Researchers find epigenetic tie to neuropsychiatric disorders

Dysfunction in dopamine signaling profoundly changes the activity level of about 2,000 genes in the brain’s prefrontal cortex and may be an underlying cause of certain complex neuropsychiatric disorders, such as schizophrenia, according to UC Irvine scientists.

This epigenetic alteration of gene activity in brain cells that receive this neurotransmitter showed for the first time that dopamine deficiencies can affect a variety of behavioral and physiological functions regulated in the prefrontal cortex.

The study, led by Emiliana Borrelli, a UCI professor of microbiology & molecular genetics, appears online in the journal Molecular Psychiatry.

“Our work presents new leads to understanding neuropsychiatric disorders,” Borrelli said. “Genes previously linked to schizophrenia seem to be dependent on the controlled release of dopamine at specific locations in the brain. Interestingly, this study shows that altered dopamine levels can modify gene activity through epigenetic mechanisms despite the absence of genetic mutations of the DNA.”

Dopamine is a neurotransmitter that acts within certain brain circuitries to help manage functions ranging from movement to emotion. Changes in the dopaminergic system are correlated with cognitive, motor, hormonal and emotional impairment. Excesses in dopamine signaling, for example, have been identified as a trigger for neuropsychiatric disorder symptoms.

Borrelli and her team wanted to understand what would happen if dopamine signaling was hindered. To do this, they used mice that lacked dopamine receptors in midbrain neurons, which radically affected regulated dopamine synthesis and release.

The researchers discovered that this receptor mutation profoundly altered gene expression in neurons receiving dopamine at distal sites in the brain, specifically in the prefrontal cortex. Borrelli said they observed a remarkable decrease in expression levels of some 2,000 genes in this area, coupled with a widespread increase in modifications of basic DNA proteins called histones – particularly those associated with reduced gene activity.

Borrelli further noted that the dopamine receptor-induced reprogramming led to psychotic-like behaviors in the mutant mice and that prolonged treatment with a dopamine activator restored regular signaling, pointing to one possible therapeutic approach.

The researchers are continuing their work to gain more insights into the genes altered by this dysfunctional dopamine signaling.

http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201467a.html

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Rare genetic mutation confirmed as a cause of Tourette Syndrome

Brain researchers say they have confirmed for the first time that a rare genetic mutation can cause some cases of Tourette syndrome, with the fault disrupting production of histamine in the brain.

The New Haven, CT, researchers at the Yale School of Medicine say the histamine effect "is a cause of the tics and other abnormalities of Tourette syndrome." Tics are repetitive movements and vocal sounds, and they are unwanted and involuntary - they cannot be controlled.

Publishing their research on mice in the journal Neuron, the authors raise the question of investigating treatment of Tourette syndrome by drugs that target histamine receptors in the brain.

Drugs with such a mode of action are already being explored by pharmaceutical companies for the treatment of separate brain disorders, schizophrenia and ADHD.

Information from the national gene database about histamine describes the chemical's role - it is a messenger molecule released by nerves, among other functions.

Current neurological drugs under investigation target a certain gene-encoded histamine receptor known as the histamine H3 receptor.

Christopher Pittenger, of the Yale Child Study Center and associate professor of psychiatry and psychology, says of his particular study on histamine genetics:

"These findings give us a new window into what's going on in the brain in people with Tourette. That's likely to lead us to new treatments."

Histamine also has an important role in inflammation, which is why antihistamines work to reduce allergy symptoms. Interactions with the histamine system in the brain, say the Yale researchers, "explain why some allergy medications cause people to feel sleepy."

The specific gene in this study is called HDC (the histidine decarboxylase gene), which the researchers previously found to be mutated in a family that had nine members with Tourette syndrome.

Researchers found that mice with a faulty HDC gene showed symptoms similar to those found in Tourette syndrome.

That earlier finding of a faulty gene led the authors to confirm its effects on histamine in their present study with mice.

Mice with the same mutation carried by the Tourette family developed symptoms similar to those found in the syndrome, the Yale team showed, saying that this helps to prove that the histamine disruption can cause the tics.

Brain structures and chemicals

The study also found effects to do with dopamine, another brain chemical involved in communication between nerve cells.

There were abnormalities in dopamine neurotransmitter signaling in mice and in the patients carrying the faulty HDC gene.

The disruption was to dopamine effects in the basal ganglia, which is a network of structures responsible for movement - and the part of the brain that Dr. Pittenger focuses on toward the scientific understanding of neuropsychiatric diseases.

His research biography says:

"The basal ganglia are involved both in motor control and in the formation of habits.

Abnormalities in this circuit are implicated in a variety of conditions characterized by maladaptive, inflexible behaviors - habits gone bad.

