Glasses Allow Blind Soldier to See with his tongue

I actually read about this technology several years ago in a wired article called Mixed Feelings.  The article is extremely interesting, so much so that i re-read it today.  But if you don't feel like reading the entire thing here are the parts relevant to the above video / story.  First it talks about why this works.

It turns out that the tricky bit isn't the sensing. The world is full of gadgets that detect things humans cannot. The hard part is processing the input. Neuroscientists don't know enough about how the brain interprets data. The science of plugging things directly into the brain — artificial retinas or cochlear implants — remains primitive.

So here's the solution: Figure out how to change the sensory data you want into something that the human brain is already wired to accept, like touch or sight. The brain, it turns out, is dramatically more flexible than anyone previously thought, as if we had unused sensory ports just waiting for the right plug-ins. Now it's time to build them.

Then it refers to an experiment that was the predecessor to the above device.

Paul Bach-y-Rita built his first "tactile display" in the 1960s. Inspired by the plasticity he saw in his father as the older man recovered from a stroke, Bach-y-Rita wanted to prove that the brain could assimilate disparate types of information. So he installed a 20-by-20 array of metal rods in the back of an old dentist chair. The ends of the rods were the pixels — people sitting in the chairs could identify, with great accuracy, "pictures" poked into their backs; they could, in effect, see the images with their sense of touch.

 The mouthpiece was the next itteration.

Having long ago abandoned the vaguely Marathon Man like dentist chair, the team now uses a mouthpiece studded with 144 tiny electrodes. It's attached by ribbon cable to a pulse generator that induces electric current against the tongue. (As a sensing organ, the tongue has a lot going for it: nerves and touch receptors packed close together and bathed in a conducting liquid, saliva.)

Here is the most relevant part.

During a long brainstorm session, they wondered whether the tongue could actually augment sight for the visually impaired. I tried the prototype; in a white-walled office strewn with spare electronics parts, Wicab neuroscientist Aimee Arnoldussen hung a plastic box the size of a brick around my neck and gave me the mouthpiece. "Some people hold it still, and some keep it moving like a lollipop," she said. "It's up to you."

Arnoldussen handed me a pair of blacked-out glasses with a tiny camera attached to the bridge. The camera was cabled to a laptop that would relay images to the mouthpiece. The look was pretty geeky, but the folks at the lab were used to it.

She turned it on. Nothing happened.

"Those buttons on the box?" she said. "They're like the volume controls for the image. You want to turn it up as high as you're comfortable."

I cranked up the voltage of the electric shocks to my tongue. It didn't feel bad, actually — like licking the leads on a really weak 9-volt battery. Arnoldussen handed me a long white foam cylinder and spun my chair toward a large black rectangle painted on the wall. "Move the foam against the black to see how it feels," she said.

I could see it. Feel it. Whatever — I could tell where the foam was. With Arnold ussen behind me carrying the laptop, I walked around the Wicab offices. I managed to avoid most walls and desks, scanning my head from side to side slowly to give myself a wider field of view, like radar. Thinking back on it, I don't remember the feeling of the electrodes on my tongue at all during my walkabout. What I remember are pictures: high-contrast images of cubicle walls and office doors, as though I'd seen them with my eyes. Tyler's group hasn't done the brain imaging studies to figure out why this is so — they don't know whether my visual cortex was processing the information from my tongue or whether some other region was doing the work.

The thing that really interests me is this "Thinking back on it, I don't remember the feeling of the  electrodes on my tongue at all during my walkabout. What I remember are  pictures: high-contrast images of cubicle walls and office doors, as  though I'd seen them with my eyes."

Click the title for the short BBC article that accompanies the video.

Advanced Cell Technologies CEO Interviewed on Bloomberg Radio

I posted recently that ACT has gotten approval to start a phase I trial for treating Stargardts disease. 

The CEO of ACT was interviewed on the radio on March 9th. He speaks about stem cell treatment in general, as well has the health care industry.

Click the Title of the article to listen to the interview

Advanced Cell Technologies granted orphan drug designation from FDA

I have written earlier about Advanced Cell Technologies filing an IND (Investigational New Drug) application with the FDA.  The application would allow them to start a phase 1 trial for using Embryonic Stem Cells to treat Stargardt's disease in 12 people.

