Cataract surgery can improve cognitive ability in patients with mild Alzheimer’s disease, it has been found

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Posted on 25th January 2012 by Pacific ClearVision Institute in Cataracts

Researchers at Tenon Hospital, Paris, France, say that patients whose vision improved after cataract surgery also showed improvement in cognitive ability, mood, sleep patterns and other behaviors. Lead researcher Brigitte Girard, MD, discussed her team’s results at the American Academy of Ophthalmology’s 2011 Annual Meeting.

This is the first study to specifically assess whether cataract surgery could benefit Alzheimer’s patients, although earlier research had shown that poor vision is related to impaired mood and thinking skills in older people and that cataract surgery could improve their quality of life. Thirty-eight patients, average age 85 and all exhibiting mild dementia due to Alzheimer’s disease, completed Dr. Girard’s study. All participants had debilitating cataract in at least one eye and were appropriately treated with standard cataract surgery and implantation of intraocular lenses, which replace the eyes’ natural lenses in order to provide vision correction. After surgery, distance and near vision improved dramatically in all but one of the Alzheimer’s patients.

A neuropsychologist assessed the Alzheimer’s patients for mood and depression, behavior, ability to function independently, and cognitive abilities at one month before and three months after cataract surgery. Cognitive status, the ability to perceive, understand and respond appropriately to one’s surroundings, improved in 25 percent of patients. Depression was relieved in many of them, and the level of improvement was similar to what commonly occurs after cataract surgery in elderly people who do not have dementia. No changes were found in patients’ level of autonomy, that is, their ability to function independently.

“We wanted to learn whether significant vision improvement would result in positive mood and behavior changes, or might instead upset these patients’ fragile coping strategies,” said Dr. Girard. “In future studies we intend to learn what factors, specifically, led to the positive effects we found, so that we can boost the quality of life for Alzheimer’s patients, their families and caregivers.”

Source-Medindia

Flexible Adult Stem Cells, Right There in Your Eye

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Posted on 25th January 2012 by Pacific ClearVision Institute in Retina

In the future, patients in need of perfectly matched neural stem cells may not need to look any further than their own eyes. Researchers reporting in the January issue of Cell Stem Cell, a Cell Press publication, have identified adult stem cells of the central nervous system in a single layer of cells at the back of the eye.

That cell layer, known as the retinal pigment epithelium (RPE), underlies and supports photoreceptors in the light-sensitive retina. Without it, photoreceptors and vision are lost. The new study shows that the RPE also harbors self-renewing stem cells that can wake up to produce actively growing cultures when placed under the right conditions. They can also be coaxed into forming other cell types.

“You can get these cells from a 99-year-old,” said Sally Temple of the Neural Stem Cell Institute in Rensselaer, New York. “These cells are laid down in the embryo and can remain dormant for 100 years. Yet you can pull them out and put them in culture and they begin dividing. It is kind of mind boggling.”

Temple’s group got the RPE-derived stem cells they describe from the eyes of donors in the hours immediately after their deaths. But the cells can also be isolated from the fluid that surrounds the retina at the back of the eye, which means they are accessible in living people as well.

“You can literally go in and poke a needle in the eye and get these cells from the subretinal space,” she says. “It sounds awful, but retinal surgeons do it every day.” By comparison, access to most other neural stem cell populations would require major surgery.

Temple said they were curious about the proliferative potential of the RPE given that the tissue is known to be capable of regenerating entire retinas in salamanders. But that plasticity in adulthood had seemed to be lost in mice and chicks. Still, “given the evolutionary evidence, we thought it was worth revisiting,” she said.

They placed RPE tissue taken from 22-year-old to 99-year-old cadavers into many culture conditions to see what they could make the cells do. They found one set of conditions that got the cells dividing. Not all of the RPE cells have this regenerative potential, but perhaps 10 percent of them do.

Further work showed that the cells are multipotent, which means that they can form different cell types, though the researchers admit there is more to do to fully explore the cells’ differentiation capacity.

