Othera reports positive interim results from Phase II dry AMD trial
Published:13-April-2009
By Datamonitor staff writer
137 patients enrolled at 20 leading retinal disease treatment centers across the US
Othera Pharmaceuticals, a specialty pharmaceutical company, has reported positive interim data from its Phase II trial of OT-551 in treating geographic atrophy, an advanced form of dry age-related macular degeneration for which there is no FDA-approved treatment.
According to Othera, the 12-month findings from the two-year Omega trial suggest an emerging trend for reducing moderate vision loss in patients with geographic atrophy (GA) who were treated with OT-551 compared with placebo. This numeric trend was more pronounced in subgroups based on GA characteristics or level of visual acuity at baseline.
The Omega study is a randomized, double-masked, dose-ranging, multi-center, Phase II study of topical OT-551 in patients with GA associated with age-related macular degeneration (AMD). Approximately 137 patients were enrolled at 20 leading retinal disease treatment centers across the US in this two-year study.
OT-551 has demonstrated a dose-dependent protective effect on photoreceptor activity in an animal model of AMD, and has been shown to reach the back of the eye after topical dosing in multiple species. This profile supports the rationale for studying the drug in patients with degenerative retinal conditions, such as GA, the company said.
Al Reaves, senior vice president of clinical development at Othera, said: "Based on these preliminary results, OT-551 continues to exhibit the excellent safety profile seen in prior studies. Given OT-551's safety profile and the positive trend on visual acuity, continued follow-up of this elderly population with GA should allow us to profile the drug's effect on visual acuity and better understand its long term safety."
Sunday, April 19, 2009
Saturday, April 11, 2009
*
Feds Give Life to New Research
UCSB To Take Advantage of New Stem Cell Policy
By Sara-Fay Katz / Staff Writer
Published Wednesday, April 8, 2009
Issue 100 / Volume 89
After eight years in the cold, stem cell research is poised to benefit from the open support of the Obama administration.
Under the Bush presidency, federal funding was distributed only to researchers experimenting on 21 existing stem cell lines, thus limiting developments in the field. When President Barack Obama lifted the ban on March 9, he made federal funding available for the study of new embryonic stem lines, and UCSB researchers stand to gain from his decision.
Dennis Clegg, chair of the Dept. of Molecular, Cellular and Developmental Biology, said the Bush-era ban had significantly hindered the progress of biological research for almost a decade.
“Back in 2001, President Bush said you could only use federal funding when using existing [stem cell] lines,” Clegg said. “So, it really slowed down the progress of stem cell research in the country. Now with the lifting of the ban, it will lessen the red tape associated with this kind of study and provide new funding for stem cell research.”
Clegg said new research into regenerative medicines such as stem cells has the potential to render many fatal diseases harmless, or at least make them readily treatable.
“We are in a very exciting time for stem cell research right now,” Clegg said. “Stem cell research has great potential for treating a variety of human diseases like macular degeneration, diabetes, Parkinson’s and Alzheimer’s.”
A co-director of strategy, planning and operations at the UCSB Center for Stem Cell Biology and Engineering, Clegg said UCSB has the power to make major advancements in the growing field.
“We have quite a bit of exciting work going on in basic molecular biology and bioengineering, and we’re partnering with other universities and institutions to bring our findings to clinical applications,” Clegg said. “I think UCSB has unique strengths that will allow us to make a significant contribution in the field of stem cell research.”
Lincoln Johnson, associate director of the Center for the Study of Macular Degeneration, said the removal of the ban now ensures more options for the treatment of human diseases using natural mechanisms.
“Not all embryonic stem cell lines are the same,” Johnson said. “So for instance, with cardiac muscle for the treatment heart disease, one stem cell line might be better than another, so it’s important to have a variety. For regenerative medicine such as constructing organs, having a wider variety of stem cells to choose from will help better match the donor organ to the recipient.”
