Sentences with phrase «damaged axons»

The purpose of this study is to assess the utility of pNF - H, a biomarker released from damaged axons of the spinal cord into the bloodstream, to predict return of function following surgery in dachshunds without pain sensation in their hind limbs due to disc herniation.

Damaged axons in the brain and spinal cord of mammals don't regenerate, and spinal cord injuries can therefore lead to permanent paralysis.

The findings raise the possibility that blocking the Phr1 protein with a drug could keep damaged axons alive and functional when the body would normally cause the axons to self - destruct.

Three days after injury, these axons are protected from degeneration because they are missing Phr1, a gene involved in removing damaged axons from the body.

Instead, the researchers found that dendritic, but not axonal, varicosities could be induced by prolonged treatment with glutamate, an excitatory neurotransmitter that is released from damaged axons.

The other is that the virus itself directly attacks neural cells and destabilizes the myelin sheath around them or damages axons to cause GBS.

A few microscopic techniques can focus light deep into the intact brains of dead animals to study its structure without damaging the axons, but much of this light is scattered away by the fatty lipid membranes that surround individual cells, making the technique less than perfect.

However, this damages the axons — the arms that protrude from neurons to make connections with other cells — making it difficult to see exactly how brain cells link up.

Not exact matches

Giza speculates that youth may be at greater risk for more severe damage from concussion because developing brains lack myelin, the covering that protects axons.

TBI commonly damages nerve fibers in the brain called axons.

Surviving axons may compensate for the damage by increasing electrical signaling and thus restoring the normal speed of information processing in the brain.

Those signals are disrupted because myelin, the insulating sheath around a nerve cell's message - transmitting axons, becomes damaged.

A drug that blocks a component of this cascade called Rho kinase reduced the damage to axons.

The HMS study reveals that the aberrant behavior of an enzyme called RIPK1 damages neuronal axons by disrupting the production of myelin, the soft gel - like substance enveloping axons to insulate them from injury.

As part of the new study, the researchers showed that intact axons without Phr1 were protected from the damage caused by vincristine, a chemotherapy drug used to treat leukemia, neuroblastoma, Hodgkin's disease and non-Hodgkin's lymphoma, among other cancers.

Experiments conducted in mice and in human ALS cells reveal that when RIPK1 is out of control, it can spark axonal damage by setting off a chemical chain reaction that culminates in stripping the protective myelin off of axons and triggering axonal degeneration — the hallmark of ALS.

Instead, the researchers discovered a different protein, p75, that binds to the axon's myelin when nerve damage occurs in these animals.

For a damaged nerve to regain function, its long, signal - transmitting extensions known as axons need to grow and establish new connections to other cells.

RIPK1, the researchers found, inflicts damage by directly attacking the body's myelin production plants — nerve cells known as oligodendrocytes, which secrete the soft substance, rich in fat and protein that wraps around axons to support their function and shield them from damage.

Sheng and his research fellow Bing Zhou, the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration.

Unlike peripheral nerves, which re-sprout axons when they are damaged, mature spinal neurons do not regrow axons in the part of the body where the injury has occurred — such as when the spinal cord is cut or crushed — which results in paralysis below the injury.

The study, «Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits,» which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.

The axons look fairly normal, but they are catastrophically damaged.

The swellings get so big that they eventually rupture, tearing the axon apart and spewing out damaged proteins.

Previous work by Freeman's lab identified another enzyme, a gene called SARM, which was the first shown to activate a process that causes axons to disintegrate when damaged.

\ n \ nMeanwhile, work in the private sector in collaboration with academic institutions, has produced an IND that is now before the FDA, for a human trial with hESC - derived oligodendrocytes to remyelinate damaged spinal chord axons.

Our goal is to use a new imaging system to monitor damage caused by AD to the brain region that contains the insulated axons (analogous to cables) connecting the neuron cell bodies (analogous to the central processing unit of a computer).

So, intraocular pressure may be elevated, axon transport fails, the axon ends up being physically damaged; the retinal ganglion cells die relatively late in the disease.

Furthermore, the success of this project can lead to the development of novel axon - regenerating therapeutics that could transform the clinical treatment of angle - closure glaucoma and other types of optic neuropathies, as well as have the potential to be adapted to regenerating the long - distance axonal projections damaged by spinal cord injury, brain trauma, and white matter stroke.

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.

My research is focused on the pathophysiology of retinal ganglion cell (RGC) axon damage in glaucoma and detecting early - stage abnormalities by means of non-invasive imaging, psychophysical testing and electrophysiological measures such as electroretinography (ERG) and visually evoked cortical potentials (VEP).

Vision loss from glaucoma occurs when axons in the optic nerve become damaged and can no longer carry visual information to the brain.

No axons were damaged.

It's these axons that a head injury can damage.

Dr. Olby wants to restore the myelin sheath to these surviving axons by taking fat cells from the patient and turning them into stem cells that can be combined with nerve cells and injected into the site of the damage, regrowing the sheath.

Obviously, researchers would love to be able to replace all the lost neurons and axons and restore normal connections in a damaged spinal cord.