There are other implications as well. For example, these cells may explain diseases in which other tissue types show up in the eye. Their presence also suggests that there might be some way to stimulate controlled repair of the eye in the millions of people who suffer from age-related macular degeneration.

“I think it might be possible,” Temple said.

Researchers Develop Gene Therapy That Could Correct a Common Form of Blindness

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Posted on 25th January 2012 by Pacific ClearVision Institute in Retina

A new gene therapy method developed by University of Florida researchers has the potential to treat a common form of blindness that strikes both youngsters and adults. The technique works by replacing a malfunctioning gene in the eye with a normal working copy that supplies a protein necessary for light-sensitive cells in the eye to function.

The findings are published Jan. 23 in the Proceedings of the National Academy of Sciences online.

Several complex and costly steps remain before the gene therapy technique can be used in humans, but once at that stage, it has great potential to change lives.

“Imagine that you can’t see or can just barely see, and that could be changed to function at some levels so that you could read, navigate, maybe even drive — it would change your life considerably,” said study co-author William W. Hauswirth, Ph.D., the Rybaczki-Bullard professor of ophthalmology in the UF College of Medicine and a professor and eminent scholar in department of molecular genetics and microbiology and the UF Genetics Institute. “Providing the gene that’s missing is one of the ultimate ways of treating disease and restoring significant visual function.”

The researchers tackled a condition called X-linked retinitis pigmentosa, a genetic defect that is passed from mothers to sons. Girls carry the trait, but do not have the kind of vision loss seen among boys. About 100,000 people in the U.S. have a form of retinitis pigmentosa, which is characterized by initial loss of peripheral vision and night vision, which eventually progresses to tunnel vision, then blindness. In some cases, loss of sight coincides with the appearance of dark-colored areas on the usually orange-colored retina.

The UF researchers previously had success pioneering the use of gene therapy in clinical trials to reverse a form of blindness known as Leber’s congenital amaurosis. About 5 percent of people who have retinitis pigmentosa have this form, which affects the eye’s inner lining.

“That was a great advance, which showed that gene therapy is safe and lasts for years in humans, but this new study has the potential for a bigger impact, because it is treating a form of the disease that affects many more people,” said John G. Flannery, Ph.D., a professor of neurobiology at the University of California, Berkeley who is an expert in the design of viruses for delivering replacement genes. Flannery was not involved in the current study.

The X-linked form of retinitis pigmentosa addressed in the new study is the most common, and is caused by degeneration of light-sensitive cells in the eyes known as photoreceptor cells. It starts early in life, so though affected children are often born seeing, they gradually lose their vision.

“These children often go blind in the second decade of life, which is a very crucial period,” said co-author Alfred S. Lewin, Ph.D., a professor in the UF College of Medicine department of molecular genetics and microbiology and a member of the UF Genetics Institute. “This is a compelling reason to try to develop a therapy, because this disease hinders people’s ability to fully experience their world.”

Both Lewin and Hauswirth are members of UF’s Powell Gene Therapy Center.

The UF researchers and colleagues at the University of Pennsylvania performed the technically challenging task of cloning a working copy of the affected gene into a virus that served as a delivery vehicle to transport it to the appropriate part of the eye. They also cloned a genetic “switch” that would turn on the gene once it was in place, so it could start producing a protein needed for the damaged eye cells to function.

After laboratory tests proved successful, the researchers expanded their NIH-funded studies and were able to cure animals in which X-linked retinitis pigmentosa occurs naturally. The injected genes made their way only to the spot where they were needed, and not to any other places in the body. The study gave a good approximation of how the gene therapy might work in humans.

“The results are encouraging and the rescue of the damaged photoreceptor cells is quite convincing,” said Flannery, who is on the scientific advisory board of the Foundation Fighting Blindness, which provided some funding for the study. “Since this type of study is often the step before applying a treatment to human patients, showing that it works is critical.”

The researchers plan to repeat their studies on a larger scale over a longer term, and make a version of the virus that proves to be safe in humans. Once that is achieved, a pharmaceutical grade of the virus would have to be produced and tested before moving into clinical trials in humans. The researchers will be able to use much of the technology they have already developed and used successfully to restore vision.