Despite the avenues of stem cell research opened by the Obama administration, Johnson said the field is still in its infancy.
“There’s a lot of research to be done, but having more cell lines and more funding will speed up the process,” Johnson said. “The better the research and the more people involved, the greater influence UCSB might have on policy formation.”
In addition to getting the go-ahead for more stem cell research, professor of chemical engineering Frank Doyle said UCSB has plans to open a new bioengineering building that will be suited for new developments in national research.
“We are in the planning stages of trying to set up a bioengineering building and we’re probably about four years away from realizing this dream,” Doyle said. “It would be a home to a rich range of engineers, chemists, biologists and physicists. I think what were hoping this building will be home to a big thrust of research on the campus, particularly an interface between medicine and engineering.”
For those interested in learning more about stem cell research, UCSB offers a class this quarter in Life Sciences Building 1001 - MCDB 146: Stem Cell Biology in Health and Disease taught by Professor Clegg. Students can also consult the UCSB Center for Stem Cell Biology and Engineering’s Web site, www.stemcell.ucsb.edu.
Feds Give Life to New Research
UCSB To Take Advantage of New Stem Cell Policy
By Sara-Fay Katz / Staff Writer
Published Wednesday, April 8, 2009
Issue 100 / Volume 89
After eight years in the cold, stem cell research is poised to benefit from the open support of the Obama administration.
Under the Bush presidency, federal funding was distributed only to researchers experimenting on 21 existing stem cell lines, thus limiting developments in the field. When President Barack Obama lifted the ban on March 9, he made federal funding available for the study of new embryonic stem lines, and UCSB researchers stand to gain from his decision.
Dennis Clegg, chair of the Dept. of Molecular, Cellular and Developmental Biology, said the Bush-era ban had significantly hindered the progress of biological research for almost a decade.
“Back in 2001, President Bush said you could only use federal funding when using existing [stem cell] lines,” Clegg said. “So, it really slowed down the progress of stem cell research in the country. Now with the lifting of the ban, it will lessen the red tape associated with this kind of study and provide new funding for stem cell research.”
Clegg said new research into regenerative medicines such as stem cells has the potential to render many fatal diseases harmless, or at least make them readily treatable.
“We are in a very exciting time for stem cell research right now,” Clegg said. “Stem cell research has great potential for treating a variety of human diseases like macular degeneration, diabetes, Parkinson’s and Alzheimer’s.”
A co-director of strategy, planning and operations at the UCSB Center for Stem Cell Biology and Engineering, Clegg said UCSB has the power to make major advancements in the growing field.
“We have quite a bit of exciting work going on in basic molecular biology and bioengineering, and we’re partnering with other universities and institutions to bring our findings to clinical applications,” Clegg said. “I think UCSB has unique strengths that will allow us to make a significant contribution in the field of stem cell research.”
Lincoln Johnson, associate director of the Center for the Study of Macular Degeneration, said the removal of the ban now ensures more options for the treatment of human diseases using natural mechanisms.
“Not all embryonic stem cell lines are the same,” Johnson said. “So for instance, with cardiac muscle for the treatment heart disease, one stem cell line might be better than another, so it’s important to have a variety. For regenerative medicine such as constructing organs, having a wider variety of stem cells to choose from will help better match the donor organ to the recipient.”
Despite the avenues of stem cell research opened by the Obama administration, Johnson said the field is still in its infancy.
“There’s a lot of research to be done, but having more cell lines and more funding will speed up the process,” Johnson said. “The better the research and the more people involved, the greater influence UCSB might have on policy formation.”
In addition to getting the go-ahead for more stem cell research, professor of chemical engineering Frank Doyle said UCSB has plans to open a new bioengineering building that will be suited for new developments in national research.
“We are in the planning stages of trying to set up a bioengineering building and we’re probably about four years away from realizing this dream,” Doyle said. “It would be a home to a rich range of engineers, chemists, biologists and physicists. I think what were hoping this building will be home to a big thrust of research on the campus, particularly an interface between medicine and engineering.”
