Posts Tagged ‘schizophrenia’

By Rafi Letzter

Scientists in Switzerland dosed test subjects with LSD to investigate how patients with severe mental disorders lose track of where they end and other people begin.

Both LSD and certain mental disorders, most notably schizophrenia, can make it difficult for people to distinguish between themselves and others. And that can impair everyday mental tasks and social interactions, said Katrin Preller, one of the lead authors of the study and a psychologist at the University Hospital of Psychiatry in Zurich. By studying how LSD breaks down people’s senses of self, the researchers aimed to find targets for future experimental drugs to treat schizophrenia.

“Healthy people take having this coherent ‘self’ experience for granted,” Preller told Live Science, “which makes it difficult to explain why it’s so important.”

Depression, she said, also relates to the sense of self. Whereas people with schizophrenia can lose track of themselves entirely, people with depression tend to “ruminate” on themselves, unable to break obsessive, self-oriented patterns of thought.

But this kind of phenomenon is challenging to study, Preller said.

“If you want to investigate self-experience, you have to manipulate it,” Preller said. “And there are very few substances that can actually manipulate sense of self while patients are lying in our MRI scanner.”

One of the substances that can, however, is LSD. And that’s why this experiment happened in Zurich, Preller said. Switzerland is one of the few countries where it’s possible to use LSD on human beings for scientific research. (Doing so is still quite difficult, though, requiring lots of oversight.)

The experiment itself didn’t sound like the most exciting use of the drug for the test subjects, all of whom were physically healthy and did not have schizophrenia or other illnesses After taking the drug, the subjects lay inside MRI machines with video goggles strapped to their faces, trying to make eye contact with a computer-generated avatar. Once they accomplished this, the subjects then tried to look off at another point in space that the avatar was also looking at. This is the kind of social task, Preller said, that’s very difficult if your sense of self has broken down.

Every study subject tried the task three times: once sober, once on LSD, and once after taking both LSD and a substance called ketanserin. This substance blocks LSD from interacting with a particular serotonin receptor in the brain, which researchers call “5-HT2.”

Previous studies on animals had suggested that 5-HT2 played a key role in LSD’s ability to mess with sense of self. The researchers suspected that blocking the receptor in humans might somewhat reduce the effect of LSD.

But it turned out to more than “somewhat” block the effect: There was no difference between the performance of subjects who took ketanserin and the placebo group.

“This was surprising to us, because LSD interacts with a lot of receptors [in the brain], not just 5-HT2,” Preller said.

But LSD’s most dramatic measurable effects entirely abated when subjects first took ketanserin.

That tentatively indicates that 5-HT2 plays an important role in regulating sense of self in the brain, Preller said. The next step, she added, is to work on drugs that target that receptor and see if they might alleviate some of the symptoms of severe psychiatric illnesses that affect the sense of self.

The paper detailing the study’s results was published today (March 19) at The Journal of Neuroscience.

https://www.livescience.com/62059-schizophrenia-lsd-sense-self.html#?utm_source=ls-newsletter&utm_medium=email&utm_campaign=03202018-ls

Advertisements


Illustration by Paweł Jońca

by Helen Thomson

In March 2015, Li-Huei Tsai set up a tiny disco for some of the mice in her laboratory. For an hour each day, she placed them in a box lit only by a flickering strobe. The mice — which had been engineered to produce plaques of the peptide amyloid-β in the brain, a hallmark of Alzheimer’s disease — crawled about curiously. When Tsai later dissected them, those that had been to the mini dance parties had significantly lower levels of plaque than mice that had spent the same time in the dark.

Tsai, a neuroscientist at Massachusetts Institute of Technology (MIT) in Cambridge, says she checked the result; then checked it again. “For the longest time, I didn’t believe it,” she says. Her team had managed to clear amyloid from part of the brain with a flickering light. The strobe was tuned to 40 hertz and was designed to manipulate the rodents’ brainwaves, triggering a host of biological effects that eliminated the plaque-forming proteins. Although promising findings in mouse models of Alzheimer’s disease have been notoriously difficult to replicate in humans, the experiment offered some tantalizing possibilities. “The result was so mind-boggling and so robust, it took a while for the idea to sink in, but we knew we needed to work out a way of trying out the same thing in humans,” Tsai says.