Gene Identified as a New Target for Treatment of Aggressive Childhood Eye Tumor

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Posted on 25th January 2012 by Pacific ClearVision Institute in Retina

New findings from the St. Jude Children’s Research Hospital — Washington University Pediatric Cancer Genome Project (PCGP) have helped identify the mechanism that makes the childhood eye tumor retinoblastoma so aggressive. The discovery explains why the tumor develops so rapidly while other cancers can take years or even decades to form.

The finding also led investigators to a new treatment target and possible therapy for the rare childhood tumor of the retina, the light-sensing tissue at the back of the eye. The study appears in the January 11 advance online edition of the scientific journal Nature.

Researchers have known for decades that loss of a tumor suppressor gene named RB1 launches retinoblastoma during fetal development. But the other steps involved in the rapid transformation from a normal cell to a malignant tumor cell that occurs in this cancer were unknown.

This study linked the RB1 mutation to abnormal activity of other genes linked to cancer without changing the makeup of the genes themselves. Evidence suggests that epigenetic factors, including reversible chemical changes that influence how genes are switched on and off in tumor cells, are altered when RB1 is mutated.

“The dogma in the field has been that once RB1 is mutated, the genome of the affected cell becomes unstable, chromosomes begin to break and recombine, and mutations quickly develop in the pathways that are essential for cancer progression,” said Michael Dyer, Ph.D., member of the St. Jude Department of Developmental Neurobiology and a Howard Hughes Medical Institute Early Career Scientist. “What we found through the Pediatric Cancer Genome Project was exactly the opposite. These tumors contain very few mutations or chromosomal rearrangements.”

Dyer is one of the paper’s corresponding authors. The others are James Downing, M.D., St. Jude scientific director, and Richard Wilson, Ph.D. director of The Genome Institute at Washington University in St. Louis.

Worldwide, retinoblastoma is found in more than 5,000 children each year, including about 300 in the U.S. Most are age 5 or younger, and some are infants when the cancer is discovered, making them among the youngest cancer patients.

While 95 percent of patients are cured with current therapies if their tumors are discovered before they spread beyond the eye, Dyer said the prognosis is much worse for children in developing countries whose cancer is often advanced when it is discovered. For up to half of those patients, retinoblastoma remains a death sentence. Researchers are working to develop curative treatments that preserve vision without radiation or surgical removal of the eye. Success is particularly important for children with tumors in both eyes.

For this study, researchers sequenced the complete normal and cancer genomes of four St. Jude patients with retinoblastoma. The human genome is the complete set of instructions needed to assemble and sustain an individual.

The effort, a first for retinoblastoma, was part of the PCGP that St. Jude and Washington University officials launched in 2010. The three-year project aims to complete whole-genome sequencing of normal and tumor DNA from 600 children and adolescents battling some of the most challenging cancers. Organizers believe the results will provide the foundation for the next generation of clinical care.

The retinoblastoma tumors sequenced contained about 15-fold fewer mutations than have been found in nearly all other cancers sequenced so far. In one patient’s tumor, RB1 was the only mutation.

The findings prompted Dyer to integrate the whole-genome sequencing results with additional tests that looked at differences in the patterns of gene activity in tumor and normal tissue. In particular, researchers focused on genes that, when mutated, promote cancer development. “To our surprise and excitement, what we found was that instead of cancer genes having genetic mutations, they were being epigenetically regulated differently than normal cells,” Dyer said.

The genes included SYK, which is required for normal blood development and has been linked to other cancers. Drugs targeting the SYK protein are already in clinical trials for adults with leukemia and rheumatoid arthritis.

SYK has no role in normal eye development. When researchers checked SYK protein levels in normal and retinoblastoma tissue, they found high levels of the protein in 82 tumor samples and absent in normal tissue. “We see changes in the SYK gene in retinoblastoma that probably give the cancer cell a growth advantage or provide other key factors with regard to how retinoblastoma is initiated,” Wilson said.