For those interested in learning more about stem cell research, UCSB offers a class this quarter in Life Sciences Building 1001 - MCDB 146: Stem Cell Biology in Health and Disease taught by Professor Clegg. Students can also consult the UCSB Center for Stem Cell Biology and Engineering’s Web site, www.stemcell.ucsb.edu.
Sunday, April 5, 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
(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.
"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
(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.
"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.
Monday, March 30, 2009
MD Linked with Range of Illnesses
TUESDAY, Mar. 10 (HealthDay News) -- Elderly patients with age-related macular degeneration are more likely than their counterparts without the eye disease to experience a wide range of illnesses, including depression, hip fracture and blindness, according to a report published in the March issue of the Archives of Ophthalmology.
Ashley Wysong, of Duke University School of Medicine in Durham N.C., and colleagues studied Medicare claims data on 32,702 adults aged 68 years and older who were newly diagnosed with age-related macular degeneration in 1994 and 32,702 matched controls, who were all followed up in 2004 to ascertain the prevalence of a range of health conditions.
Rates of blindness, vision loss, depression, hip fracture and nursing home residence were higher among the patients with age-related macular degeneration versus those without, and they had a higher prevalence of 11 other general health conditions such as congestive heart failure, dementia and liver disease, the investigators found.
"This nationally longitudinal study documents increased rates of visual and functional health complications that occurred within 10 years of an age-related macular degeneration diagnosis," the authors write. "These findings demonstrate that the health issues of the age-related macular degeneration population are multifaceted, especially when viewed in a 10-year period, highlighting the importance of a multidisciplinary, integrated approach to the care of elderly persons with an age-related macular degeneration diagnosis."
Ashley Wysong, of Duke University School of Medicine in Durham N.C., and colleagues studied Medicare claims data on 32,702 adults aged 68 years and older who were newly diagnosed with age-related macular degeneration in 1994 and 32,702 matched controls, who were all followed up in 2004 to ascertain the prevalence of a range of health conditions.
Rates of blindness, vision loss, depression, hip fracture and nursing home residence were higher among the patients with age-related macular degeneration versus those without, and they had a higher prevalence of 11 other general health conditions such as congestive heart failure, dementia and liver disease, the investigators found.
"This nationally longitudinal study documents increased rates of visual and functional health complications that occurred within 10 years of an age-related macular degeneration diagnosis," the authors write. "These findings demonstrate that the health issues of the age-related macular degeneration population are multifaceted, especially when viewed in a 10-year period, highlighting the importance of a multidisciplinary, integrated approach to the care of elderly persons with an age-related macular degeneration diagnosis."
Saturday, March 21, 2009
New Technique May Spot Evidence of Macular Degeneration Years Earlier
New Technique May Spot Evidence of Macular Degeneration Years Earlier
February 26, 2009
Adapted from Rochester University
A layer of "dark cells" in the retina that is responsible for maintaining the health of the light-sensing cells in our eyes has been imaged in a living retina for the first time.
The ability to see this nearly invisible layer could help doctors identify the onset of many diseases of the eye long before a patient notices symptoms. The findings are reported in the February, 2009 issue of Investigative Ophthalmology and Visual Science.
"Our goal is to figure out why macular degeneration, one of the most prevalent eye diseases, actually happens," says David Williams, director of the Center for Visual Science and professor in the Institute of Optics at the University of Rochester. "Macular degeneration affects one in 10 people over the age of 65, and as the average age of the U.S. population continues to increase, it is only going to get more and more common. We know these dark retinal cells are compromised by macular degeneration, and now that we can image them in the living eye, we might be able to detect the disease at a much earlier stage."
