At this point, there is no effective treatment for TON and the mechanisms of
the optic nerve cell death have been largely unclear.
Not exact matches
And like other retinal ganglion
cells in the eye, the ipRGCs grow long fibers that snake out to join the
optic nerve.
Anatomical investigations have shown, however, that there are many more receptor
cells in the retina than there are fibers in the
optic nerve.
Roughly 2 % of people over age 35 have chronic glaucoma, in which fluid builds up inside the eyeball, leading to increased pressure and eventual death of
cells in the
optic nerve.
«Our data clearly showed that one of the protein receptors on white blood
cells called CXCR3 brings white blood
cells to the
optic nerve in response to production of its binding partner CXCL10 by damaged
nerve tissue,» said Zhang.
When the
optic nerve is injured, there are tears and swelling in the affected area that causes the
nerve cells to die.
«It would seem that the ganglion
cells — which «have long tails that bundle together to become the
optic nerve and send messages to the brain» — would be the final section of the eye, not the first one that intercepts light.
«Our work could lead not only to a better understanding of the biology of the
optic nerve, but also to a
cell - based human model that could be used to discover drugs that stop or treat blinding conditions,» says study leader Donald Zack, M.D., Ph.D., the Guerrieri Family Professor of Ophthalmology at the Johns Hopkins University School of Medicine.
«We hope that these
cells can eventually lead to new treatments for glaucoma and other forms of
optic nerve disease.»
These electrodes pulse to stimulate
cells in the retina, transmitting visual information along the
optic nerve to the brain, creating the perception of patterns of light.
The impulse starts with excitation of the left retina, then travels down the
optic nerve to
cells in the midbrain and brain stem, which excite neurons near both eyes that cause the pupils to constrict.
A healthy
optic nerve has axons transmitting information from the eye to the brain along the
nerve after considerable information processing and synaptic transmission between various
cell types within the retina.
Scientists at the Virginia Tech Carilion Research Institute (VTCRI) have revealed the pathology of
cells and structures stricken by
optic nerve hypoplasia, a leading cause of childhood blindness in developed nations.
Optic nerve hypoplasia is closely related to
optic nerve atrophy, in which the
optic nerve develops normally initially, but later degenerates as its
cells die off.
NERVE PROTECTORS The glowing cells in this micrograph of a mouse's optic nerve help shield electrical signals passing between eyes and b
NERVE PROTECTORS The glowing
cells in this micrograph of a mouse's
optic nerve help shield electrical signals passing between eyes and b
nerve help shield electrical signals passing between eyes and brain.
The drops protected the animals» retinal ganglion
cells and
optic nerves, both of which are generally damaged by the disease.
These
cells normally don't mingle with neurons from the diencephalon, which gives rise to less advanced structures such as the hypothalamus and
optic nerves.
«We used a mouse model of the KPro to, first of all, identify the inflammatory factors that cause damage to the eye, and then we also quantified the amount of
nerve cell death in the back of the eye that mediates the
optic neuropathy, and, lastly, we looked at blocking these factors with antibodies,» said Reza Dana, M.D., M.Sc., MPH, Director of the Cornea and Refractive Surgery Service at Massachusetts Eye and Ear and the Claes H. Dohlman Professor of Ophthalmology at Harvard Medical School.
When these photoreceptors detect light, they send a signal to specialized neurons in the retina called retinal ganglion
cells, or RGCs, which then transmit visual information to the brain by firing electrical pulses along the
optic nerve.
Some of the
cells in this layer (the photoreceptors) convert light into an electrical signal that is then amplified and processed by other
cells before being sent to the brain via the
optic nerve.
In 2010, they decided to collaborate to learn about zinc's impact on retinal ganglion
cells, which receive visual signals and form the
optic nerve that delivers information to the brain.3
They discovered that zinc is released from
cells within an hour after the
optic nerve is injured acutely — but they were surprised to find that it didn't come from retinal ganglion
cells.
In one -, four - and 10 - week - old animals, the donor
cells not only took, but actually migrated to the right place, started assuming the characteristics of retinal
cells and extended into the
optic nerve, which links the eye to the brain.
Millions of
nerve fibers running from the ganglion
cells dive through the eye's «blind spot» and form the
optic nerve that carries impulses to the brain.