Scientists identified the waves of electrical activity that constantly ripple through the brain almost 100 years ago, but they have struggled to assign these oscillations a definitive role in behaviour or brain function. Studies have strongly linked brainwaves to memory consolidation during sleep, and implicated them in processing sensory inputs and even coordinating consciousness. Yet not everyone is convinced that brainwaves are all that meaningful. “Right now we really don’t know what they do,” says Michael Shadlen, a neuroscientist at Columbia University in New York City.

Now, a growing body of evidence, including Tsai’s findings, hint at a meaningful connection to neurological disorders such as Alzheimer’s and Parkinson’s diseases. The work offers the possibility of forestalling or even reversing the damage caused by such conditions without using a drug. More than two dozen clinical trials are aiming to modulate brainwaves in some way — some with flickering lights or rhythmic sounds, but most through the direct application of electrical currents to the brain or scalp. They aim to treat everything from insomnia to schizophrenia and premenstrual dysphoric disorder.

Tsai’s study was the first glimpse of a cellular response to brainwave manipulation. “Her results were a really big surprise,” says Walter Koroshetz, director of the US National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “It’s a novel observation that would be really interesting to pursue.”


A powerful wave

Brainwaves were first noticed by German psychiatrist Hans Berger. In 1929, he published a paper describing the repeating waves of current he observed when he placed electrodes on people’s scalps. It was the world’s first electroencephalogram (EEG) recording — but nobody took much notice. Berger was a controversial figure who had spent much of his career trying to identify the physiological basis of psychic phenomena. It was only after his colleagues began to confirm the results several years later that Berger’s invention was recognized as a window into brain activity.

Neurons communicate using electrical impulses created by the flow of ions into and out of each cell. Although a single firing neuron cannot be picked up through the electrodes of an EEG, when a group of neurons fires again and again in synchrony, it shows up as oscillating electrical ripples that sweep through the brain.

Those of the highest frequency are gamma waves, which range from 25 to 140 hertz. People often show a lot of this kind of activity when they are at peak concentration. At the other end of the scale are delta waves, which have the lowest frequency — around 0.5 to 4 hertz. These tend to occur in deep sleep (see ‘Rhythms of the mind’).

At any point in time, one type of brainwave tends to dominate, although other bands are always present to some extent. Scientists have long wondered what purpose, if any, this hum of activity serves, and some clues have emerged over the past three decades. For instance, in 1994, discoveries in mice indicated that the distinct patterns of oscillatory activity during sleep mirrored those during a previous learning exercise. Scientists suggested that these waves could be helping to solidify memories.

Brainwaves also seem to influence conscious perception. Randolph Helfrich at the University of California, Berkeley, and his colleagues devised a way to enhance or reduce gamma oscillations of around 40 hertz using a non-invasive technique called transcranial alternating current stimulation (tACS). By tweaking these oscillations, they were able to influence whether a person perceived a video of moving dots as travelling vertically or horizontally.

The oscillations also provide a potential mechanism for how the brain creates a coherent experience from the chaotic symphony of stimuli hitting the senses at any one time, a puzzle known as the ‘binding problem’. By synchronizing the firing rates of neurons responding to the same event, brainwaves might ensure that the all of the relevant information relating to one object arrives at the correct area of the brain at exactly the right time. Coordinating these signals is the key to perception, says Robert Knight, a cognitive neuroscientist at the University of California, Berkeley, “You can’t just pray that they will self-organize.”


Healthy oscillations

But these oscillations can become disrupted in certain disorders. In Parkinson’s disease, for example, the brain generally starts to show an increase in beta waves in the motor regions as body movement becomes impaired. In a healthy brain, beta waves are suppressed just before a body movement. But in Parkinson’s disease, neurons seem to get stuck in a synchronized pattern of activity. This leads to rigidity and movement difficulties. Peter Brown, who studies Parkinson’s disease at the University of Oxford, UK, says that current treatments for the symptoms of the disease — deep-brain stimulation and the drug levodopa — might work by reducing beta waves.

