By JEAN ENERSEN / KING 5 News
Beatrice Dean has had the dry form of macular degeneration for 20 years.
"You get to the point where you don't read any longer, you don't write, you just don't see things straight on,” she said.
A National Institute of Health study found that certain eye vitamins can help, to a point. Dr Richard Bensinger of Swedish Medical Center says this was the first breakthrough.
"It showed a very significant slowing of the condition, not a cure, or stoppage,” he said.
Now the Acucela biotech firm in Bothell is working on a pill that may finally stop the disease altogether.
Founder Ryo Kubota says the goal is to prevent dry form from progressing into the more severe wet form, which can cause blindness overnight.
"Primarily it will be preventative and slow down the disease, but in animal test studies that we've done, we've show in can reduce the already accumulated toxic byproducts,” said Dr. Kubota.
In theory, the drug works by blocking the damage before it starts.
Who will get macular degeneration?
"There really is no risk factor that's known except for everybody's favorite, smoking,” said Dr. Kubota.
Dr. Kobota hopes this research will make all the difference since macular degeneration cases are expected to rise as baby boomers get older.
“We're hoping this drug to be on the market in five to 10 years,” he said.
Human trials are just beginning. We'll keep you up to date on the research and when the study will begin recruiting locally.
Saturday, March 14, 2009
Saturday, March 7, 2009
Brain Adapts to Age-Related Eye Disease
Brain Adapts to Age-Related Eye Disease
Neurons seek input from undamaged areas to compensate, study finds
Posted March 3, 2009
TUESDAY, March 3 (HealthDay News) -- When macular degeneration causes one to start losing his or her sight, the affected neurons simply start seeking visual input from other, non-affected parts of the eye, Massachusetts Institute of Technology researchers report.
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"This study shows us one way that the brain changes when its inputs change. Neurons seem to want to receive input: When their usual input disappears, they start responding to the next best thing," senior author Nancy Kanwisher, of MIT's McGovern Institute for Brain Research, said in an university news release.
The researchers found when the cells in the fovea, the part of the retina responsible for the central field of vision, were damaged by macular degeneration (MD) -- the neuron attached to them begin responding to stimuli in an undamaged section -- a type of internal reorganization of the eye's visual map as opposed to the cortex's work being shifting to other neurons.
"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information-processing strategy," Kanwisher said.
The findings are published in the March 4 issue of the Journal of Neuroscience.
Macular degeneration, the most common form of adult blindness, affects almost 2 million people in the United States. Patients often compensate for lack of central vision by rolling their eyes upward so they can utilize the preferred retinal locus (PRL), an undamaged area under and adjacent to the affected part of the retina.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said.
Neurons seek input from undamaged areas to compensate, study finds
Posted March 3, 2009
TUESDAY, March 3 (HealthDay News) -- When macular degeneration causes one to start losing his or her sight, the affected neurons simply start seeking visual input from other, non-affected parts of the eye, Massachusetts Institute of Technology researchers report.
People Who Read This Also Read
Learning to Relax by Paying Attention
'Fasting Signal' Offers Clues to Insulin Resistance in the Obese
Good Parents, Bad Results
Do Teenagers Need Vitamins of Their Own?
Retinal Gene Is Linked to Childhood Blindness
"This study shows us one way that the brain changes when its inputs change. Neurons seem to want to receive input: When their usual input disappears, they start responding to the next best thing," senior author Nancy Kanwisher, of MIT's McGovern Institute for Brain Research, said in an university news release.
The researchers found when the cells in the fovea, the part of the retina responsible for the central field of vision, were damaged by macular degeneration (MD) -- the neuron attached to them begin responding to stimuli in an undamaged section -- a type of internal reorganization of the eye's visual map as opposed to the cortex's work being shifting to other neurons.
"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information-processing strategy," Kanwisher said.
The findings are published in the March 4 issue of the Journal of Neuroscience.
Macular degeneration, the most common form of adult blindness, affects almost 2 million people in the United States. Patients often compensate for lack of central vision by rolling their eyes upward so they can utilize the preferred retinal locus (PRL), an undamaged area under and adjacent to the affected part of the retina.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said.