When researchers used the experimental drugs to block SYK in human retinoblastoma cells growing in the laboratory or in the eye of a mouse, the cells died. Dyer said work is now under way to reformulate one of the experimental drugs, a SYK-inhibitor called R406, so it can be delivered directly into the eye. If successful, those efforts are expected to lead to a Phase I trial in retinoblastoma patients.

Cataract surgery can improve cognitive ability in patients with mild Alzheimer’s disease, it has been found.

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Posted on 3rd January 2012 by Pacific ClearVision Institute in Cataracts |General

Researchers at Tenon Hospital, Paris, France, say that patients whose vision improved after cataract surgery also showed improvement in cognitive ability, mood, sleep patterns and other behaviors. Lead researcher Brigitte Girard, MD, discussed her team’s results at the American Academy of Ophthalmology’s 2011 Annual Meeting.

This is the first study to specifically assess whether cataract surgery could benefit Alzheimer’s patients, although earlier research had shown that poor vision is related to impaired mood and thinking skills in older people and that cataract surgery could improve their quality of life. Thirty-eight patients, average age 85 and all exhibiting mild dementia due to Alzheimer’s disease, completed Dr. Girard’s study. All participants had debilitating cataract in at least one eye and were appropriately treated with standard cataract surgery and implantation of intraocular lenses, which replace the eyes’ natural lenses in order to provide vision correction. After surgery, distance and near vision improved dramatically in all but one of the Alzheimer’s patients.

A neuropsychologist assessed the Alzheimer’s patients for mood and depression, behavior, ability to function independently, and cognitive abilities at one month before and three months after cataract surgery. Cognitive status, the ability to perceive, understand and respond appropriately to one’s surroundings, improved in 25 percent of patients. Depression was relieved in many of them, and the level of improvement was similar to what commonly occurs after cataract surgery in elderly people who do not have dementia. No changes were found in patients’ level of autonomy, that is, their ability to function independently.

Sleep patterns improved and night time behavior problems decreased in most study patients. Other studies have shown that when cataracts are removed, levels of the sleep-regulating hormone melatonin become normalized. Dr. Girard notes that this may have been a key factor in the Alzheimer’s patients’ improved sleep patterns.

“We wanted to learn whether significant vision improvement would result in positive mood and behavior changes, or might instead upset these patients’ fragile coping strategies,” said Dr. Girard. “In future studies we intend to learn what factors, specifically, led to the positive effects we found, so that we can boost the quality of life for Alzheimer’s patients, their families and caregivers.”

New Evidence of an Unrecognized Visual Process

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Posted on 3rd January 2012 by Pacific ClearVision Institute in General |Retina

We don’t see only what meets the eye. The visual system constantly takes in ambiguous stimuli, weighs its options, and decides what it perceives. This normally happens effortlessly. Sometimes, however, an ambiguity is persistent, and the visual system waffles on which perception is right. Such instances interest scientists because they help us understand how the eyes and the brain make sense of what we see.

Most scientists believe rivalry occurs only when there’s “spatial conflict” — two objects striking the same place on the retina at the same time as our eyes move. But the retina isn’t the only filter or organizer of visual information. There’s also the “non-retinal reference frame” — objects such as mountains or chairs that locate things in space and make the world appear stable even when our eyes are moving.

“We asked: what if visual ambiguities are not presented on the same spot on the retina, but on the objects [in the frame] as they move around,” says California Institute of Technology cognitive scientist Jeroen J.A. van Boxtel. Indeed, he and colleague Christof Koch found evidence of rivalry in this reference frame, with surprising effects on the better-understood spatial conflict. The findings, which will appear in an upcoming issue of Psychological Science, a journal published by the Association of Psychological Science, offer intriguing clues to how the visual system works.

In their experiments, van Boxtel and Koch created spatial conflict with a “motion quartet,” which changes the arrangement of four dots. If the dots are displaced in certain ways, the visual system isn’t sure if the movement is vertical or horizontal. If the dots move to an altogether different space, there’s no rivalry. Then the researchers upped the perceptual ante by creating an object reference frame with three white discs and shifting it, too, along with or in opposition to the smaller dots.