People with Alzheimer’s disease show a reduction in gamma oscillations5. So Tsai and others wondered whether gamma-wave activity could be restored, and whether this would have any effect on the disease.

They started by using optogenetics, in which brain cells are engineered to respond directly to a flash of light. In 2009, Tsai’s team, in collaboration with Christopher Moore, also at MIT at the time, demonstrated for the first time that it is possible to use the technique to drive gamma oscillations in a specific part of the mouse brain6.

Tsai and her colleagues subsequently found that tinkering with the oscillations sets in motion a host of biological events. It initiates changes in gene expression that cause microglia — immune cells in the brain — to change shape. The cells essentially go into scavenger mode, enabling them to better dispose of harmful clutter in the brain, such as amyloid-β. Koroshetz says that the link to neuroimmunity is new and striking. “The role of immune cells like microglia in the brain is incredibly important and poorly understood, and is one of the hottest areas for research now,” he says.

If the technique was to have any therapeutic relevance, however, Tsai and her colleagues had to find a less-invasive way of manipulating brainwaves. Flashing lights at specific frequencies has been shown to influence oscillations in some parts of the brain, so the researchers turned to strobe lights. They started by exposing young mice with a propensity for amyloid build-up to flickering LED lights for one hour. This created a drop in free-floating amyloid, but it was temporary, lasting less than 24 hours, and restricted to the visual cortex.

To achieve a longer-lasting effect on animals with amyloid plaques, they repeated the experiment for an hour a day over the course of a week, this time using older mice in which plaques had begun to form. Twenty-four hours after the end of the experiment, these animals showed a 67% reduction in plaque in the visual cortex compared with controls. The team also found that the technique reduced tau protein, another hallmark of Alzheimer’s disease.

Alzheimer’s plaques tend to have their earliest negative impacts on the hippocampus, however, not the visual cortex. To elicit oscillations where they are needed, Tsai and her colleagues are investigating other techniques. Playing rodents a 40-hertz noise, for example, seems to cause a decrease in amyloid in the hippocampus — perhaps because the hippo-campus sits closer to the auditory cortex than to the visual cortex.

Tsai and her colleague Ed Boyden, a neuro-scientist at MIT, have now formed a company, Cognito Therapeutics in Cambridge, to test similar treatments in humans. Last year, they started a safety trial, which involves testing a flickering light device, worn like a pair of glasses, on 12 people with Alzheimer’s.

Caveats abound. The mouse model of Alzheimer’s disease is not a perfect reflection of the disorder, and many therapies that have shown promise in rodents have failed in humans. “I used to tell people — if you’re going to get Alzheimer’s, first become a mouse,” says Thomas Insel, a neuroscientist and psychiatrist who led the US National Institute of Mental Health in Bethesda, Maryland, from 2002 until 2015.

Others are also looking to test how manipulating brainwaves might help people with Alzheimer’s disease. “We thought Tsai’s study was outstanding,” says Emiliano Santarnecchi at Harvard Medical School in Boston, Massachusetts. His team had already been using tACS to stimulate the brain, and he wondered whether it might elicit stronger effects than a flashing strobe. “This kind of stimulation can target areas of the brain more specifically than sensory stimulation can — after seeing Tsai’s results, it was a no-brainer that we should try it in Alzheimer’s patients.”

His team has begun an early clinical trial in which ten people with Alzheimer’s disease receive tACS for one hour daily for two weeks. A second trial, in collaboration with Boyden and Tsai, will look for signals of activated microglia and levels of tau protein. Results are expected from both trials by the end of the year.

Knight says that Tsai’s animal studies clearly show that oscillations have an effect on cellular metabolism — but whether the same effect will be seen in humans is another matter. “In the end, it’s data that will win out,” he says.

The studies may reveal risks, too. Gamma oscillations are the type most likely to induce seizures in people with photosensitive epilepsy, says Dora Hermes, a neuroscientist at Stanford University in California. She recalls a famous episode of a Japanese cartoon that featured flickering red and blue lights, which induced seizures in some viewers. “So many people watched that episode that there were almost 700 extra visits to the emergency department that day.”