Wednesday, February 25, 2009
Should everyone with AMD be taking high-dose vitamins?
Only those patients with intermediate to advanced forms of AMD should be taking the high-dose multivitamin formula. Ask your doctor if you should be taking this vitamin supplement.
Is it safe to take high doses of vitamin E?
AREDS researchers say it is unclear if the possible increased risk associated with very high doses - 500IU to 2000IU - of vitamin E applies to people taking 400IU. An increased risk of mortality was not found among those taking about 400IU of vitamin E.
The National Institutes of Health Office of Dietary Supplements has a fact sheet on vitamin E that summarizes the research on vitamin E and different chronic diseases.
Is it safe to take high doses of vitamin E?
AREDS researchers say it is unclear if the possible increased risk associated with very high doses - 500IU to 2000IU - of vitamin E applies to people taking 400IU. An increased risk of mortality was not found among those taking about 400IU of vitamin E.
The National Institutes of Health Office of Dietary Supplements has a fact sheet on vitamin E that summarizes the research on vitamin E and different chronic diseases.
Tuesday, February 17, 2009
Will vitamins make my vision better?
Will vitamins make my vision better?
Vitamin therapy for AMD will help slow the progression of AMD. Vitamins are not a cure for AMD and will not give back any vision that has already been lost.
Should everyone with AMD be taking high-dose vitamins?
Only those patients with intermediate to advanced forms of AMD should be taking the high-dose multivitamin formula. Ask your doctor if you should be taking this vitamin supplement.
Vitamin therapy for AMD will help slow the progression of AMD. Vitamins are not a cure for AMD and will not give back any vision that has already been lost.
Should everyone with AMD be taking high-dose vitamins?
Only those patients with intermediate to advanced forms of AMD should be taking the high-dose multivitamin formula. Ask your doctor if you should be taking this vitamin supplement.
Thursday, February 12, 2009
Vitamins and AMD
Are vitamins helpful for AMD?
The Age-Related Eye Disease Study (AREDS) showed that taking high-dose anti-oxidant vitamins and zinc significantly slowed the rate of progression of vision loss in patients who had more advanced forms of AMD.
AREDS II is an ongoing study to understand the role of certain other vitamins. More information
What vitamins should I take?
The following vitamin combination was proven effective in the AREDS study:
* Vitamin C, 500 mg
* Vitamin E, 400 IU
* Beta-Carotene, 15 mg
* Zinc, as zinc oxide, 80 mg
* Copper, as cupric oxide, 2 mg
The Age-Related Eye Disease Study (AREDS) showed that taking high-dose anti-oxidant vitamins and zinc significantly slowed the rate of progression of vision loss in patients who had more advanced forms of AMD.
AREDS II is an ongoing study to understand the role of certain other vitamins. More information
What vitamins should I take?
The following vitamin combination was proven effective in the AREDS study:
* Vitamin C, 500 mg
* Vitamin E, 400 IU
* Beta-Carotene, 15 mg
* Zinc, as zinc oxide, 80 mg
* Copper, as cupric oxide, 2 mg
Thursday, February 5, 2009
Vision Loss from Macular Degeneration
By Jacob Teitelbaum, MD on January 30, 2009 in Complementary Medicine
Does the center of your visual field seemed blurred?
Age-Related Macular Degeneration (ARMD) is the most common cause of age related vision loss (besides needing reading glasses). Fortunately, natural treatments are very helpful for both prevention and treatment.
BACKGROUND
The macula is in the central part of the retina that is used for more detailed vision, so it tends to affect the center of our visual field. As it has the largest concentration of cells, it also needs more oxygen then the rest of the retina. ARMD is a degenerative condition of the macula. It is the most common cause of vision loss in the United States in those 50 or older, and increases with age. ARMD is caused by hardening of the arteries that nourish the retina. Fortunately, macular degeneration does not cause total blindness since it does not affect the peripheral vision.
There are 2 types of ARMD:
Wet ARMD
Around 10% of cases are called "Wet" ARMD, as new, but fragile, blood vessels try to regrow in to support the macula. These fragile new vessels sometimes leak (hence the name "Wet") causing rapid vision loss in the center of 1 eye.