In 1997, Williams' team was the first to image individual photoreceptor cells in the living eye, using a technique called adaptive optics, which was borrowed from astronomers trying to get clearer images of stars. To image the dark cells behind the photoreceptors, however, Williams employed adaptive optics with a new method to make the dark cells glow brightly enough to be detected.
The cells, called retinal pigment epithelial, or RPE cells, are nearly black, and form a layer that recharges the photoreceptor cells of the eye after they are exposed to light, Williams explains. The photoreceptors contain molecules called photopigments. When light strikes these molecules, they absorb the light and change shape, sending a signal to the brain indicating they've "seen" light.
Once a photopigment molecule absorbs light, says Williams, it needs to get recharged, so it is shuttled out of the photoreceptor and down to the RPE cells. The RPE cells recharge the photopigment molecules and send them back to the photoreceptors to start the process again. In addition, the RPE layer keeps the photoreceptors healthy by collecting and storing toxic waste products that are produced during the process of regenerating the photopigment. In macular degeneration, for reasons that are not yet completely clear, the RPE cells are unable to provide this support for the photoreceptors and both kinds of cells eventually die.
Given their critical role supporting the photoreceptors, Williams says that scientists will benefit from being able to image RPE cells in patients to see what is malfunctioning in individual cells.
Williams and his team now hope to learn exactly how RPE cells are related to macular degeneration. At the moment, scientists aren't sure how the disease starts, but being able to monitor the health of individual RPE cells may help doctors begin to piece together a picture of what mechanisms are malfunctioning in the retina. Williams also says that since the technique may eventually be able to spot illness in the RPE long before the patient experiences symptoms, doctors could start patients on therapies early enough to possibly slow or stop the onset of macular degeneration. Currently, when a patient begins treatment, a great deal of irreparable damage has been done.
February 26, 2009
Adapted from Rochester University
A layer of "dark cells" in the retina that is responsible for maintaining the health of the light-sensing cells in our eyes has been imaged in a living retina for the first time.
The ability to see this nearly invisible layer could help doctors identify the onset of many diseases of the eye long before a patient notices symptoms. The findings are reported in the February, 2009 issue of Investigative Ophthalmology and Visual Science.
"Our goal is to figure out why macular degeneration, one of the most prevalent eye diseases, actually happens," says David Williams, director of the Center for Visual Science and professor in the Institute of Optics at the University of Rochester. "Macular degeneration affects one in 10 people over the age of 65, and as the average age of the U.S. population continues to increase, it is only going to get more and more common. We know these dark retinal cells are compromised by macular degeneration, and now that we can image them in the living eye, we might be able to detect the disease at a much earlier stage."
In 1997, Williams' team was the first to image individual photoreceptor cells in the living eye, using a technique called adaptive optics, which was borrowed from astronomers trying to get clearer images of stars. To image the dark cells behind the photoreceptors, however, Williams employed adaptive optics with a new method to make the dark cells glow brightly enough to be detected.
The cells, called retinal pigment epithelial, or RPE cells, are nearly black, and form a layer that recharges the photoreceptor cells of the eye after they are exposed to light, Williams explains. The photoreceptors contain molecules called photopigments. When light strikes these molecules, they absorb the light and change shape, sending a signal to the brain indicating they've "seen" light.
Once a photopigment molecule absorbs light, says Williams, it needs to get recharged, so it is shuttled out of the photoreceptor and down to the RPE cells. The RPE cells recharge the photopigment molecules and send them back to the photoreceptors to start the process again. In addition, the RPE layer keeps the photoreceptors healthy by collecting and storing toxic waste products that are produced during the process of regenerating the photopigment. In macular degeneration, for reasons that are not yet completely clear, the RPE cells are unable to provide this support for the photoreceptors and both kinds of cells eventually die.
Given their critical role supporting the photoreceptors, Williams says that scientists will benefit from being able to image RPE cells in patients to see what is malfunctioning in individual cells.
