August 24 Research Roundup: Stem Cells for Muscle, Autism, Dementia and More

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There are plenty of great scientific research stories out this week. Here’s a look at just a few of them.

Stem Cell Matrix Can Help Build Muscle in Elderly and Duchene Muscular Dystrophy Patients

Researchers at the Georgia Institute of Technology published research in the journal Science Advances describing the developing of a molecular matrix that can deliver muscle stem cells to injured muscle tissue. It notes that, for example, elderly patients with muscle injuries have problems healing, and diseases like Duchene muscular dystrophy (DMD) are linked to problems with muscle regeneration.

Young Jang, an assistant professor in Georgia Tech’s School of Biological Sciences and one of the article’s principal investigators, stated, “Any muscle injury is going to attract immune cells. Typically, this would help muscle stem cells repair damage. But in aged or dystrophic muscles, immune cells lead to the release of a lot of toxic chemicals like cytokines and free radicals that kill the new stem cells.”

They developed a hydrogel molecular matrix that allows stem cells to be successfully delivered in mice. The technique was also successful in mice with muscle tissue deficiency that modeled for DMD. The hydrogel protects the stem cells, allowing them to multiply and thrive inside the matrix. The gel is applied to injured muscle and the cells attach to the tissues and help them heal.

Autism and Related Disorders Linked to Egg Cell’s Problems in Creating Large Proteins

The genetic factors that cause fragile X syndrome and possibly other autism-related disorders have been linked to defects in cell’s ability to manufacture unusually large proteins. Specifically, researchers at Carnegie Institute for Science, Ethan Greenblatt and Allan Spradling, identified mutations in the Fmr1 gene. These mutations can cause problems in the brain and reproductive system, and lead to fragile X syndrome, the most common type of inherited autism. It can also lead to premature ovarian failure.

The researchers, who published their research in the journal Science, conducted work on Fmr1’s effects on the protein-manufacturing process in fruit fly eggs. “Our results surprised us,” Spradling stated. “We found that egg cells lacking Fmr1 were at first completely normal; but over time, if they were stored, they lost function much faster than stored eggs with normal Fmr1, which is reminiscent of the human ovarian failure syndrome. What’s more, when fertilized, these Fmr1-lacking eggs created offspring with severe nervous system defects, which is reminiscent of fragile X syndrome.”

“Rogue Proteins” Linked to ALS and Frontotemporal Dementia

Inherited forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia—similar to early-onset Alzheimer’s—have been linked to gene mutations tied to an abnormal buildup of the RNA-binding protein, TDP-43, in the brain. Researchers at Columbia University and New York Genome Center published research in the journal eLife, showing that TDP-43 and at least three other RNA-binding proteins also behave abnormally in ALS and dementia patients that don’t have the mutation.

“It turns out that if you analyze the biochemical properties of RNA-binding proteins you see it’s not just TDP-43 but several others that are also perturbed,” stated Aaron Gitler, genetics professor at Stanford University, who discussed the trial in the same issue of eLife. “This is a new concept in how we think about these diseases—not just as TDP-43 diseases, but as RNA-binding protein diseases.”

“Our data suggests that we may be able to distinguish one subpopulation of ALS patients from the other,” stated study co-author Neil Schneider, a neurology professor who heads Columbia University Irving Medical Center’s Eleanor and Lou Gehrig ALS Center. “This could lead to a therapeutic intervention that works selectively on those patients.”

Who Knew? Eating a Healthy Diet Can Keep your Cells Young … If You’re A Woman

Yet another reason to eat your fruits and veggies, researchers at the University of Michigan School of Public Health published research in the American Journal of Epidemiology that showed eating diets rich in fruits, vegetables, whole grains and low in sugar, sodium and processed meat can keep your telomeres from shortening. If you think of DNA as being like shoelaces, telomeres are those little plastic things at the ends that keep them from unraveling (an aglet). Every time your cells divide, telomeres get a tiny bit shorter, which is linked to aging. But telomeres also can get shortened due to behavioral, environmental and psychological factors. Shorter telomeres are linked to increased risk for heart disease, type 2 diabetes and some cancers.

Cindy Leung, assistant professor of nutritional sciences at the University of Michigan, led a group that looked at the diets of almost 5,000 healthy adults and scored their diets and examined their cells’ telomere length. What is a bit surprising was that these results weren’t as obvious in men as they were in women.

“We have seen some gender differences in previous nutrition and telomere studies,” Leung said in a statement. “In our study, as well as in previous studies, men tended to have lower diet quality scores than women. Men also had higher intakes of sugary beverages and processed meats, both of which have been associated with shorter telomeres in prior studies. It’s possible that not all foods affect telomere length equally and you need higher amounts of protective foods in order to negate the harmful effects of others. However, more research is needed.”

It’s also possible that men overstate the number of fruits and vegetables they actually eat.

Possible Gene Therapy for Retinitis Pigmentosa

Researchers at the University of Pennsylvania’s School of Veterinary Medicine and Perelman School of Medicine, in collaboration with University of Florida scientists, developed a gene therapy that appears to treat retinitis pigmentosa, a progressive disease of the eye that causes night and peripheral vision problems before leading to blindness. Their work on dogs was published in the Proceedings of the National Academy of Sciences.

The team used a two-part therapy that included a way of knocking out the defective genes and replacing them. “It’s a one treatment fits all,” stated William Beltran, professor of ophthalmology and director of the Division of Experimental Retinal Therapies at Penn Vet and co-lead author of the study. "This treatment targets a region of the rhodopsin gene that is homologous in humans and dogs and is separate from where the mutations are located. That gives us great hope about making this a translational treatment.”

Early work knocked down both the mutant and normal rhodopsin genes in dogs, which prevented the disease but also caused loss of the key cellular compartment of rod photoreceptors. This required they try adding back a healthy copy.

How Does Exercise Cut the Risk of Age-Associated Cognitive Decline?

Exercise has been associated with lower rates of cognitive decline in older individuals. Why that is isn’t completely clear. Researchers at Deakin University and Swinburne University of Technology, both in Australia, published work in IOS Press looking at the possible mechanisms. They looked at a number of studies and evaluated factors including increased neurogenesis and neuroplasticity, reduction in stress and anxiety, reduced inflammation and improved insulin sensitivity.

The authors conclude, “Overall, the current research supports the potential for exercise to improve cognitive outcomes via increased BDNF-facilitated neurogenesis and neuroplasticity, improvement in vascular function, reduced stress and inflammation, and improved insulin sensitivity. However, at present the relative contribution of exercise to these mechanisms has not been specified. Neither have the relative strengths of the influence of these mechanisms on cognition, as current research in the area typically isolates one specific potential mediator at a time. Exercise, as opposed to many other potential cognitive interventions, is extremely cost-effective and has no intrinsic negative side effects, which makes it a promising candidate for ameliorating the rate of cognitive decline in our aging population.”

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