Dry ARMD
The other 90% of cases are called "Dry" ARMD, and these have a very gradual progression.
PREVENTION and TREATMENT
A number of studies have shown that good nutrition can slow or prevent the development of macular degeneration. For example, it has been proven that people with diets high in antioxidant containing fruits and vegetables (especially leafy green vegetables and colorful berries) have a lower incidence of macular degeneration. This is associated with high levels of the nutrient flavonoids, as well as lutein and zeaxanthin (both found in egg yolks), and lycopene (in tomatoes). In fact, those with high levels of these nutrients had only half the risk of ARMD. Fish oils and nuts were also very protective. Red wine is protective, but beer can worsen ARMD.
Research suggests that a mix of nutrients is more effective than individual ones for ARMD. I recommend a product called "Ocudyne II" capsules by Nutricology (easily found in many online shops) along with:
* Vitamin C 1,000 mg 2-3x day
* Vitamin E (must be natural and mixed tocopherols) 600 units/day
* Selenium 200 mcg a day
* Ginkgo Biloba (standardized to 24%) 40-80 mg 3x day
* Bilberry extract (25% extract) 40-80 mg 3x day
* Zinc 25-50 mg a day
* Eat fish (especially tuna or salmon at least 2x week) ot take fish oil
Other helpful tips include:
* Protect your eyes with sunglasses that have UV protection. Ultraviolet rays are believed to cause damage to the pigment cells in the retina.
* Quit smoking. Smoking worsens circulation to the retinal blood vessels.
To make reading easier:
* Use a halogen light. These have less glare than standard light bulbs.
* Shine the light directly on your reading material. This improves the contrast and makes the print easier to see.
* Use a hand-held magnifier. A cheap drugstore magnifier can increase the print size dramatically.
For wet ARMD, your eye doctor may recommend laser treatments, which can be added to the treatments above.
Does the center of your visual field seemed blurred?
Age-Related Macular Degeneration (ARMD) is the most common cause of age related vision loss (besides needing reading glasses). Fortunately, natural treatments are very helpful for both prevention and treatment.
BACKGROUND
The macula is in the central part of the retina that is used for more detailed vision, so it tends to affect the center of our visual field. As it has the largest concentration of cells, it also needs more oxygen then the rest of the retina. ARMD is a degenerative condition of the macula. It is the most common cause of vision loss in the United States in those 50 or older, and increases with age. ARMD is caused by hardening of the arteries that nourish the retina. Fortunately, macular degeneration does not cause total blindness since it does not affect the peripheral vision.
There are 2 types of ARMD:
Wet ARMD
Around 10% of cases are called "Wet" ARMD, as new, but fragile, blood vessels try to regrow in to support the macula. These fragile new vessels sometimes leak (hence the name "Wet") causing rapid vision loss in the center of 1 eye.
Dry ARMD
The other 90% of cases are called "Dry" ARMD, and these have a very gradual progression.
PREVENTION and TREATMENT
A number of studies have shown that good nutrition can slow or prevent the development of macular degeneration. For example, it has been proven that people with diets high in antioxidant containing fruits and vegetables (especially leafy green vegetables and colorful berries) have a lower incidence of macular degeneration. This is associated with high levels of the nutrient flavonoids, as well as lutein and zeaxanthin (both found in egg yolks), and lycopene (in tomatoes). In fact, those with high levels of these nutrients had only half the risk of ARMD. Fish oils and nuts were also very protective. Red wine is protective, but beer can worsen ARMD.
Research suggests that a mix of nutrients is more effective than individual ones for ARMD. I recommend a product called "Ocudyne II" capsules by Nutricology (easily found in many online shops) along with:
* Vitamin C 1,000 mg 2-3x day
* Vitamin E (must be natural and mixed tocopherols) 600 units/day
* Selenium 200 mcg a day
* Ginkgo Biloba (standardized to 24%) 40-80 mg 3x day
* Bilberry extract (25% extract) 40-80 mg 3x day
* Zinc 25-50 mg a day
* Eat fish (especially tuna or salmon at least 2x week) ot take fish oil
Other helpful tips include:
* Protect your eyes with sunglasses that have UV protection. Ultraviolet rays are believed to cause damage to the pigment cells in the retina.