This application was approved on March 2nd and the trial is now able to move forward.  This could be a very promising treatment for those with Stargardt's Disease.

“We are pleased that the FDA has, for the first time, granted orphan drug status for the use of an embryonic stem cell derived therapy in treating an unmet medical need,” said Edmund Mickunas, Vice President Regulatory. “We believe that our terminally differentiated RPE cells represent a promising treatment for patients with SMD and expect to be in a position to accelerate clinical development and hopefully make RPE cellular therapy available to the majority of patients sooner.”

Here is a description of the treatment.

Degenerative diseases of the retina are among the most common causes of untreatable blindness in the world, and as many as ten million people in the United States have photoreceptor degenerative disease. While most of these patients have Age-Related Macular Degeneration (AMD), a smaller number have Stargardt’s, an Orphan disease and to date an untreatable form of juvenile macular degeneration leading to blindness in a much younger group of patients than are affected by AMD. ACT’s treatment for eye disease uses stem cells to re-create a type of cell in the retina that supports the photoreceptors needed for vision. These cells, called retinal pigment epithelium (RPE), are often the first to die off in SMD and AMD, which in turn leads to loss of vision.

While there is currently no treatment for SMD, several years ago ACT and its collaborators discovered that human embryonic stem cells could be a source of RPE cells. Subsequent studies found that the cells could restore vision in animal models of macular degeneration. In a Royal College of Surgeons (RCS) rat model, implantation of RPE cells resulted in 100% improvement in visual performance over untreated controls, without any adverse effects. The cells survived for more than 220 days and sustained extensive photoreceptor rescue. Functional rescue was also achieved in the ‘Stargardt’s’ mouse with near-normal functional measurements recorded at more than 70 days.

Click the title for the full Press Release

Macular Degeneration Cause discovered on a molecular level

Researchers at University College London have discovered the chemical proccess that causes Macualr Degeneration.  They state it is caused by the interaction of two protiens blood protein Factor H, and C-reactive protein.  These proteins work together to clear out the debris of dead cells in the retina, but if the levels are not optimal or if someone has a genetically different form of Factor H then dead cells are not cleaned up properly and for a deposite called drusen.  These deposits take the place of new cells and also restrict the bloodflow to neighboring cells causing them to die.  At least that is how I understood it.  here is the article in full.

Researchers at University College London say they have gleaned a key insight into the molecular beginnings of age-related macular degeneration, the No. 1 cause of vision loss in the elderly, by determining how two key proteins interact to naturally prevent the onset of the condition.

In a paper to be published in a forthcoming issue of the Journal of Biological Chemistry, the team reports for the first time how a common blood protein linked to the eye condition reins in another protein that, when produced in vastly increased amounts in the presence of inflammation or infection, can damage the eye.

"By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly," said Zuby Okemefuna, the lead author of the paper to be published Jan. 8.

Age-related macular degeneration, or AMD, is painless but affects the macula, the part of the retina that allows one to see fine detail. One form of the debilitating condition, known as "wet" AMD, occurs when abnormal and fragile blood vessels grow under the macula, leaking blood and fluid and displacing and damaging the macula itself. The second form, "dry" AMD, occurs when light-sensitive cells in the macula slowly break down.

It is believed that both forms start on a common molecular route and then deviate into dry or wet AMD, explained the research leader, Steve Perkins.

"The earliest hallmark of AMD is the appearance of protein, lipid and zinc deposits under the retinal pigment epithelial cells," he said, adding that the yellowish deposits, usually discovered by an ophthalmologist, are commonly known as "drusen."

The researchers studied two proteins involved in drusen formation -- blood protein Factor H and a second blood protein known as C-reactive protein -- and showed that Factor H binds to C-reactive protein when C-reactive protein is present in large amounts, as in the case of infection, to reduce the potentially damaging effects of an overactive immune system.

