Here's a drug to reverse permanent deafness

PTI | Jan 11, 2013, 07.18 AM IST
READ MORE LY411575|inner ear|Harvard scientists|drug|deafness
LONDON: Harvard scientists have developed a drug which they claim can cure permanent deafness by stimulating the inner ear. The drug, codenamed LY411575, works by triggering the regeneration of sensory hair cells.

Until now it has not been possible to restore the cells once they have been lost due to factors such as loud noise exposure, infection and toxic drugs, the Daily Mail said.

This type of deafness, often suffered by rock musicians and DJs, is generally assumed to be irreversible. Scientists succeeded in partially restoring hearing to mice that had been deafened by loud noise and believe the research could lead to effective treatments for in humans.

The new approach involves reprogramming inner ear cells by inhibiting a protein, Notch. Previous research shows Notch signals help prevent stem cells in the cochlea transforming themselves into new sensory hair cells.
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Botox jab may aid recovery in stroke survivors

PTI | Jan 9, 2013, 07.06 AM IST
READ MORE Neuroscience Research Australia|Botox
MELBOURNE: Injecting botox into the arm muscles of stroke survivors may aid their long-term recovery, according to new research.
Researchers at Neuroscience Research Australia found that when botox is injected into the arm muscles of stroke survivors, with severe spasticity, it changes electrical activity in the brain which assists in long-term recovery.
Researchers monitored nerve activity in the arms and brains of stroke survivors before and after botulinum toxin (botox) injections in rigid and stiff muscles in the arm.
They found that botox indeed improved arm muscles, but also altered brain activity in the cortex. "Botulinum toxin is used to treat a range of muscular and neurological conditions and shows that this treatment results in electrical and functional changes within brain itself," said William Huynh, lead author.
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New drug can help paralyzed people walk again

PTI | Jan 9, 2013, 01.23 PM IST
READ MORE the rest|Placebo|Ohio State University|Frank|Axon
LONDON: Scientists have developed a pill which they claim could help paralyzed people walk again.

The new drug allowed mice with no movement in their lower limbs to walk with 'well-coordinated steps' and even to replicate swimming motions, researchers said.

The experimental drug, called LM11A-31, was developed by Professor Frank Longo, of Stanford University, California.

The researchers gave three different oral doses of LM11A-31, as well as a placebo, to different groups of mice beginning four hours after injury and then twice daily for a 42 day experimental period, the 'Daily Mail' reported.

In tests, the experimental medication did not increase pain in the mice and showed no toxic effects on the animals.

It also efficiently crossed the blood brain barrier, which protects the central nervous system from potentially harmful chemicals carried around in the rest of the bloodstream.

An injury to the spinal cord stops the brain controlling the body and this is the first time an oral drug has been shown to provide an effective therapy.

"This is a first to have a drug that can be taken orally to produce functional improvement with no toxicity in a rodent model," Professor Sung Ok Yoon, of Ohio State University, Columbus, said.

"So far, in the spinal cord injury field with rodent models, effective treatments have included more than one therapy, often involving invasive means. Here, with a single agent, we were able to obtain functional improvement," Yoon said.

The small molecule in the study was tested for its ability to prevent the death of cells called oligodendrocytes.

These cells surround and protect axons, long projections of a nerve cell, by wrapping them in a myelin sheath that protect the fibres.

In addition to functioning as axon insulation, myelin allows for the rapid transmission of signals between nerve cells.

The drug preserved oligodendrocytes by inhibiting the activation of a protein called p75. Yoon's lab previously found p75 is linked to the death of these specialised cells after a spinal cord injury. When they die, axons that are supported by them degenerate.

"Because we know oligodendrocytes continue to die for a long period of time after an injury, we took the approach that if we could put a brake on that cell death, we could prevent continued degeneration of axons," she said.

The study was published in the Journal of Neuroscience.
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