Exercise Plus IGF1 Gene Therapy Prolong Survival in Mouse Model of ALS

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By Karla Gale

NEW YORK (Reuters Health) Nov 15 - In a mouse model of amyotrophic lateral

sclerosis (ALS), researchers have found that exercise initiated early in

life prolongs survival, as does gene therapy with insulin-like growth factor

1 (IGF-1), according to a presentation this week at the annual meeting of

the Society for Neuroscience in Washington, DC.

" There have been reports that exercise is neuroprotective in animal models

of Huntington's disease, Parkinson's disease, and ALS, " presenter Dr.

Kaspar told Reuters Health. " Other studies have suggested that exercise

increases serum levels of IGF-1, which may be responsible for

exercise-mediated neuroprotection. "

However, extreme exercise, as practiced by many athletes, seems to have the

opposite effect, increasing the odds of developing ALS, he added.

To tease out the effects of exercise on ALS, Dr. Kaspar, from the Ohio State

University in Columbus, and his colleagues used a mouse model of ALS, the

lifespan of which averages 120 days.

According to background materials, the authors found that exercise on a

running wheel, if initiated at 90 days of age, provided significant motor

function benefits and extended the animals' lifespan approximately 11 days.

If exercise was started when they were younger, they lived about a month

longer.

Moreover, treatment with IGF-1 using an adenovirus vector extended their

lifespan to an extent similar to that observed with exercise.

However, there appeared to be a synergistic effect when exercised animals

received gene therapy with IGF-1; these animals lived an average of 210

days.

" From our work, we know that gene changes are occurring within the spinal

cord motor neurons and in muscle that is induced by exercise. We believe

these gene changes lead to neural protection, " Dr. Kaspar said. For example,

they theorize that trophic factors and antiapoptotic factors are upregulated

during exercise.

" We're now planning to increase the intensity exercise in this model of

ALS, " the researcher said, " with the ultimate goal of developing gene

therapies or pharmaceutical therapies to slow down disease progression in

humans. "