Seven male and female participants viewed the changing arrangements in four conditions. In one, both dots and discs remained stationary (creating spatial rivalry); in each of two, either dots or discs moved right or left; in the fourth, both moved horizontally together (creating ambiguity in the frame). Each time, participants had to press a button indicating whether the dots moved horizontally or vertically. The presses were analyzed for perceived movement “bias” (more horizontal or vertical) and duration — evidence either of rivalry or visual clarity.

The results: Even when the dots moved to another space altogether — so there was no spatial conflict — the moving discs created the effect of perceptual ambiguity. But the researchers also found that visual rivalry disappeared when the dots were stationary and the disks moved (that is, the dots were not linked to the disks). It was as if the brain had bigger fish — object-frame rivalry — to fry.

In subsequent experiments — one changing the vertical relationship of the dots and one placing the dots outside the white discs — the researchers got results similar to those they would have gotten without the frame. Their conclusion: The visual system is working out object-frame rivalry as it would spatial rivalry, probably with the same brain regions and processes.

What the Brain Sees After the Eye Stops Looking

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Posted on 3rd January 2012 by Pacific ClearVision Institute in General |Retina

When we gaze at a shape and then the shape disappears, a strange thing happens: We see an afterimage in the complementary color. Now a Japanese study has observed for the first time an equally strange illusion: The afterimage appears in a “complementary” shape — circles as hexagons, and vice-versa.

“The finding suggests that the afterimage is formed in the brain, not in the eye,” the author, Hiroyuki Ito of Kyushu University, wrote in an email. More specifically, the illusion is produced in the brain’s shape-processing visual cortex, not the eye’s light-receiving, message-sending retina. The findings appear in an upcoming issue of Psychological Science, a journal published by the Association for Psychological Science.

Ito conducted three experiments with 82, 92, and 44 participants respectively. In the first two, he showed participants yellow circles or hexagons — outlined or filled, static or rotating on a gray ground. In each, after they observed the images for 10 seconds, the images disappeared, leaving only the blank gray field. The observers were asked to indicate which of seven shapes, on a piece of paper, the afterimage most resembled.

In the third experiment, Ito split the visual field between the two eyes. In the left eye, participants saw rotating circles and hexagons, as well as rotating asterisk-like “stars” — shapes that were neither round nor angular. The right eye viewed static circles in all conditions. When the circles, hexagons, and stars disappeared, the left field was black, which suppressed the formation of afterimages, and the right was white, which heightened it.

In Experiments 1 and 2, participants tended to see circles after hexagons and hexagons after circles. In the third, the right eye produced the most angular afterimages when rotating circles had been projected in the left eye; the most rounded ones after the rotating hexagons; and after the “stars,” images that were neither circular nor edged.

How did Ito infer that the brain, not the eye, was producing these afterimages? He eliminated the theory that the afterimage was a manifestation of “retinal bleaching” — when the photoreceptors on the retina become ineffective or fatigued through prolonged exposure to light. Viewing static circles or hexagons produce circular or hexagonal bleached areas on the retina. However, the afterimage shapes were not in the bleached shapes. A spinning circle or hexagon produces a circular trace of light on the retina, causing circular shape of retinal bleaching just as painting on the retina. However, spinning circles produced hexagonal afterimages and vice versa.

Retinal bleaching could not produce “an afterimage shape different from the [typical] retinal bleaching shape.” Neither could the retina transfer information taken in by the left eye to produce an afterimage in the right eye. “The only site that can happen is the brain.”

The research adds to science’s understanding of the role of the brain in vision. “People tend to think that afterimages are meaningless by-products arising from the physiological characteristics of the eye,” wrote Ito. “But I think that the afterimages reflect brain activities and provide us the means to know those activities in a directly visible form.”

Hereditary Predisposition of Melanoma of the Eye Discovered

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Posted on 3rd January 2012 by Pacific ClearVision Institute in General |Retina

Ohio State University researchers have discovered a hereditary cancer syndrome that predisposes certain people to a melanoma of the eye, along with lung cancer, brain cancer and possibly other types of cancer.