These include obsessive-compulsive disorder, Tourette syndrome, and drug addiction."

The Tourette Syndrome Association of America - a non-profit whose mission "is to identify the cause of, find the cure for, and control the effects of Tourette Syndrome" - helped to fund the Yale study, which also received financial support from the Allison Family Foundation and the National Institutes of Health.

The US Centers for Disease Control and Prevention (CDC) does not have a firm estimate of the number of people affected by Tourette syndrome in America, but has run studies that indicate a prevalence of between 3 and 6 children out of every 1,000 in the population.

Other researchers, from the Massachusetts General Hospital and the University of Chicago, have also found family genetics behind Tourette's - and obsessive compulsive disorder (OCD), too. Their PLOS Genetics study published in October 2013 found insights into genetic architecture.

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What Is Echophenomenon?

Echophenomenon is the involuntary repetition of another person’s words or actions. When words are imitated, this may be defined as echolalia. When a person compulsively repeats the actions of someone else, it is called echopraxia. People can suffer from either echolalia and echopraxia, or both.

It should be understood that there is a very big distinction between willfully repeating another person’s actions or words, and doing it without conscious purpose. In the former, it’s an annoying, often teasing gesture that frequently occurs among school children, particularly siblings. In the latter, the movement or sounds being repeated aren’t on purpose and certainly aren’t meant to tease or annoy others.

The distinction is valuable because there are some people who suffer from echopraxia, or more generally echopathy, that may live in very mainstreamed environments. People with Tourette syndrome may suffer this condition, and in a school setting, the movements of others student might be picked up on by the child and reproduced in an echopractic fashion. Obviously teaching other students in a class not to mind this behavior would be important for mainstreaming success.

It shouldn’t be assumed that echopraxia is only suffered by people with Tourette syndrome, and all people with Tourette’s do not suffer it. There are many illnesses or conditions where echopraxia may occur. Some people with autism are echopractic, and the condition occasionally presents in people with schizophrenia. Other illnesses that are associated with echopathy include Ganser Disorder and occasionally major depressive disorder. From time to time, medical literature presents information about others who have suffered from echopraxia, and this includes those who have suffered brain tumors and some types of seizure disorders.

Due to the variety of conditions associated with echopraxia, it’s hard to say exactly what causes it in all cases or how it is best treated. Most times treating the underlying disease is the best way to minimize echopathy. Parents may find it particularly challenging to help children with this condition when they talk to doctors. Any demonstration of new movements or behaviors by the parent could result in new tics on the part of the echopractic child.

Children, mostly to their benefit, are also extremely observant, and may note small movements in others that might easily be turned into a repetitive movement by self. Of course it can be said that, for anyone, the condition of having unwanted repetitious movements is extremely difficult. This is especially the case, since many times people with this condition are quite cognizant that the behavior is unusual, possibly uncomfortable, and very often draws unwanted attention.

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Marijuana and Schizophrenia: New Study Explains How It Could Help

Researchers believe a lack of marijuana-like chemicals may be responsible for some of the core symptoms of schizophrenia.

The traditional belief that marijuana is bad for schizophrenia has been challenged time and time again by studies which suggest an opposite effect. Now a team of researchers at the University of Texas have found evidence that seems to explain why it helps.

Published in the August issue of Neuropsychopharmacology, their findings demonstrate a link between symptoms of schizophrenia and a lack of cannabinoid activity. Cannabinoids are a group of chemicals found in marijuana as well as the human brain, where they help to regulate normal function.

According to Alexandre Seillier, Ph.D, who co-authored the study, chemicals like THC may actually work to counter the negative symptoms of schizophrenia. Those who warn patients to avoid THC may be oversimplifying its role in the disorder, he explained to us.

“When people say THC is bad, it’s not always the case.”

Dr. Seillier believes the results offer a “possible explanation for why people use THC to medicate some of the symptoms of schizophrenia.” Likewise, research from other groups exists showing schizophrenics who use cannabis experience less negative symptoms than non-users.

In the new study, researchers used a drug called URB597 to increase levels of a natural cannabinoid (called anandamide) in rat models of schizophrenia. This caused a reversal in social withdrawal – one of the core symptoms of schizophrenia – leading the researchers to believe that a lack of cannabinoids may underlie the disease, or at least certain symptoms of it.

“The idea is maybe they have less to start with and when we increase the (endo)cannabinoids we restore normal physiological level.”

The study also identified an interesting difference between activity of the brain’s cannabinoids (called endocannabinoids) and cannabinoids found outside the body. While an increase in endocannabinoids reduced social withdrawal in schizophrenic rats, it had the opposite effect in normal rats. However, using chemicals that stimulate cannabinoid receptors directly seemed to avoid that problem.