Williams and his team now hope to learn exactly how RPE cells are related to macular degeneration. At the moment, scientists aren't sure how the disease starts, but being able to monitor the health of individual RPE cells may help doctors begin to piece together a picture of what mechanisms are malfunctioning in the retina. Williams also says that since the technique may eventually be able to spot illness in the RPE long before the patient experiences symptoms, doctors could start patients on therapies early enough to possibly slow or stop the onset of macular degeneration. Currently, when a patient begins treatment, a great deal of irreparable damage has been done.
Saturday, March 14, 2009
What Drives Brain Changes in Macular Degeneration
ScienceDaily (Mar. 13, 2009) — In macular degeneration, the most common form of adult blindness, patients progressively lose vision in the center of their visual field, thereby depriving the corresponding part of the visual cortex of input. Previously, researchers discovered that the deprived neurons begin responding to visual input from another spot on the retina — evidence of plasticity in the adult cortex.
Just how such plasticity occurred was unknown, but a new MIT study sheds light on the underlying neural mechanism.
"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," said Nancy Kanwisher of the McGovern Institute for Brain Research at MIT and senior author of the study appearing in the March 4 issue of the Journal of Neuroscience.
"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," said Kanwisher, the Ellen Swallow Richards Professor of Cognitive Neuroscience in MIT's Department of Brain and Cognitive Sciences.
Macular degeneration affects 1.75 million people in the United States alone. Loss of vision begins in the fovea of the retina — the central area providing high acuity vision that we use for reading and other visually demanding tasks. Patients typically compensate by using an adjacent patch of undamaged retina. This "preferred retinal locus" (PRL) is often below the blind region in the visual field, leading patients to roll their eyes upward to look at someone's face, for example.
The visual cortex has a map of the visual field on the retina, and in macular degeneration the neurons mapping to the fovea no longer receive input. But several labs, including Kanwisher's, previously found that the neurons in the visual cortex that once responded only to input from central vision begin responding to stimuli at the PRL. In other words, the visual map has reorganized.
"We wanted to know if the chronic, prior use of the PRL causes the cortical change that we had observed in the past, according to what we call the use-dependent hypothesis," said first author Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab. "Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behavior, according to the use-independent hypothesis?"
The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging (fMRI) to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.
Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.
But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.
This finding suggests that the long-term change in visual behavior is not driving the brain's remapping. Instead, the brain changes appear to be a relatively passive response to visual deprivation.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex." Kanwisher said. If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well.
Chris Baker of the Laboratory of Brain and Cognition (NIMH) and Eli Peli of the Schepens Eye Research Institute also contributed to this study, which was supported by the NIH, Kirschstein-NRSA, and Dr. and Mrs. Joseph Byrne.
Adapted from materials provided by Massachusetts Institute of Technology.
Just how such plasticity occurred was unknown, but a new MIT study sheds light on the underlying neural mechanism.
"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," said Nancy Kanwisher of the McGovern Institute for Brain Research at MIT and senior author of the study appearing in the March 4 issue of the Journal of Neuroscience.
"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," said Kanwisher, the Ellen Swallow Richards Professor of Cognitive Neuroscience in MIT's Department of Brain and Cognitive Sciences.
Macular degeneration affects 1.75 million people in the United States alone. Loss of vision begins in the fovea of the retina — the central area providing high acuity vision that we use for reading and other visually demanding tasks. Patients typically compensate by using an adjacent patch of undamaged retina. This "preferred retinal locus" (PRL) is often below the blind region in the visual field, leading patients to roll their eyes upward to look at someone's face, for example.
The visual cortex has a map of the visual field on the retina, and in macular degeneration the neurons mapping to the fovea no longer receive input. But several labs, including Kanwisher's, previously found that the neurons in the visual cortex that once responded only to input from central vision begin responding to stimuli at the PRL. In other words, the visual map has reorganized.
"We wanted to know if the chronic, prior use of the PRL causes the cortical change that we had observed in the past, according to what we call the use-dependent hypothesis," said first author Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab. "Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behavior, according to the use-independent hypothesis?"