The hereditary cancer syndrome is caused by an inherited mutation in a gene called BAP1, researchers say. The findings suggest that BAP1 mutations cause the disease in a small subset of patients with hereditary uveal melanoma and other cancers.

Uveal melanoma is a cancer of the eye involving the iris, ciliary body, or choroid, which are collectively known as the uvea. These tumors arise from the pigment cells, also known as melanocytes that reside within the uvea giving color to the eye. This is the most common type of eye tumor in adults.

The findings are reported in the Journal of Medical Genetics.

“We are describing a new cancer genetic syndrome that could affect how patients are treated,” said first author Dr. Mohamed H. Abdel-Rahman, researcher at the Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute. “If we know that a patient has this particular gene mutation, we can be more proactive with increased cancer screenings to try to detect these other potential cancers when they are beginning to grow.”

Study leader Dr. Frederick H. Davidorf, professor emeritus of ophthalmology at Ohio State University, explained that BAP1 seems to play an important role in regulating cell growth and proliferation, and that loss of the gene helps lead to cancer.

“If our results are verified, it would be good to monitor these patients to detect these cancers early when they are most treatable,” said Davidorf, who treats ocular oncology patients at Ohio State along with researcher and physician Dr. Colleen Cebulla.

The study involved 53 unrelated uveal melanoma patients with high risk for hereditary cancer, along with additional family members of one of the study participants. Of the 53 patients in the study, researchers identified germline variants in BAP1 in three patients.

“We still don’t know exactly the full pattern of cancers these patients are predisposed to, and more studies are needed,” said Abdel-Rahman, also an assistant professor of ophthalmology and division of human genetics at Ohio State University College of Medicine.

“So far, we’ve identified about six families with this hereditary cancer syndrome. We are working with researchers at Nationwide Children’s Hospital to develop a clinical test to screen for the BAP1 gene mutation,” he said. “Families with this cancer syndrome should be screened for inherited mutations that increase their risk for developing several other cancers.”

Other Ohio State researchers involved in the study include Robert Pilarski, James B. Massengill, Benjamin N. Christopher and Getachew Boru, along with Peter Hovland of the Colorado Retina Associates in Denver.

Funding from the Patti Blow Research Fund in Ophthalmology and the American Cancer Society supported this research.

New Insights Into How the Nervous System Becomes Wired During Early Development

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Posted on 3rd January 2012 by Pacific ClearVision Institute in General |Retina

Thanks to a new study of the retina, scientists at UC Santa Barbara have developed a greater understanding of how the nervous system becomes wired during early development.

The findings reflect the expansion of developmental neurobiology and vision research at UCSB. The work is described in a recent publication of The Journal of Neuroscience.

The research team examined the connectivity of nerve cells, called neurons, in mice. Neurons communicate with one another via synapses where the dendrites and axon terminals of different cells form contacts. This is where nerve signals are transmitted from one neuron to another.

Scientists have understood for some time how neuronal activation at developing synapses contributes to the patterns of connectivity observed in maturity, explained Ben Reese, senior author and professor in UCSB’s Neuroscience Research Institute and the Department of Psychological & Brain Sciences.

Incoming activity plays a critical role in sculpting neuronal form and the elaboration of synaptic connections. The new research shows, by contrast, how relationships between neighboring cells of the same type independently regulate neuronal size and connectivity.

The researchers circumvented the difficulty of visualizing the three-dimensional relationships between neurons within the brain by working within the retina. The retina is an outgrowth of the brain during embryonic development, and is a precisely layered structure in which the cells, their dendrites and their axons are restricted to discrete strata. “This makes the visualization and analysis of neuronal morphology and connectivity far simpler,” said Reese.

The scientists used two genetically modified mouse models to modulate the density of one particular type of retinal neuron, a class of cone bipolar cell. Cone bipolar cells relay information from the population of cone photoreceptors to the retinal ganglion cells. The latter are neurons that in turn project information to locations within the brain where further visual processing of the retinal image takes place.