* Quit smoking. Smoking worsens circulation to the retinal blood vessels.
To make reading easier:
* Use a halogen light. These have less glare than standard light bulbs.
* Shine the light directly on your reading material. This improves the contrast and makes the print easier to see.
* Use a hand-held magnifier. A cheap drugstore magnifier can increase the print size dramatically.
For wet ARMD, your eye doctor may recommend laser treatments, which can be added to the treatments above.
Wednesday, January 28, 2009
Researchers Hope to Mime 1000 Neurons With High-Res Artificial Retina
By Sally Adee
19 December 2008—Researchers from three major California universities are working on an artificial retina that could give limited sight to people with degenerative diseases of the retina, such as macular degeneration. Such a prosthesis is a more realistic future treatment than stem-cell therapy, gene therapy, or eye transplants, its developers say. The Californian researchers have been treating people using a 60-pixel retina in a clinical trial for two years. But they are now gunning for a system with a resolution of 1000 pixels, they reported Tuesday at the IEEE International Electron Devices Meeting (IEDM), in San Francisco. And in contrast with systems in trials today, the researchers hope to develop a system that would be completely sealed into the eye, without any external components.
James Weiland, an associate professor of ophthalmology at the University of Southern California’s Biomimetic MicroElectronic Systems (BMES) Engineering Research Center, reported on an experimental system that includes a 1000-pixel test chip. He expects to have the high-res retina at a point where they can begin clinical trials in about five years.
In the artificial retina, a camera mounted on glasses outside the eye sends the visual signals to two RF coils inside the front half of the eye. An electronics module inside the eye’s vitreous humor—the gelatinous saline sac that fills the space between the lens of the eye and the retina at the back of the eye—translates the RF signals into voltages for use in the high-res retina chip. Lying against the retina is a grid of 1000 electrodes on a flexible substrate; these electrodes apply voltage signals to the retina, which interprets them as photons. The rest of the visual process takes place as usual, and the system mimics relatively normal vision.
The group, which includes researchers from the BMES center, the California Institute of Technology, in Pasadena, and the University of California, Santa Cruz, which developed earlier prototypes in collaboration with Second Sight Medical Products. The first was the Argus 16, with 16 electrodes; the next, Argus II, has 60. Both have been in clinical trials. The Argus II implant enabled blind clinical-test subjects to follow a straight line for about 6 meters without deviating from the path. But the key to a medical device’s ability to grant true independence is whether it allows the person to identify faces or read. Artificial-eye researchers estimate that such tasks will require between 600 and 1000 electrodes.
Ideally, that artificial retina would be contained entirely within a person’s eyeball. In order to create a fully self-contained high-resolution system, the team must consider many different pieces: a parylene coating to protect the prosthesis from the corrosive effects of being inside the body for 60 years or more, a flexible substrate that can conform to the idiosyncracies of different individuals’ retinal curves, and, most important, wireless power.
Instead of batteries, the device uses inductive coils that pick up energy transmitted from outside the body. The researchers are also relying on insights from MEMS fabrication: the implant coils, interconnects, and 1000 electrodes are formed during a single parylene micromachining process.
“This is a really breathtaking system,” says MIT electrical engineering professor Jesus del Alamo, who organized the panel at IEDM where Weiland discussed the group’s research. “They have every piece of the system in place—they have even designed their own software.”
But there is more work to be done. “You need to get everything into the eye,” says Jamal Deen, a professor of electrical and computer engineering at McMaster University, in Ontario, “including the camera.”
So far, the camera, image-processing hardware, power amplifier, and data modulator are external, but Weiland hopes to implant even the camera part of the system by fixing it to the lens of the eye. His collaborators at USC are working on miniaturizing the camera system so that it can be placed onto the lens in a routine surgical procedure similar to cataract surgery. “If we can make a camera the size of the lens, we can implant it there,” he says. “But again, the challenge is making a self-contained camera without a larger control circuit.”
