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If this pans out....
2 page article....I suggest reading it all.
2 page article....I suggest reading it all.
Potential New Weapon against Lou Gehrig's Disease
Mouse model suggests that a combination of therapies may stave off the onset of this neurodegenerative disorder
A protein that helps combat stress on cells caused by environmental influences like rising ambient temperatures appears to block the onset of amyotrophic lateral sclerosis (ALS), at least in a mouse model of the neurodegenerative illness.
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ALS ravages two distinct populations of motor neurons—one in the brain, the other in the spinal cord. The endings of the spinal cord cells interface with neighboring muscle cells, normally signaling muscles to contract or relax to create motion. But researchers at Wake Forest University Baptist Medical Center in Winston?Salem, N.C., found that ALS-affected neurons undergo a process known as "denervation" that severs the connection.
The scientists report in The Journal of Neuroscience, however, that they were able to preserve these neuromuscular links in mice genetically engineered to develop ALS by injecting heat protein 70 (Hsp70) into their backs, thus delaying the onset of the disease. This protein is secreted in large quantities by neurons in response to stressors. Hsp70 maintains proper nerve cell function by binding to the neurons and chaperoning proper protein folding inside. Previous models of ALS demonstrated that neurons sustain damage when stressed, because Hsp70 levels do not rise to corresponding levels.
"By keeping [muscle and nerve] cells talking to each other, you keep both cells healthy," says study co-author Carol Milligan, an assistant professor of neurobiology at W.F.U. Medical Center. "That keeps the motor neurons healthier longer." She notes that most existing and developing ALS therapies target cell bodies as opposed to the neuromuscular junction.
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Mouse model suggests that a combination of therapies may stave off the onset of this neurodegenerative disorder
A protein that helps combat stress on cells caused by environmental influences like rising ambient temperatures appears to block the onset of amyotrophic lateral sclerosis (ALS), at least in a mouse model of the neurodegenerative illness.
>
ALS ravages two distinct populations of motor neurons—one in the brain, the other in the spinal cord. The endings of the spinal cord cells interface with neighboring muscle cells, normally signaling muscles to contract or relax to create motion. But researchers at Wake Forest University Baptist Medical Center in Winston?Salem, N.C., found that ALS-affected neurons undergo a process known as "denervation" that severs the connection.
The scientists report in The Journal of Neuroscience, however, that they were able to preserve these neuromuscular links in mice genetically engineered to develop ALS by injecting heat protein 70 (Hsp70) into their backs, thus delaying the onset of the disease. This protein is secreted in large quantities by neurons in response to stressors. Hsp70 maintains proper nerve cell function by binding to the neurons and chaperoning proper protein folding inside. Previous models of ALS demonstrated that neurons sustain damage when stressed, because Hsp70 levels do not rise to corresponding levels.
"By keeping [muscle and nerve] cells talking to each other, you keep both cells healthy," says study co-author Carol Milligan, an assistant professor of neurobiology at W.F.U. Medical Center. "That keeps the motor neurons healthier longer." She notes that most existing and developing ALS therapies target cell bodies as opposed to the neuromuscular junction.
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