Flu may save you from common cold

Researchers have found that people who suffered from influenza were 70 per cent less likely to have acquired rhinoviruses, or the common cold.

For the study samples from 44,230 cases of acute respiratory illness, in 36,157 patients, were tested for 11 types of respiratory viruses over nine years at National Academy of Sciences (NHS) Greater Glasgow and Clyde board in UK.

“One really striking pattern in our data is the decline in cases of the respiratory virus rhinovirus, which is typically a mild common cold causing virus, occurring during winter, around the time that flu activity increases,” said a researcher.

During the study, the most striking interaction they found was between influenza A viruses and rhinoviruses, a type of virus that can cause the common cold.

Computer modelling of the data found that the inhibitory interactions between influenza and rhinoviruses appeared to occur within individual people as well as at a population level.

According to the study, patients with influenza were approximately 70 per cent less likely to also be infected with rhinovirus, than were patients infected with the other virus types.

“We believe respiratory viruses may be competing for resources in the respiratory tract. There are various possibilities we’re investigating, such as these viruses are competing for cells to infect in the body, or the immune response to one virus makes it harder for another unrelated virus to infect the same person,” the researcher said.

Limitations of the study include that the correlations observed cannot show what is causing these interactions and that samples were only taken from people with symptoms of a respiratory infection, so it may not capture how the viruses behave in people who don’t develop symptoms.

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Researchers identified a brain protein that could be more direct target for treating anxiety

Anxiety is an important mental state and related disorders may lead to many severe sufferings. In which patients suffer from intense fears and anxiety or from sudden, inexplicable panic  attacks. Whereas in extreme cases, the sufferer sometimes leaves their home and which can have many other serious impacts on their family, friend and work circles.

Recently, scientists  have discovered a synaptic protein which, when inactivated, has an anxiolytic effect in mice. This research will play an important role to study anxiety disorders.

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Nearly ten percent of the total populous suffers from anxiety disorders, however, available treatment alternatives only can help a proportion of them.

Patients with anxiety disorders are commonly investigated with increased neuronal activity in the amygdala, a brain region that plays a key role in processing emotions such as anxiety or fear. Overactivation of the amygdala is found to be actively involved in causing severe anxiety.

Many anxiolytic medications for instance Benzodiazepines bring this overactivation to normal by strengthening the function of inhibitory synapses. 

Synapses are actually connections between nerve cells in the brain, at which information is transmitted from one nerve cell to another. At inhibitory synapses, this information transmission lowers a reduction in the activity of the neighboring nerve cells.

In the amygdala, for instance, this hinders the transmission of stimuli that trigger fear and anxiety. Anxiolytic medications such as Benzodiazepines strengthen this inhibitory effect.

Unfortunately, this medication also impacts synapses in the brain those are not targeted ones. This can lead to many other side effects such as pronounced sedation and impaired concentration.

In the search for new, more specific targets for anxiolytic medications several studies take place. During such a study, healthy animals investigate an empty test chamber, rodents with a pathological anxiety phenotype split into a corner because they are afraid. Conversely, when the scientists inhibit the production of the recently discovered protein IgSF9b in these mice, they started wandering around the chamber again.

A researcher said, “Blocking IgSF9b in pathologically anxious mice has an anxiolytic effect and normalizes anxiety behavior in these animals. This protein could, therefore, be a target for pharmacological approaches to treating anxiety disorders.”

The author who led a study, said,  “Our research shows that protein structures at inhibitory synapses in the centromedial amygdala, and particularly the protein IgSF9b, constitute promising new targets for potential treatments. It thus provides an important contribution toward understanding the biological causes of anxiety disorders and for the development of new anxiolytic medications.”

There's a Link Between Autism And Epilepsy, And Scientists Might Have Figured It Out

Researchers have discovered why a mutated gene causes seizures in some children who have autism.
Autism spectrum disorder is a highly prevalent neurodevelopmental disorder - affecting one in 68 children - characterized by a range of symptoms, including difficulty with communication and social interactions.

One third of children who have autism spectrum disorder also have epilepsy. It's related to a gene that is mutated in patients with autism. But scientists didn't know why the mutation causes seizures.
The new discovery shows the mutation acts like a bad gardener in the brain.

It shrinks the neurons' tiny branches and leaves - its dendrite arbors and synapses - that let brain cells relay vital messages and control the brain's activity.

That shrinkage can cause a breakdown in message delivery.

In people with the mutation, inhibitory neurons- that are supposed to keep things tranquil in the brain and slam the brake on excitatory neurons - don't grow enough branches and leaves to communicate their calming message, according to the research. That can lead to seizures.

The mutation, CNTNAP2 or "catnap2," works as a team with another mutated gene, CASK, implicated in intellectual disability. As a result, scientists now have a new target for drugs to treat the disorder.

"Now we can start testing drugs to treat the seizures as well as other problems in autism," says lead author, professor of psychiatry and behavioral sciences.

