Quest Magazine

ALS 'Lake Link' Tenuous

Recent media reports have raised the question of a possible link between an increased risk of developing amyotrophic lateral sclerosis (ALS) and living near Lake Mascoma in Western New Hampshire.

The Union Leader in New Hampshire and other news outlets have reported that the risk of developing ALS is 25 times higher than average for people living around Lake Mascoma, located in Enfield and Lebanon, N.H. The source of this statistic was not explained.

NM Research: Successful Substitute?

A protein present in skeletal muscles during fetal development and in the heart after birth can apparently compensate for a similar protein that's missing in a small percentage of patients with the muscle disease known as nemaline myopathy.

MDA research grantee Nigel Laing at the University of Western Australia in Perth was part of a multinational team of scientists, who published their findings May 25, 2009, in the Journal of Cell Biology.

MD Research: Muscle-Repair Booster

In experiments in mice, Michael Rudnicki, an MDA grantee at the Sprott Center for Stem Cell Research at Ottawa Hospital Research Institute (OHRI), and colleagues, found the WNT7a protein stimulates muscle repair by causing proliferation (an increase in number) of "satellite stem cells." They say the protein probably operates similarly in humans. The findings were published June 5, 2009, in the journal Cell Stem Cell.

Cardiac Actin Can Substitute for Skeletal-Muscle Actin

A protein present in skeletal muscles during fetal development and in the heart after birth can apparently compensate for a similar protein that's missing in a small percentage of patients with the muscle disease known as nemaline myopathy.

MDA research grantee Nigel Laing at the University of Western Australia in Perth was part of a multinational team of scientists, who published their findings May 25, 2009, in the Journal of Cell Biology.

WNT7a Protein Boosts Muscle Repair

In experiments in mice, Michael Rudnicki, an MDA grantee at the Sprott Center for Stem Cell Research at Ottawa Hospital Research Institute (OHRI), and colleagues, found the WNT7a protein stimulates muscle repair by causing proliferation (an increase in number) of "satellite stem cells." They say the protein probably operates similarly in humans. The findings were published June 5, 2009, in the journal Cell Stem Cell.

Stem Cell Research Brings New Hope for Muscular Dystrophy Treatment

A discovery that strengthens the body’s ability to repair muscle tissue could lead to new treatments for people with muscular dystrophy and other degenerative muscle diseases.

Kids’ Respiratory Needs

The proceedings of a symposium titled "Pulmonary Management of Pediatric Patients with Neuromuscular Disorders" have been published as a supplement to the May 2009 issue of the journal Pediatrics.

The symposium was held Feb. 20, 2008, at Scottish Rite Hospital in Dallas, and was sponsored by MDA, as well as Respironics and Hill-Rom Services.

Topics, all of which pertain specifically to children with neuromuscular disorders, include

Holes in the Walls

Proteins that keep large molecules from moving freely across blood-vessel walls in the spinal cord appear to be deficient in people with ALS (amyotrophic lateral sclerosis), MDA-supported researchers say. They don't yet know, however, whether a lower-than-normal level of some of these so-called "tight junction" proteins, is helpful or harmful in the disease process.

Utrophin Gets In

MDA grantee James Ervasti and colleagues at the University of Minnesota-Twin Cities in Minneapolis have found that a protein known as utrophin, injected into mice lacking the dystrophin protein and showing a disease resembling Duchenne muscular dystrophy (DMD), conferred significant benefits.

The experiments Ervasti and colleagues describe online May 26, 2009, in PLoS Medicine, are the first to show benefit from the direct injection into DMD mice of utrophin protein, rather than utrophin genes or gene modifiers.

Holes in the Walls

Proteins that keep large molecules from moving freely across blood-vessel walls in the spinal cord appear to be deficient in people with ALS (amyotrophic lateral sclerosis), MDA-supported researchers say. They don't yet know, however, whether a lower-than-normal level of some of these so-called "tight junction" proteins, is helpful or harmful in the disease process.

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