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Researchers reverse important symptom of schizophrenia in mice by manipulating genes

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This is an announcement of no small importance that appeared on the Columbia University website. The researchers say they have reversed one of the most important symptoms of schizophrenia in mice by reversing the SETD1A gene mutation, a gene already known and previously linked by other studies to schizophrenia. Specifically, the researchers reversed the impairment of spatial working memory.

For schizophrenia, there are currently no real treatments. This pathology, which influences the functioning of the brain as well as behavior and mood, must be linked to a sort of cognitive impairment. However, the drugs that exist today for schizophrenia mostly control the psychotic symptoms and not the cognitive ones. This new study shows that it is possible, in a sense, to repair brain cells made dysfunctional by schizophrenia, at least in mice, bringing their level of working memory back to a pre-existing state.

The study, published in Neuron, therefore shows what Joseph Gogos, a researcher at Columbia’s Brain Behavior Institute and senior author of the study, defines as a “promising path” to treat schizophrenia, particularly damage to working memory, not always treated with antipsychotic drugs. An inoperative working memory makes it difficult to maintain any kind of relationship and even damages everyday life by literally putting on by people with schizophrenia who can no longer interact with other people.

The researchers worked on the SETD1A gene. The latter produces a protein that can influence the activity of other important genes. The researchers worked on a group of memory-deficient mice, mice that had some difficulty, for example, in moving into a simple maze. These mice presented neurons from the different prefrontal cortex of normal mice. Specifically, mice lacking SETD1A had short and poorly developed neuronal branches.

This prevented them from establishing the necessary connections with other groups of brain neurons, as Jun Mukai, the study’s first author and former researcher in the Gogos laboratory, explains. By manipulating the SETD1A gene they discovered that it was linked to another gene, called LSD1. By inhibiting the latter, the memory of the mice greatly improved so that their axons began to grow again, becoming similar to those of healthy mice.

Researchers say SETD1A influences a number of other genes and proteins that, combined, can cause memory deficits. This finding could be useful, according to the researchers, to make personalized drugs for people with SETD1A gene mutations and, in a broader view, even to treat schizophrenia itself.

Johnathan Flint

Johnathan is a recent graduate of the Missouri University of Science and Technology with a Bachelor of Medicine, and is an avid reader of numerous medical journals. He recently joined Health Shiner as an editor, researcher and content contributor, and brings a great deal of knowledge and wisdom to our reporting.

2462 White Oak Drive, Weston Missouri, 64098
Ph: 816-640-5682
Email: [email protected]
Johnathan Flint
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Medical Research

Deaf people have “rewired” brains that influence learning according to a new study

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According to a new study published in Nature Scientific Reports, the brains of people with congenital deafness can develop differently and this can influence the ways in which these same people learn to learn. This study, according to the same researchers, may prove useful precisely to develop new methods of teaching “tailor-made” for all people who have never had the opportunity to use hearing during their existence.

According to Colin Johnson, a researcher at the College of Science of the State University of Oregon, people who are born deaf can have a life that is severely compromised even with regards to school and teaching in general. Often these people, in fact, as specified by the researcher, generally fail to reach an adequate level of education and this leads to cascade to other consequences that certainly do not improve the standard of living.

Researchers have discovered that it is a particular protein mutation that causes hearing loss and that it can also alter the wiring of different groups of neurons. The protein, known as otoferlina, has the sole task of encoding the sound in the sensory hair cells that are found in the inner ear.

If this protein undergoes a genetic modification, total hearing loss can occur. This mutation weakens the link between the protein and a calcium synapse in the ear and this lack of interaction is the basis of hearing loss.

Studying this protein in humans has always been difficult due to its size and due to the fact that it is characterized by low solubility. That is why Johnson and colleagues have studied zebrafish that share a similarity in genetic, molecular and cellular levels with humans.

Thanks to these studies, the researcher has discovered a smaller version of the otoferlina that could be used for gene therapy but only in those brains that have not yet undergone a complete rewiring such as that of adults.

“If you grow up without that protein, it’s not just a matter of replacing the gene. If you are deaf and grow deaf, it seems that the physical wiring of your brain is a little different. This complicates the goal of doing gene therapy. We need to go further and look at these hair cells and the brain itself. Does the brain process information differently? This is an area we need to focus on,” explains Johnson.