Methanol harms sight mainly by damaging mitochondria in
cells in the eye's retina and
optic nerve.
In fact, so much of the progress that we're making in laboratories, including mine, is on developing neuroprotective therapies that can protect the retina from degeneration, regenerate
optic nerve fibers all the way back to their targets in the brain, and even replace damaged retinal ganglion
cells with self - therapies that completely rebuild the
optic nerve.
Summary: In glaucoma, permanent vision loss and blindness occur when retinal ganglion
cells (RGCs) that make up the
optic nerve are lost.
These
nerve cells, known as retinal ganglion
cells (RGCs), use electrical impulses to send visual information — entering the eye through the
optic nerve — to the brain where images are perceived.
Clinical, histopathological, and molecular variables included patient age, gender, extraocular extension, tumor location (ciliary body or not),
optic nerve invasion, angiotropism, neurotropism, melanoma
cell type, BAP1 mutation, and monosomy 3.
(E) Retinal ganglion
cell axons exit the eye as the
optic nerve (white arrow), pass under the brain and out of view then reappear on the contralateral side (arrowhead).
The reprogrammed
cells formed all seven classes of retinal
cells normally found in the eyes, including the retinal ganglion
cells, which have axons (
optic nerves) that extend to the brain.
We have two neurobiologists who are studying retinal ganglion
cell and
optic nerve biology — and that's me and Andy Huberman — and we also have two optical imaging engineers with very different backgrounds — and that's Vivek Srinivasan and Alf Dubra.
We are using these new tools to image the structural features of individual
cells, such as the
cell body and the axons of the
cells, which are long fibers that extend from each neuron, together forming the
optic nerve that transmits visual information to the brain.
These key understandings are the first significant steps toward slowing or preventing the
cell death process using targeted interventions to protect the
optic nerve from glaucoma's damage.
There's no retinal ganglion
cell regeneration or replacement after
optic nerve injury.
GenSight's treatment is for people with damaged photoreceptor
cells but intact ganglion
cells; it inserts the gene into the ganglion
cells, whose axons form the basis of the
optic nerve.
We've devised ways to test patients using new imaging technologies to measure the health of their retinal ganglion
cells and of their fibers entering the
optic nerve.
The processor then sends that pattern wirelessly to a chip implanted above the retina, where 60 electrodes stimulate undamaged
cells, creating signals that travel up the
optic nerve.
The macula is densely packed with photoreceptor
cells called rods and cones that react to light and send electrical
nerve impulses to the
optic nerve and into the brain.
The pattern of RGC loss in patients as well as information obtained from laboratory research all point to the fact that an important site of pathology occurs at the
optic nerve head, a region where the axonal
cell processes of RGCs exit the eye on their way to the visual centers of the brain.
Replacing rods and cones is challenging, because these
cells have to establish connections with
nerve fibers that feed signals into the
optic nerve, which sends those signals to the brain to interpret.
Dr. Otteson studied how retinal ganglion
cells turn on and off the genes that regulate the normal patterns of connections during
optic nerve development.
In this study, we will examine whether glial
cells and certain proteins secreted from these
cells influence axon regeneration and guidance in the
optic nerve in adult mice.
Second, they will determine which components of the EDN system are involved in both degeneration of the
optic nerve and retinal
cell death.
Understanding the role of glial
cells in glaucoma as well as what happens to the
optic nerve where the retinal
nerve axons leave the eye may present new therapeutic targets and even potential biomarkers of glaucoma.
Towards this goal, we first discovered that
optic nerves regenerate physically on the surface of astrocytes which are the support
cells in the
optic nerve.
On the surface, the disease appears relatively simple, with high pressure (intra-ocular pressure, or IOP) within the eye associated with the death of
cells in the retina and
optic nerve dysfunction.
Right now all therapy for glaucoma is directed at lowering eye pressure, but the idea that we could develop therapies and test them in people that really target the retinal ganglion
cells and the axon fibers going into the
optic nerve — that, I think, is the most exciting new frontier for the premise of restoring vision and protecting vision in glaucoma.
The retina and
optic nerve have specialized
cells that manage these byproducts to prevent harmful accumulation.
Some eye diseases, including glaucoma, damage the retinal ganglion
cells (RGCs) that make up the
optic nerve.