Tag Archives: retina

CRISPR Gene Editing Grows New Neurons In Diseased Brains

Transferring lab grown neurons into animal brains reduces the cells’ viability — their chances of integrating well into the tissue — and the efficiency with which they can restore function. So scientists at Shanghai Research Center for Brain Science and BrainInspired Intelligence fashioned a method to regenerate neurons inside the brain. The method is similar to how one would revive a dying plant: by nurturing it with the right conditions for it to grow new leaves.

Building up on a previous study, Haibo Zhou, a postdoctoral researcher in Hui Yang’s lab, and colleagues, set up a method to convert non neuronal brain cells called “glia” into neurons. They did this by turning down a gene called PTBP1 in glia of different parts of the mouse brain, using the gene-editing tool CRISPR. Depending on which brain region was targeted, the glia gave rise to different kinds of neurons.

Reducing PTBP1 levels presumably reverted glia to unspecified stem cells, which adopted varied neuronal identities based on which glia were targeted and the environmental signals they received. This was evident from the team’s successful attempts at restoring two different types of neurons and alleviating the symptoms associated with the loss of each.

Parkinson’s disease occurs due to loss of dopamine-producing neurons and manifests as tremors, stiffness, and loss of balance. To test their method in rejuvenating this group of neurons, the team first got rid of them using a toxic compound in mice. The authors then converted glia into dopamine-producing neurons, and the new cells showed the same activity as their original counterparts.

This rescue was not limited to just the neuron population. It also partially restored the normal motor behavior of the animal. This is a huge step forward from drug induced alleviation of symptoms because it puts forth a more permanent solution.

The team also tackled retinal diseases caused by death of retinal ganglion cells, or RGCs, which leads to permanent blindness. Turning down PTBP1 in glia of the retina transformed them into RGCs. Astoundingly, these renewed neurons not only responded to light independently, but also sent their projections to the visual cortex correctly, restoring circuit function. This led to a partial recovery of eyesight in the treated mice.

Source: https://www.salon.com/

Nanotubes In the Eye That Help Us See

Researchers  find a new structure by which cells in the retina communicate with each other, regulating blood supply to keep vision intact. A new mechanism of blood redistribution that is essential for the proper functioning of the adult retina has just been discovered in vivo by researchers at the University of Montreal Hospital Research Centre (CRCHUM).

For the first time, we have identified a communication structure between cells that is required to coordinate blood supply in the living retina,” said Dr. Adriana Di Polo, a neuroscience professor at Université de Montréal and holder of a Canada Research Chair in glaucoma and age-related neurodegeneration, who supervised the study.

We already knew that activated retinal areas receive more blood than non-activated ones,” she said, “but until now no one understood how this essential blood delivery was finely regulated.”

The study was conducted on mice by two members of Di Polo’s lab: Dr. Luis Alarcon-Martinez, a postdoctoral fellow, and Deborah Villafranca-Baughman, a PhD student. Both are the first co-authors of this study.

In living animals, as in humans, the retina uses the oxygen and nutrients contained in the blood to fully function. This vital exchange takes place through capillaries, the thinnest blood vessels in all organs of the body. When the blood supply is dramatically reduced or cut off—such as in ischemia or stroke—the retina does not receive the oxygen it needs. In this condition, the cells begin to die and the retina stops working as it should.

The study has been published in Nature.


Bionic Eye With Better Vision Than Humans

The world’s first 3D artificial eyeball — capable of outperforming the human eye in some ways — may help droves of people who are partially or fully blind in as little as five years, according to experts.

Researchers from Hong Kong University of Science and Technology have devised an electrochemical eye whose structure and performance mimic those of the ones humans are born with.

The device design has a high degree of structural similarity to a human eye with the potential to achieve high imaging resolution when individual nanowires are electrically addressed,” researchers of Hong Kong University of Science and Technology wrote in a paper published in the journal Nature.

The device converts images through tiny sensors that mirror the lightdetecting photoreceptor cells in a human eyeThe Sun reported. Those sensors reside within a membrane made of aluminum and tungsten which is shaped into a half sphere for the purpose of mimicking a human retina.