Johnathan Flint

Johnathan is a recent graduate of the Missouri University of Science and Technology with a Bachelor of Medicine, and is an avid reader of numerous medical journals. He recently joined Health Shiner as an editor, researcher and content contributor, and brings a great deal of knowledge and wisdom to our reporting.

2462 White Oak Drive, Weston Missouri, 64098
Ph: 816-640-5682
Email: [email protected]
Johnathan Flint
Continue Reading

Medical Research

Ghrelin can increase the urge to exercise according to a new discovery

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As some researchers have observed when performing experiments on mice, limiting access to food can increase the levels of a particular hormone, called ghrelin, and this in turn can increase the motivation to exercise, something that naturally leads, in a chain effect, slimming.

In the study, published in the Journal of Endocrinology, it is described how the increase in the level of this hormone pushed mice to voluntarily start exercising or physical activity. This finding, according to the same researchers, could lead, through the limitation of food intake or through the so-called “intermittent fasting,” overweight people to be encouraged to exercise more.

On the other hand, the restriction of food the same regular exercise are the two main ways and the most economic strategies to prevent and treat obesity, a sort of global “epidemic” that requires much more effective intervention strategies. However, adhering to a regular training regime can be difficult for many because motivation is lacking.

This hormone, also called the “hunger hormone,” can not only stimulate the appetite but, as demonstrated by Yuji Tajiri and colleagues from the Kurume University medical school, Japan, it can also stimulate the same desire to exercise. The mice genetically modified in the laboratory for not having ghrelin of their body, in fact, ran less than the control mice, which instead had normal ghrelin levels.

According to Tajiri, the results achieved by this study indicate “that hunger, which promotes ghrelin production, could also be involved in increasing motivation to voluntary exercise when nutrition is limited. Therefore, maintaining a healthy diet, with regular meals or fasting, could also encourage motivation for exercising in overweight people.”

Johnathan Flint

Johnathan is a recent graduate of the Missouri University of Science and Technology with a Bachelor of Medicine, and is an avid reader of numerous medical journals. He recently joined Health Shiner as an editor, researcher and content contributor, and brings a great deal of knowledge and wisdom to our reporting.

2462 White Oak Drive, Weston Missouri, 64098
Ph: 816-640-5682
Email: [email protected]
Johnathan Flint
Continue Reading

Medical Research

Exposure to sunlight can modify intestinal microbiome

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Exposure of the skin to ultraviolet light from the sun can modify the intestinal microbiome according to a new study published in Frontiers in Microbiology. To mediate this change would be vitamin D and this would also explain the protective effect of ultraviolet light itself with regard to inflammatory bowel diseases.

It is well known that exposure to sunlight gives greater production of vitamin D in the skin. It is known, however, through studies published in recent years, also that the same greater quantity of vitamin D can alter the human intestinal microbiome. It follows that solar radiation on the skin can change the human intestinal microbiome but this has only been shown in rodents. This new study shows that this effect is also real for humans.

The researchers performed experiments on 21 healthy volunteer women. The 21 patients underwent three one-minute ultraviolet exposure sessions throughout the body for a week. Throughout the treatment, stool samples were taken and intestinal bacteria were analyzed. Blood samples were also taken to analyze vitamin D levels. The researchers discovered that the exposure of the skin to ultraviolet rays significantly increased the intestinal microbial diversity and this happened only in those people who had not taken vitamin D supplements in the course of experiments.

As explained by Bruce Vallance, a researcher at the University of British Columbia who led the study, exposure to UVB rays increased the richness and uniformity of the subjects’ microbiome. Before exposure to rays, women who did not take supplements showed a less diversified intestinal microbiome than women who already took vitamin D supplements. Among the bacteria that increased the most were the Lachnospiraceae, a genus of bacteria already previously linked with vitamin D.

“UVB light is able to modulate the composition of the intestinal microbiome in humans, through the synthesis of vitamin D,” says Vallance. Now researchers would like to discover the underlying causes but according to Vallance, it is likely that exposure to UVB light somehow affects the immune system of the skin and this, in turn, has a favorable influence on the intestinal environment for different species of bacteria.

Johnathan Flint

Johnathan is a recent graduate of the Missouri University of Science and Technology with a Bachelor of Medicine, and is an avid reader of numerous medical journals. He recently joined Health Shiner as an editor, researcher and content contributor, and brings a great deal of knowledge and wisdom to our reporting.

2462 White Oak Drive, Weston Missouri, 64098
Ph: 816-640-5682
Email: [email protected]
Johnathan Flint
Continue Reading
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