encoded in the pattern of electrical impulses traveling the optic nerve. The scientists developed better ways to visualize and interpret the resulting neural activity patterns when the retina is stimulated.
Using high-performance video cameras and near-infrared illumination, the Los Alamos team imaged tiny changes in the light scattering and birefringence properties of neural tissue that are associated with nerve electrical activity, the retina that were produced by stimulation. The team also advised the consortium on the use of compatible technologies to map the human brain function stimulated by the devices or by normal biological vision.
The Laboratory team developed theory—supported with experimental data—of how electrical activity of nerve cells produces polarized light signals that were used to image retinal function. They created a computer model of the retina directly predicting the dynamics of retinal neurons firing as function of patterns of stimulation. They also created theoretical models of the response of nerve cells to electrical stimulation, which suggest new strategies to stimulate patterns of neural activity with higher resolution and a greater specificity, useful to a wider range of individuals with visual impairment.
The need to improve the retina and electronics interface was the largest technical recording and stimulating arrays, and developed new techniques for coating electrode arrays that might enable advanced neural interfaces in the future, with many more channels and greater tolerance for the challenging environment of electronics implanted in biological tissue.
About the Artificial Retina Project
The DOE Artificial Retina Project is a multi-institutional collaborative effort to develop and implant a device containing an array of microelectrodes into the eyes of people blinded by retinal disease. The ultimate goal is to design a device to help restore limited vision that enables reading, unaided mobility and facial recognition.
The 10-year project involved researchers from DOE national laboratories (Argonne, Lawrence Livermore, Los Alamos, Oak Ridge, and Sandia), universities (Doheny Eye Institute at the University of Southern California, California Institute of Technology, North Carolina State University, University of Utah, and the University of California—Santa Cruz), and private industry (Second Sight Medical Products, Inc.). Members of the Los Alamos artificial retina team include team leader John George and members Garrett Kenyon, Michael Ham, Xin-cheng Yao, David Rector, Angela Yamauchi, Beth Perry, Benjamin Barrows, Bryan Travis, Andrew Dattelbaum, Jurgen Schmidt, James Maxwell and Karlene Maskaly.
The DOE Office of Science funded the Los Alamos portion of the Artificial Retina Project. Laboratory Directed Research and Development (LDRD), the National Institutes of Health and the National Science Foundation have sponsored different aspects of basic R&D on neuroimaging, computational modeling and analysis of neural function, and materials and fabrication techniques that enabled the Los Alamos role in this project. The work supports the Lab’s Global Security mission area and the Science of Signatures and Information, Science, and Technology science pillars.
Temporal Processing in the Olfactory System: Can We See a Smell?
Sensory processing circuits in the visual and olfactory systems receive input from complex, rapidly changing environments. Although patterns of light and plumes of odor create different distributions of activity in the retina and olfactory bulb, both structures use what appears on the surface similar temporal coding strategies to convey information to higher areas in the brain. We compare temporal coding in the early stages of the olfactory and visual systems, highlighting recent progress in understanding the role of time in olfactory coding during active sensing by behaving animals. We also examine studies that address the divergent circuit mechanisms that generate temporal codes in the two systems, and find that they provide physiological information directly related to functional questions raised by neuroanatomical studies of Ramon y Cajal over a century ago. Consideration of differences in neural activity in sensory systems contributes to generating new approaches to understand signal processing.
Bionic eye maker has vision of the future
Robert Greenberg got tired of hearing from senior engineers that it wasn’t possible to build his product idea: a bionic eye that gives sight to the blind.
"A lot of the folks straight out of school didn’t know any better, so I hired them instead," quipped Greenberg, chief executive of Second Sight Medical Products Inc., a Sylmar biotech company. "They didn’t know how hard it was going to be, that it was impossible. And so they tried."
Greenberg can laugh now that he once thought developing the device would take a year and $1 million. Some 20 years and $200 million later, the first bionic eye has helped more than 20 European patients regain some of their sight.
Called the Argus II Retinal Prosthesis System, the device recently was approved by the Food and Drug Administration. Second Sight, which has 100 employees, is allowed to sell the bionic eye system to patients in the U.S. with advanced retinitis pigmentosa, a degenerative eye disease that can cause blindness.
"We are a far cry from restoring 20/20 vision," said Brian V. Mech, Second Sight’s vice president of business development, who holds a doctorate in materials science and an MBA from the UCLA Anderson School of Management.
"We are taking blind people back up to low vision, and that is pretty significant."
Mech likes to show videos of once-sightless patients who, after receiving the retinal prosthesis, are able to follow a person walking down the street and discern a street curb without using their canes.
"Until our product, these patients had no other option to obtain the ability to see," Mech said of the $100,000 device, part of which rests on a pair of Oakley Inc. sunglass frames. The cost to European patients has been paid by insurance companies in most cases.
Palo Alto attorney Dean Lloyd, who lost his vision 17 years ago, got the bionic eye system as part of the U.S. testing process. It allows him to see “boundaries and borders, not images” but has had a profound effect on his life.
Lloyd cites an incident before he received the eye system that still rankles. In the middle of a courtroom trial, an opposing attorney said Lloyd didn’t stand a chance with his case because he couldn’t even keep his socks straight: Lloyd had mixed up his black, courtroom socks with his white athletic ones.
"What did I do after the surgical procedure that I hadn’t been able to do?" Lloyd said. "I went home and sorted all of my socks."
The story of how the bionic eye came to be made in Sylmar underscores the state’s long record of medical device advances and involves top university researchers who were brought to Southern California to work on the project.
Greenberg likened the degree of difficulty to “shrinking a television set to the size of a pea, then throwing it into the ocean and expecting it to work.”
For Greenberg, it began in the early 1990s when he was a doctoral candidate in the Department of Biomedical Engineering at Johns Hopkins University in Baltimore.
Some of the first work was being done there, testing patients who had lost their vision because of retinitis pigmentosa, to see if electrically stimulating their retinas would produce results. It did.
"Using one electrode, the patient saw one spot of light," Greenberg said. "Second electrode, and the patient was seeing two spots of light. During that experiment, I was hooked."
Greenberg said he thought: “This is just engineering. Put more spots and you could make more pixels, like lights on a scoreboard or pixels on your computer monitor. You could see images.”
There was a breakthrough of another sort a few years later, in Washington. There, Greenberg was working as a medical officer and a lead reviewer for the FDA’s Office of Device Evaluation when he met entrepreneur Alfred E. Mann.
Mann had already established himself as a medical device developer through Mannkind Corp. and several other Southern California companies. During the 1980s, the self-made billionaire founded Pacesetter Systems, which made cardiac pacemakers. From there, he moved on to insulin pumps and related equipment.
Another Mann-funded company, Advanced Bionics Corp., took on cochlear implants, which could restore hearing to the deaf. It was the electrode-based cochlear implant that formed the rough basis of Second Sight’s first bionic eye.
In 1998, Second Sight opened with the financial backing of Mann and Sam Williams, another successful entrepreneur whose company, Williams International, designed and built small, efficient turbofan jet engines.
"Sam Williams was blind from retinitis pigmentosa, the disease that we are treating," Mech said. "He had invested along with Al in Advanced Bionics, which restores hearing for deaf people, and they were already on the market in the ’90s. Sam said to Al, ‘Why can’t we do the same for blind people?’"