The lead author on the study, Sammy Lee, was a postdoctoral researcher working in Reese’s lab and supported by a C.J. Martin National Health & Medical Research Council fellowship from Australia during the course of the study. Lee labeled individual cone bipolar cells with a fluorescent dye through a new microinjection procedure developed by Patrick Keeley, a graduate student in the Reese lab.

“What Dr. Lee has shown is that cone bipolar cells modulate the size of their dendritic fields (branched extensions of the neuron) in association with the local density of like-type neurons,” said Reese. “One line of mice has conspicuously fewer cone bipolar cells, each now with a larger dendritic territory, while the other line shows heightened densities and correspondingly smaller dendritic fields.”

Other studies have suggested such homotypic (like-type) modulation of dendritic field size, but the current study directly shows this modulation following genetic manipulation of neuronal density, according to Reese.

Additionally, the researchers found that connectivity with the afferent population of cone photoreceptors is impacted directly, with the larger dendritic fields being innervated by more cones, and the smaller dendritic fields connecting with fewer cones. At any individual cone, the number of dendritic endings associating with that cone was not observed to change, so that the total number of connections made by a cone bipolar cell was remarkably plastic, defined solely by the number of cone contacts formed.

“This developmental plasticity in dendritic growth and synapse number may be well-suited to ensure uniform coverage and connectivity between two populations of neurons — afferents and their targets — when the number of cells in each population is specified independently,” said Reese.

Other studies from Reese’s lab, recently reported in The Proceedings of the National Academy of Sciences and Investigative Ophthalmology and Visual Science, showed how neuronal number is tightly specified genetically, yet is highly variable between different strains of mice. “Wiring together two populations, each of which may vary nearly two-fold in size, yet independent of each other, might best be served by such homotypic plasticity during early development,” he said.

Studies like these may prove relevant for re-establishing connectivity following nerve cell re-specification or replacement in degenerative diseases, particularly as advances in stem cell biology make this an increasing possibility, said Reese.

Reese’s research is funded by the National Eye Institute of the National Institutes of Health. In addition to clinical research NIH funds basic research furthering the fundamental understanding of biological processes; in this case, neural development.

Nanometer-Scale Growth of Cone Cells Tracked in Living Human Eye

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Posted on 3rd January 2012 by Pacific ClearVision Institute in General |Retina

Humans see color thanks to cone cells, specialized light-sensing neurons located in the retina along the inner surface of the eyeball. The actual light-sensing section of these cells is called the outer segment, which is made up of a series of stacked discs, each about 30 nanometers (billionths of a meter) thick. This appendage goes through daily changes in length.

Scientists believe that a better understanding of how and why the outer segment grows and shrinks will help medical researchers identify potential retinal problems. But the methods usually used to image the living human eye are not sensitive enough to measure these miniscule changes. Now, vision scientists at Indiana University in Bloomington have come up with a novel way to make the measurements in a living human retina by using information hidden within a commonly used technique called optical coherence tomography (OCT). They discuss their results in the Optical Society’s (OSA) open-access journal Biomedical Optics Express.

To make an OCT scan of the retina, a beam of light is split into two. One beam scatters off the retina while the other is preserved as a reference. The light waves begin in synch, or in phase, with each other; when the beams are reunited, they are out of phase, due to the scattering beam’s interactions with retinal cells. Scientists can use this phase information to procure a precise measurement of a sample’s position. But since in this case their samples were attached to live subjects, the researchers had to adapt these typical phase techniques to counteract any movements that the subjects’ eyes might insert into the data.

Instead of measuring the phase of a single interference pattern, the researchers measured phase differences between patterns originating from two reference points within the retinal cells: the top and bottom of the outer segment. The team used this hidden phase information to measure microscopic changes in hundreds of cones, over a matter of hours, in two test subjects with normal vision. Researchers found they could resolve the changes in length down to about 45 nanometers, which is just slightly longer than the thickness of a single one of the stacked discs that make up the outer segment. The work shows that the outer segments of the cone cells grow at a rate of about 150 nanometers per hour, which is about 30 times faster than the growth rate of a human hair.