The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging (fMRI) to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.
Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.
But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.
This finding suggests that the long-term change in visual behavior is not driving the brain's remapping. Instead, the brain changes appear to be a relatively passive response to visual deprivation.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex." Kanwisher said. If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well.
Chris Baker of the Laboratory of Brain and Cognition (NIMH) and Eli Peli of the Schepens Eye Research Institute also contributed to this study, which was supported by the NIH, Kirschstein-NRSA, and Dr. and Mrs. Joseph Byrne.
Adapted from materials provided by Massachusetts Institute of Technology.
Saturday, March 7, 2009
MIT study sheds light on brain changes in macular degeneration
MIT study sheds light on brain changes in macular degeneration
Wednesday, March 4, 2009
CBC News
The brain adapts to find new visual information when a person gets eye disease causing blindness, according to a study from the Massachusetts Institute of Technology.
Researchers found that when people lose their sight because of macular degeneration, the affected neurons simply start seeking visual input from other, non-affected parts of the eye.
Their findings were published Wednesday in the Journal of Neuroscience.
"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," wrote lead researcher Nancy Kanwisher of the McGovern Institute for Brain Research at MIT.
It appears the long-term change in visual behaviour is not driving the brain's remapping; rather, it's the brain's relatively passive response to visual deprivation.
Macular degeneration is the most common form of adult blindness. It affects 800,000 people in Canada. Those suffering from it progressively lose vision in the central visual field of their retina, or their fovea. That means the corresponding part of the visual cortex in the brain also loses input.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said in a news release. "If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well."
Previously, researchers found deprived neurons would begin responding to visual input from another spot on the retina, essentially building a new visual map on the cortex. That information provided evidence of plasticity in the adult cortex. However, there were still questions as to how that happened.
MIT's study sheds light on the underlying neural mechanism.
"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," said Kanwisher.
Typically, people suffering from MD will compensate by using an adjacent patch of undamaged retina. They'll roll their eyes upward to look at someone's face instead of focusing straight on, for instance. That undamaged patch becomes their new "preferred retinal locus," or PRL.
The researchers wanted to find out if the cortical change was caused by chronic prior use of the PRL, said another study author, Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab.
"Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behaviour," he wrote.
The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.
Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.
But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.
Wednesday, March 4, 2009
CBC News
The brain adapts to find new visual information when a person gets eye disease causing blindness, according to a study from the Massachusetts Institute of Technology.
Researchers found that when people lose their sight because of macular degeneration, the affected neurons simply start seeking visual input from other, non-affected parts of the eye.
Their findings were published Wednesday in the Journal of Neuroscience.
"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," wrote lead researcher Nancy Kanwisher of the McGovern Institute for Brain Research at MIT.
It appears the long-term change in visual behaviour is not driving the brain's remapping; rather, it's the brain's relatively passive response to visual deprivation.
Macular degeneration is the most common form of adult blindness. It affects 800,000 people in Canada. Those suffering from it progressively lose vision in the central visual field of their retina, or their fovea. That means the corresponding part of the visual cortex in the brain also loses input.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said in a news release. "If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well."
Previously, researchers found deprived neurons would begin responding to visual input from another spot on the retina, essentially building a new visual map on the cortex. That information provided evidence of plasticity in the adult cortex. However, there were still questions as to how that happened.
MIT's study sheds light on the underlying neural mechanism.
"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," said Kanwisher.
Typically, people suffering from MD will compensate by using an adjacent patch of undamaged retina. They'll roll their eyes upward to look at someone's face instead of focusing straight on, for instance. That undamaged patch becomes their new "preferred retinal locus," or PRL.
The researchers wanted to find out if the cortical change was caused by chronic prior use of the PRL, said another study author, Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab.
"Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behaviour," he wrote.
The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.
Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.
But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.
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