“We tried one CB1 receptor agonist and indeed it was different. It produced the same beneficial effects in the schizophrenia-like rats but did not produce deleterious effects in the normal rats.”

Whether this is the case for THC has yet to be determined, but Dr. Seillier hopes to have the answer soon. His next study will look at the effects of THC in schizophrenia in order to further clarify the role of marijuana in treating the disorder.

The study was funded by the Brain & Behavior Research Foundation and the National Institute of Mental Health (NIMH).

Source

http://www.truthonpot.com/2013/07/31/marijuana-and-schizophrenia-new-study-explains-how-it-could-help/

Heavy Marijuana Use Linked to Better Memory, Brain Function in Schizophrenia

Marijuana helps patients with schizophrenia, according to new research from Canada.

A study published in the scholarly journal Psychiatry Research found that heavy cannabis users performed better on memory tasks than those who avoided marijuana.

Magnetic resonance imaging (MRI) scans also revealed better brain function in an area responsible for complex thinking and decision making, reports TruthOnPot.com.

University of Montreal researchers studied 145 patients with a dual diagnosis -- "cannabis dependence" and schizophrenia -- and 14 patients with schizophrenia only. "Our results suggest that emotional memory and prefrontal lobe functioning are preserved in dual-diagnosis patients," the researchers wrote.

Researchers saw no difference between the emotional responses of the two groups during resting states, although patients were evaluated based on emotional memory.

The authors suggest that the better performance of marijuana users could reflect a "more general difference" in memory.

An earlier MRI study found "less impaired brain functioning" in schizophrenic cannabis users as compared to schizophrenic non-users, the authors of the new study noted. Likewise, another study published just this month suggested that some symptoms of schizophrenia could be due to a lack of cannabinoids on the brain.

Almost half of schizophrenic patients also suffer from a substance use disorder (they are, in effect, self medicating for their symptoms). Tobacco, alcohol and cannabis are the most frequently used.

Some scientists, even if the face of statistics that have shown no corresponding rise in rates of schizophrenia with the rise of cannabis use, continue to insist that marijuana causes problems when it comes to schizophrenia. But the latest study only "adds to the growing literature showing that some key functions (negative symptoms, social skills, cognition) are preserved" in patients who use cannabis heavily.

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Could cannabis have antipsychotic properties?

In addition to psychoactive chemicals, cannabis contains components that may have a protective effect in mental illness.

When Dr Tim Karl, a senior scientist at NeuRA, says he believes that marijuana has potential as a treatment for schizophrenia, he’s adding fuel to a very contentious fire.

Marijuana – or cannabis, as it is otherwise known – is a controversial substance, particularly in light of evidence that it can trigger the development of schizophrenia in some people.

But cannabis, says Dr Karl, is made up of dozens of chemical components that can have widely varying effects on the brain.

Dr Karl and his team are investigating a component called cannabidiol, or CBD. CBD is thought to reduce the psychoactive effects of the most well-known component of cannabis, THC.

THC (Δ9-tetrahydrocannabinol) is the main active chemical in cannabis, and is known to increase psychotic symptoms in people with schizophrenia.

"We’re looking at whether CBD just has the capacity to block the effects of THC, or whether it has an independent anti-psychotic effect," says Dr Karl.

"If CBD is shown to have anti-psychotic properties, I believe it could have therapeutic potential."

First hand experience

Dr Karl says his interest in schizophrenia developed in part from working in an emergency psychiatric ward in Germany after he finished high school.

"I saw people who had had psychotic episodes, people who were suicidal. I felt deeply sorry for them because their options were so limited," he says.

Dr Karl saw first-hand the limited effectiveness of the drugs available to those patients in the psychiatric ward – and the need to develop more effective alternatives with fewer side-effects.

The majority of Dr Karl’s work will be done in mice bred to carry a genetic risk factor for schizophrenia, a gene called neuregulin 1These mice are genetically predisposed for schizophrenia(NRG1). These mice are susceptible to the effects of THC in a similar way to people who are genetically predisposed to experiencing psychosis if they use cannabis during adolescence.

The team has already begun looking at the effects of CBD in mice using various strains of cannabis with different THC:CBD ratios.

"This research will tell us whether particular strains of cannabis are more likely than others to induce psychotic-like symptoms, based on their THC:CBD ratio," says Dr Karl.

Dr Karl says this research will clarify whether CBD has a protective effect and therefore potential as an anti-psychotic therapeutic.

They will also gain a better understanding of the risks involved in early cannabis abuse and the interactive nature of genetic and environmental risk factors for schizophrenia.

"I don't believe that my work will cure schizophrenia, but it will give insights into the biological mechanisms of the disorder and might help us develop better treatments," he says.

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