He cautions that it will take several years to put the whole system together and start clinical trials. But those trials will lean heavily on what is learned from trials of the implant being tested today. So potential patients should not wait for the new chip. “The 1000-channel device is likely more than five years away from even starting clinical testing,” says Weiland. “In the meantime, our 60-channel device has been in clinical trials for over two years, and sometimes we run into difficulty recruiting for the trial because some prospective participants are aware of the research efforts on higher-channel-count devices.”
19 December 2008—Researchers from three major California universities are working on an artificial retina that could give limited sight to people with degenerative diseases of the retina, such as macular degeneration. Such a prosthesis is a more realistic future treatment than stem-cell therapy, gene therapy, or eye transplants, its developers say. The Californian researchers have been treating people using a 60-pixel retina in a clinical trial for two years. But they are now gunning for a system with a resolution of 1000 pixels, they reported Tuesday at the IEEE International Electron Devices Meeting (IEDM), in San Francisco. And in contrast with systems in trials today, the researchers hope to develop a system that would be completely sealed into the eye, without any external components.
James Weiland, an associate professor of ophthalmology at the University of Southern California’s Biomimetic MicroElectronic Systems (BMES) Engineering Research Center, reported on an experimental system that includes a 1000-pixel test chip. He expects to have the high-res retina at a point where they can begin clinical trials in about five years.
In the artificial retina, a camera mounted on glasses outside the eye sends the visual signals to two RF coils inside the front half of the eye. An electronics module inside the eye’s vitreous humor—the gelatinous saline sac that fills the space between the lens of the eye and the retina at the back of the eye—translates the RF signals into voltages for use in the high-res retina chip. Lying against the retina is a grid of 1000 electrodes on a flexible substrate; these electrodes apply voltage signals to the retina, which interprets them as photons. The rest of the visual process takes place as usual, and the system mimics relatively normal vision.
The group, which includes researchers from the BMES center, the California Institute of Technology, in Pasadena, and the University of California, Santa Cruz, which developed earlier prototypes in collaboration with Second Sight Medical Products. The first was the Argus 16, with 16 electrodes; the next, Argus II, has 60. Both have been in clinical trials. The Argus II implant enabled blind clinical-test subjects to follow a straight line for about 6 meters without deviating from the path. But the key to a medical device’s ability to grant true independence is whether it allows the person to identify faces or read. Artificial-eye researchers estimate that such tasks will require between 600 and 1000 electrodes.
Ideally, that artificial retina would be contained entirely within a person’s eyeball. In order to create a fully self-contained high-resolution system, the team must consider many different pieces: a parylene coating to protect the prosthesis from the corrosive effects of being inside the body for 60 years or more, a flexible substrate that can conform to the idiosyncracies of different individuals’ retinal curves, and, most important, wireless power.
Instead of batteries, the device uses inductive coils that pick up energy transmitted from outside the body. The researchers are also relying on insights from MEMS fabrication: the implant coils, interconnects, and 1000 electrodes are formed during a single parylene micromachining process.
“This is a really breathtaking system,” says MIT electrical engineering professor Jesus del Alamo, who organized the panel at IEDM where Weiland discussed the group’s research. “They have every piece of the system in place—they have even designed their own software.”
But there is more work to be done. “You need to get everything into the eye,” says Jamal Deen, a professor of electrical and computer engineering at McMaster University, in Ontario, “including the camera.”
So far, the camera, image-processing hardware, power amplifier, and data modulator are external, but Weiland hopes to implant even the camera part of the system by fixing it to the lens of the eye. His collaborators at USC are working on miniaturizing the camera system so that it can be placed onto the lens in a routine surgical procedure similar to cataract surgery. “If we can make a camera the size of the lens, we can implant it there,” he says. “But again, the challenge is making a self-contained camera without a larger control circuit.”
He cautions that it will take several years to put the whole system together and start clinical trials. But those trials will lean heavily on what is learned from trials of the implant being tested today. So potential patients should not wait for the new chip. “The 1000-channel device is likely more than five years away from even starting clinical testing,” says Weiland. “In the meantime, our 60-channel device has been in clinical trials for over two years, and sometimes we run into difficulty recruiting for the trial because some prospective participants are aware of the research efforts on higher-channel-count devices.”
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