Source:  https://www.nature.com/

How To Restore Sight To The Blind

For more than a decade, researchers have been working to create artificial digital retinas that can be implanted in the eye to allow the blind to see again. Many challenges stand in the way, but researchers at Stanford University may have found the key to solving one of the most vexing: heat. The artificial retina requires a very small computer chip (nanocoputer) with many metal electrodes poking out. The electrodes first record the activity of the neurons around them to create a map of cell types. This information is then used to transmit visual data from a camera to the brain. Unfortunately, the eye produces so much data during recording that the electronics get too darn hot.

The chips required to build a high-quality artificial retina would essentially fry the human tissue they are trying to interface with,” says E.J. Chichilnisky, a professor in the Neurosurgery and Ophthalmology departments, who is on Stanford’s artificial retina team.

Members of the team, including Chichilnisky and his collaborators in Stanford’s Electrical Engineering and Computer Science departments, recently announced they have devised a way to solve that problem by significantly compressing the massive amounts of visual data that all those neurons in the eye create. They discuss their advance in a study published in the IEEE Transactions on Biomedical Circuits and Systems.

To convey visual information, neurons in the retina send electrical impulses, known as spikes, to the brain. The problem is that the digital retina needs to record and decode those spikes to understand the properties of the neurons, but that generates a lot of heat in the digitization process, even with only a few hundred electrodes used in today’s prototypes. The first true digital retina will need to have tens of thousands of such electrodes, complicating the issue further. Boris Murmann, a professor of electrical engineering on the retina project, says the team found a way to extract the same level of visual understanding using less data. By better understanding which signal samples matter and which can be ignored, the team was able to reduce the amount of data that has to be processed. It’s a bit like being at a party trying to extract a single coherent conversation amid the din of a crowded room — a few voices matter a lot, but most are noise and can be ignored.

We compress the data by being more selective, ignoring the noise and baseline samples and digitizing only the unique spikes,” Murmann says. Previously, digitization and compression were done separately, leading to a lot of extra data storage and data transfer. “Our innovation inserts compression techniques into the digitization process,” says team member Subhasish Mitra, a professor of electrical engineering and of computer science. This approach retains the most useful information and is easier to implement in hardware.

Source: https://engineering.stanford.edu/

How To Reverse Congenital Blindness

Researchers funded by the  American National Eye Institute (NEI) have reversed congenital blindness in mice by changing supportive cells in the retina called Müller glia into rod photoreceptors. The findings advance efforts toward regenerative therapies for blinding diseases such as age-related macular degeneration and retinitis pigmentosa. A report of the findings appears online today in Nature. NEI is part of the National Institutes of Health.

This is the first report of scientists reprogramming Müller glia to become functional in the mammalian ,” said Thomas N. Greenwell, Ph.D., NEI program director for retinal neuroscience. “Rods allow us to see in low light, but they may also help preserve cone photoreceptors, which are important for color vision and high visual acuity. Cones tend to die in later-stage eye diseases. If rods can be regenerated from inside the eye, this might be a strategy for treating diseases of the eye that affect photoreceptors.”

Photoreceptors are light-sensitive cells in the retina in the back of the eye that signal the brain when activated. In mammals, including and humans, photoreceptors fail to regenerate on their own. Like most neurons, once mature they don’t divide.

Scientists have long studied the regenerative potential of Müller glia because in other species, such as zebrafish, they divide in response to injury and can turn into photoreceptors and other retinal neurons. The zebrafish can thus regain vision after severe retinal injury. In the lab, however, scientists can coax mammalian Müller glia to behave more like they do in the fish. But it requires injuring the tissue.

From a practical standpoint, if you’re trying to regenerate the retina to restore a person’s vision, it is counterproductive to injure it first to activate the Müller glia,” said Bo Chen, Ph.D., associate professor of ophthalmology and director of the Ocular Stem Cell Program at the Icahn School of Medicine at Mount Sinai, New York.

We wanted to see if we could program Müller glia to become rod photoreceptors in a living mouse without having to injure its retina,” added Chen, the study’s lead investigator.

Source: https://www.nih.gov/