"In the eye, during the normal processes of aging, cells will die naturally for all sorts of reasons," Okemefuna said. "The blood supply to the eye will bring C-reactive protein with it, and a low level of C-reactive protein activity will enable the normal processes of clearance of dead cells at the retina through mild inflammation. In conditions of high inflammation, the levels of C-reactive protein in the retina will increase dramatically."

Uncontrolled C-reactive protein activity causes damage to the retina, which is followed by more inflammation and then even more damage to the retina, and so forth.

"It's the debris of broken up retinal cells, some of which is caused by this cycle, that is deposited as drusen," Okemefuna said.

The team also found that a genetically different form of Factor H does not bind to the C-reactive protein quite as well as the normal one, making people who carry the modified protein more vulnerable to an immune system attack in the eye and, thus, drusen buildup.

"In normal individuals, further damage to the retina by prolonged exposure to high levels of C-reactive protein is prevented by Factor H. C-reactive protein also prevents Factor H from clumping together and initiating the processes that lead to drusen formation," Perkins said. "Both these 'good' activities of Factor H are much reduced in the genetically different form of Factor H."

While there is no known cure for AMD, existing therapies aim to treat the symptoms and delay progression.

"It is interesting how the interaction of these two blood proteins protects the eye during crisis," Perkins said. "The two proteins also can be involved in a rare and often fatal cause of kidney failure in children. We now are better positioned to begin to work out preventative strategies for these diseases."

Ruodan Nan, Ami Miller and Jayesh Gor also were co-authors on the study, which was funded over the past three years by University College London, the Biotechnology and Biological Sciences Research Council, the Mercer Fund of the Fight for Sight Charity and the Henry Smith Charity.

Click the title to read the full article.

Eat your Friuts and Vegetables.

A study has been published in the Journal of Food Science stating that nutrients in Green leafy vegetables and colored fruits and vegies can greatly aid vision.  Here is an excerpt from the article.

To reach the conclusion, authors from the University of Georgia compiled the results of multiple studies on the effects of the carotenoids lutein and zeaxanthin on visual performance. These carotenoids play an important role in human vision, including a positive impact on the retina.

After reviewing the various studies, the authors concluded that macular pigments, such as lutein and zeaxanthin do have an effect on visual performance. Lutein and zeaxanthin can reduce disability and discomfort from glare, enhance contrast, and reduce photostress recovery times. They can also reduce glare from light absorption and increase the visual range.

The article also states getting a healthy amound of lutein and zeaxanthin can reduce the risk of age related macular degeneration and cataracts.

I posted in a previous article one mans claims of the benefits of lutein.

Click the title for the full article.

Phase II trial for Wet Age related Macular Degeneration (In Europe)

A company called ThromboGenics is holding a phase II trail for treating West AMD with microplasmin.

Here is a description of what the drug does.

It was recently discovered that one-third of patients with AMD have focal vitreomacular adhesion, a condition in which the vitreous gel in the center of the eye has an abnormally strong adhesion to the retina at the back of the eye. The same adhesion occurs in patients with wet AMD. Microplasmin is designed to treat vitreomacular adhesion by separating the vitreous gel from the retina, potentially preventing the progression of wet AMD.

The MIVI5 (Microplasmin for IntraVitreous Injection) trial will enroll approximately 100 patients across up to 20 European medical centers. The goal is the non-surgical resolution of vitreomacular adhesion. Safety and efficacy will also be evaluated during a one-year follow-up period.

Click the Title for the full article

Video of Corey Haas 9 year old boy from gene therapy trial

In my post yesterday I spoke of 12 patients who went through gene therapy to restore their sight.  Here is a video of the youngest participant Corey Haas and his family


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Microchip in the Eye Seeks to Restore Vision

This technology isn't my favorite, but it is something that is making progress.

Patients who receive the implant will wear a pair of glasses that has a tiny camera attached to it. The camera will send images to a microchip implanted in the eyeball that channels the input to the brain.

It won’t entirely restore normal vision, say the researchers, but it will offer just enough sight to help a blind person navigate a room.

This is a good solution for those who are completely blind.  I'd prefer not needing an external camera to see.  The upside would be that you could possibly alter the camera to see infared and other light spectrums.

click the title for full story