"Patients with the mutation also have language delay and intellectual disability. So a drug targeting the mutation could have multiple benefits."

Next, researchers will do high-throughput screening of molecules with the goal of reversing these abnormalities in patients with autism.

Catnap2 is an adhesive molecule that helps cells stick together, in this case helping the synapses adhere to the dendrites. It's a difficult molecule to target with drugs, the author says.

But catnap2's partner, CASK, is a social butterfly enzyme that interacts with many other molecules.
Drugs can more easily inhibit or activate the enzyme, so researchers will screen drugs to activate it, because that appears to maintain healthy dendrite branches.

When scientists blocked CASK in the study, dendrites didn't grow.

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Here`s how protein impacts intellectual disability

A new study has paved the way for the potential treatments of intellectual disability and other neurodevelopmental disorders.

Your brain needs just the right balance between excitatory "on" signals and inhibitory "calm down" signals. Now scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown that a protein helps balance nerve cell communication.

"This paper adds a new dimension to our understanding of the molecular mechanisms that impact intellectual disability," said researcher Brock Grill. "Our study is the first to identify a defect in neuron communication caused by altering the activity of a gene called HUWE1, which causes intellectual disability, including Juberg-Marsidi-Brooks syndrome."

Studying neuronal communication is important because the brain needs to balance excitatory neurotransmitters (to increase signal transmission) and inhibitory neurotransmitters (to calm nerve cells down). An imbalance in the excitatory/inhibitory ratio is a central feature of many neurodevelopmental disorders--which occurs through gene overexpression or a loss of gene function.

For the study, Grill and his colleagues investigated neuronal communication balance using a simple model circuit in the nematode C. elegans, a small, transparent worm. Despite its small size, this worm shares half its genetic make-up with humans, which makes it an ideal model to study the genetics of neuron function.

The researchers took a close look at GABA, the principal inhibitory neurotransmitter in C. elegans and the human brain. In C. elegans, the protein responsible for regulating GABA transmission is called EEL-1; in humans, the equivalent protein is known as HUWE1.

The researchers studied the function of EEL-1/HUWE1 in the worm motor circuit and found that decreasing or increasing the protein alters GABA transmission, upending the excitatory/inhibitory balance, a shift that leads to impaired locomotion and increased sensitivity to electroshock-induced seizure.

"Using a simple model circuit, we've identified a key player required to achieve a balance of excitation and inhibition," Grill noted. "This opens up a new concept for why HUWE1 causes intellectual disability. HUWE1 affects only the release of the GABA neurotransmitter, not the levels or function of the GABA receptor, Grill noted. He said more research is needed into how this actually affects the brain.

"The paper is an important step in understanding how increased or decreased activity of HUWE1 can alter circuit function and lead to intellectual disability," said first author Karla Opperman.

The study represents important progress in understanding the molecular underpinnings of intellectual disability. In particular, results from the study show for the first time that mutations that cause Juberg-Marsidi-Brooks syndrome result in loss of HUWE1 function and can impair nerve cell function.The study is published online in the journal Cell Reports.

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researchers identify pathway that may protect against cocaine addiction

A study by researchers  gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signalling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behaviour in mice.

Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.

A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not. 

Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value.

In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.

Mice that quickly stopped seeking the drug were found to have stronger connections along the indirect pathway — a neural tract that forms indirect projections into the mid-brain and contains cells called medium spiny neurons expressing dopamine D2 receptors (D2-MSNs). A parallel pathway — known as the direct pathway -- forms direct projections into the mid-brain neurons and contains medium spiny neurons expressing D1 receptors (D1-MSNs). These two pathways are thought to work together in complementary but sometimes opposing ways to affect behaviour.

Researchers were very surprised by the results of the study because we were originally looking for vulnerability factors for developing compulsive drug use. Instead,they found changes that only happened in subjects that show a resilience to becoming compulsive drug users. Resilient mice had a strong inhibitory circuit that allowed them to exert better control over their drug intake.

To test this observation, researchers used lasers to activate individual neurons, and found that stimulating D2-MSNs in the nucleus accumbens decreased cocaine seeking in the mice. Blocking D2-MSN signalling with a chemical process increased motivation to obtain cocaine.

This research advances the understanding of how the recruitment, activation and the interaction among brain circuits can either restrain or increase motivation to take drugs.

Previous studies have shown that people with lower levels of dopamine D2 receptors in the striatum, a brain region associated with reward and working memory, are more likely to develop compulsive behaviours toward stimulant drugs.

Dopamine is a key neurotransmitter involved in reward-based learning and addiction. Cocaine disrupts communication between neurons at the synapse, the small junction between nerve cells, by blocking the re-absorption of dopamine into the transmitting neuron. As a result, dopamine continues to stimulate the receiving neuron, causing feelings of alertness and euphoria.