Researchers reverse important symptom of schizophrenia in mice by manipulating genes

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.

Scientists discover that Valium does not work alone and needs the help of a gene

A group of researchers has discovered a particular gene, called Shisa7, which plays an important role with regard to the regulation of inhibitory neural circuits and the sedative effects of certain anxiolytics based on benzodiazepines.

This means that the classic Valium, for example, used to treat things like anxiety, muscle spasms or even sleep disorders, does not work alone to calm the nerves but needs the important contribution of a gene that is defined in the press release as “sticky.”

In fact, prior to this study, it was thought that the benzodiazepines essentially worked by themselves to trigger the calming responses of the A GABA type receptors (GABAA). Experiments that Ling Gang Wu, senior researcher at the National Institute for Neurological Disorders and the Ictus (NINDS), and Ronald S. Petralia, of the National Institute of Deafness and Other Communication Disorders (NIDCD), showed that Shisa7 attaches directly to GABAA receptors accelerating responses and increasing their effectiveness in the presence of Valium.

“These results suggest that Shisa7 directly models inhibitory synaptic responses in a variety of conditions, including the presence of benzodiazepines,” reports Chris J. McBain, a researcher at the Enice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). The researchers carried out experiments on modified mice from which the Shisa7 gene was eliminated. These mice, after undergoing Valium injections, were not affected by any calming effect compared to the control group mice.

Furthermore, in other experiments, the researchers discovered that Shisa7 could also influence sleepiness levels and the hypnotic effects of benzodiazepines. Such discoveries could help in the development of new drugs or treatments aimed at GABAA receptors.

Human cells that produce testosterone grown in the laboratory

One way to grow human cells to produce testosterone in the laboratory was developed by a group of researchers at the University of Southern California Pharmacy School.

The researchers hope that with this method it will be possible to arrive at treatments to counteract low levels of testosterone in the body by using special personalized replacement cells, as reported by Vassilios Papadopoulos, a researcher who led the study.

The researchers transformed induced pluripotent stem cells, derived from human skin or blood, into Leydig cells, which are the cells present in human testes that produce the male sex hormone.
According to the researchers, Leydig’s cells grown in the laboratory looked the same as their real counterparts.

The low level of testosterone in men, also known as hypogonadism, can lead to fertility problems and to sexual function in general and can affect mood as well as conditions such as bone density and obesity.

The level of testosterone in the body is lowered naturally in the course of the age, however more or less sudden lowering can also be caused by infections such as mumps or by treatments for cancer during childhood or adolescence.

The main therapy is that which sees the intake of testosterone which can be applied as a gel or can be taken orally or injected.

“Leydig’s human cell transplant is just a few years away,” the researcher said.

Oral anticoagulant drug retards progression of Alzheimer’s disease in mice

A group of researchers has discovered that the use of a particular drug that acts as an oral anticoagulant, dabigatran, can delay the appearance of Alzheimer’s disease in mice. The research was carried out by scientists from the Centro Nacional de Investigaciones Cardiovasculares (CNIC) and the Rockfeller University of New York while the study was published in the Journal of the American College of Cardiology .

According to the researchers, long-term anticoagulation with dabigatran effectively slowed the progression of Alzheimer’s disease in mice during experiments. Marta Cort├ęs Canteli, a researcher at the CNIC and one of the authors of the study, speaks of an “important progress” regarding effective treatments for Alzheimer’s disease.

To defeat this disease, according to the researcher, there will be a need for personalized therapies aimed at various and different processes that can contribute to the progression of the disease. Among the objectives there is, according to the researcher, cerebral circulation and precisely to treat the latter an oral anticoagulant such as dabigatran can have an effective approach for those Alzheimer’s patients who have a tendency to coagulation.

According to the researcher, in addition to other studies that will have to certify the beneficial action of this drug, there will also be a need to create new diagnostic tools to identify Alzheimer’s patients with a tendency to coagulation with greater precision and efficiency, and precisely this “will be an important research line in the coming years.”

Mushroom consumption linked to lower risk of prostate cancer

Mushroom consumption could be linked to a lower risk of prostate cancer according to a new study published in the International Journal of Cancer . The researchers used data from 36,000 Japanese men who covered several decades, ranging in age from 40 to 79 years. These men came from the Miyagi and Ohsaki areas of Japan.

The data were also collected thanks to questionnaires that included questions such as those related to the consumption of mushrooms or other particular foods, as well as questions related to physical activity and personal and family medical conditions.

Researchers discovered a link between regular mushroom consumption and a reduction in prostate cancer risk in men and this link was even more significant for men aged 50 and over and in those men where the diet was mainly made from meat and dairy products with limited consumption of vegetables and fruit.

“Although our study suggests that regular consumption of mushrooms can reduce the risk of prostate cancer, we also want to emphasize that a healthy and balanced diet is much more important than filling the trolley with mushrooms,” Shu Zhang says. Zhang is a professor of epidemiology at the Tohoku University as well as lead author of the study

Zhang adds that in the past, test-tube studies and studies on living organisms had shown that fungi can potentially prevent prostate cancer.

According to the researcher, this is to be explained by the good amount of vitamins, minerals and antioxidants present in mushrooms, in particular L-ergotionein. The latter regulates the cellular imbalance caused by unsound dietary choices and long-term exposure to environmental toxins.

Zhang himself admits that new research is needed to understand the extent of this connection also because this study was carried out only on a limited population.