Genetically "Strong" Chickpeas battle Malnutritions

          Malnutrition affects over 2 billion people worldwide and has been a growing epidemic. Researchers from the University of Saskatchewan have been finding ways to combat the growing micronutrient malnutrition by enriching certain food grains by breeding correctly and right practices. these actions are coupled together and are called biofortification. Specifically chickpeas have been analyzed and changed. After the common bean, the chickpeas are the most important crop and is a necessity in the diets of millions of people.

                                     
            Dr. Ta'ran, one of the leading researchers states that in order to increase the micronutrient content in these chickpeas, the appropriate mechanisms must be clearly understood. Mechanisms of mobilization, absorption, translocation and retranslocation in the plant seed must be analyzed. Single Nucleotide variations or SNP's was analyzed through testing. The chickpeas consisted of elite cultivars, landraces, and advanced breeding lines from the University. The study found that there is in fact variability present in chickpea germplasm for seed iron and zinc concentrations, Increasing the levels of zinc and iron genetically could be a solution to a huge problem in the US

         This article gets me excited with research. Genetically modified foods have been a huge debate over the years, but its benefits can not be shown lightly. These chickpeas can have an affect, not only in the immediate US populations, but can have an affect world-wide.

Article: http://www.sciencedaily.com/releases/2014/12/141201113130.htm
Related Article: http://www.gmo-compass.org/eng/database/plants/302.chick_peas.html

ALS Acceleration Linked to Gene Variant

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative condition that results in destruction to the motor neurons of the human body; and thus, loss of proper motor control and functionality. Death of those with this disease commonly occurs due to respiratory failure upon inability to control the muscles that regulate breathing. There are approximately 12,000 Americans that are affected by this disease.

Researchers at the Penn State College of Medicine determined that there existed an association between excess iron accumulation in the brain and ALS. This was aided primarily by the observation that there was a variant of the HFE gene (H63D HFE), linked to iron overload disease, in 30 percent of the ALS patients within their clinic.

The researchers executed a study with mice, intending to determine the effect of carrying the HFE gene variant on the progression of ALS. Mice with the gene variant were crossbred with standard mice typically used for ALS research. Upon examination of the mice, they found that the progression of the disease occurred at a faster rate in those mice that carried the gene variant. For the crossbred mice, lifespan was reduced by 4 percent. These mice also performed more poorly than the normal mice on testing used to evaluate grip strength of the forelimbs and hindlimbs, indicative of reduced control over motor functions. Increased oxidative stress was also noted for those mice with the gene variant, as well as, increased activation of microglial cells. In a neurodegenerative condition like ALS these microglial cells that conventionally aid bodily repair, can actually result in harmful inflammation. Neurofilaments, which transport nutrients through nerve cells, were also found to be more damaged in mice with the gene variant. 

The identification of a gene variant, H63D HFE, in individuals with an accelerated form of the ALS disease has implications to research oriented in treatment for patients. Treatment that may have previously appeared ineffective may actually prove to be efficacious in new studies that differentiate individuals based on whether they have the normal or accelerated form of the disease. Additionally, researchers may be able to focus on determining treatments that will be more effective in populations of patients with the gene variant specifically.

The determination of a link between the H63D HFE gene variant and an accelerated form of the ALS disease is fascinating. A neurodegenerative disease such as ALS that impairs motor function is very debilitating and unfortunate, especially considering the likely death by respiratory failure. This finding may support research in developing differentiated treatments for those with either the normal or accelerated version of the disease, which may prove to be more efficacious. I also found it very interesting that the disease acceleration was so well modeled in the mice. Hopefully this finding aids future ALS research.

Link to Article: http://www.medicalnewstoday.com/releases/285478.php

Related Links:

http://www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis/detail_als.htm

http://www.pnas.org/content/100/26/15788.full

A Certain Gene Increases the Progression of ALS

        Amoytrophic lateral sclerosis is a disease that involves the degeneration of the lower and upper motor neurons of the brainstem, resulting in those with the disease to loss of muscle control and ultimately death. One third of ALS patients are believed to have a gene that causes a faster progression of the disease. When mice were given this genetic variant, the disease progressed faster and the mice died sooner than the mice that did not have the genetic variant.
       
        About 10 years ago, researchers at Penn State found a link between the amount of iron accumulation in the brain in patients with nuerodegenerative disorders (Parkinson's and Alzheimer's disease). These researchers also found that about of third of their ALS patients had an accumulation of iron and had a genetic variant, HFE, that is associated with iron overdose diseases. In order to test the relationship between iron accumulation and the HFE variant, researchers crossbred mice with the HFE gene and standard mice.

This picture shows the difference between normal nerves and how the nerve fibers start to deteriorate and muscles weaken in those who have ALS.

        When studying the mice, James Connor, vice chair of neurosurgery research and director for the Center for Aging and Neurodegenerative Diseases, and his team found that the crossbred mice performed worse on test for hind limb and forelimb strength and had a 4% shorter life span. Their observations led them to conclude that when a mouse with the HFE variant was infected with ALS, the disease progressed much more rapidly than in the mice that did not have the variant. The grad student that was running the study, Wint Nandar, also realized that the females' disease progression was much faster in females with the variant than in males; however, normally, males with the disease would die faster than females.
 
        The researchers also found that the infected mice showed a greater degree of oxidative stress and microglial activation. Microglial cells are normally responsible for repairing the body, but when they are over-activated, they can cause inflammation, a factor that does not help with the progression of the disease. The mice with the genetic variant were also seen to have a disruption of the nuerofilaments, fibers that transport nutrients through the nerve cells, another reason why the disease can progress faster when HFE is present.

          I think that this a very important study that can be very valuable to those that are trying to find a cure for ALS, or some type of treatment. Knowing the genetic background an individuals can help researchers determine why some of their products work for some patients and not others. ALS is a very detrimental disease and anything that is going to hep researchers get a better understanding of the disease would be extremely beneficial.

Original Article: Genotype found in 30 percent of ALS patients speeds up disease progression