A brain boost

Nevertheless, there is clearly a growing excitement around treating neurological diseases using neuromodulation, rather than pharmaceuticals. “There’s pretty good evidence that by changing neural-circuit activity we can get improvements in Parkinson’s, chronic pain, obsessive–compulsive disorder and depression,” says Insel. This is important, he says, because so far, pharmaceutical treatments for neurological disease have suffered from a lack of specificity. Koroshetz adds that funding institutes are eager for treatments that are innovative, non-invasive and quickly translatable to people.

Since publishing their mouse paper, Boyden says, he has had a deluge of requests from researchers wanting to use the same technique to treat other conditions. But there are a lot of details to work out. “We need to figure out what is the most effective, non-invasive way of manipulating oscillations in different parts of the brain,” he says. “Perhaps it is using light, but maybe it’s a smart pillow or a headband that could target these oscillations using electricity or sound.” One of the simplest methods that scientists have found is neurofeedback, which has shown some success in treating a range of conditions, including anxiety, depression and attention-deficit hyperactivity disorder. People who use this technique are taught to control their brainwaves by measuring them with an EEG and getting feedback in the form of visual or audio cues.

Phyllis Zee, a neurologist at Northwestern University in Chicago, Illinois, and her colleagues delivered pulses of ‘pink noise’ — audio frequencies that together sound a bit like a waterfall — to healthy older adults while they slept. They were particularly interested in eliciting the delta oscillations that characterize deep sleep. This aspect of sleep decreases with age, and is associated with a decreased ability to consolidate memories.

So far, her team has found that stimulation increased the amplitude of the slow waves, and was associated with a 25–30% improvement in recall of word pairs learnt the night before, compared with a fake treatment7. Her team is midway through a clinical trial to see whether longer-term acoustic stimulation might help people with mild cognitive impairment.

Although relatively safe, these kinds of technologies do have limitations. Neurofeedback is easy to learn, for instance, but it can take time to have an effect, and the results are often short-lived. In experiments that use magnetic or acoustic stimulation, it is difficult to know precisely what area of the brain is being affected. “The field of external brain stimulation is a little weak at the moment,” says Knight. Many approaches, he says, are open loop, meaning that they don’t track the effect of the modulation using an EEG. Closed loop, he says, would be more practical. Some experiments, such as Zee’s and those involving neuro-feedback, already do this. “I think the field is turning a corner,” Knight says. “It’s attracting some serious research.”

In addition to potentially leading to treatments, these studies could break open the field of neural oscillations in general, helping to link them more firmly to behaviour and how the brain works as a whole.

Shadlen says he is open to the idea that oscillations play a part in human behaviour and consciousness. But for now, he remains unconvinced that they are directly responsible for these phenomena — referring to the many roles people ascribe to them as “magical incantations”. He says he fully accepts that these brain rhythms are signatures of important brain processes, “but to posit the idea that synchronous spikes of activity are meaningful, that by suddenly wiggling inputs at a specific frequency, it suddenly elevates activity onto our conscious awareness? That requires more explanation.”

Whatever their role, Tsai mostly wants to discipline brainwaves and harness them against disease. Cognito Therapeutics has just received approval for a second, larger trial, which will look at whether the therapy has any effect on Alzheimer’s disease symptoms. Meanwhile, Tsai’s team is focusing on understanding more about the downstream biological effects and how to better target the hippocampus with non-invasive technologies.

For Tsai, the work is personal. Her grandmother, who raised her, was affected by dementia. “Her confused face made a deep imprint in my mind,” Tsai says. “This is the biggest challenge of our lifetime, and I will give it all I have.”

https://www.nature.com/articles/d41586-018-02391-6

Regular use of nicotine may normalize brain activity impairments linked with schizophrenia, according to a study using a mouse model, published online in Nature Medicine. The finding may explain why up to 90% of people with schizophrenia smoke—most of them heavily.

“Basically the nicotine is compensating for a genetically determined impairment,” said researcher Jerry Stitzel, PhD, of the University of Colorado Boulder. “No one has ever shown that before.”

Dr. Stitzel is part of an international research team that investigated whether a variant in the CHRNA5 gene, which is believed to increase schizophrenia risk, is associated with a reduction of neural firing in the brain’s prefrontal cortex, or hypofrontality. Researchers also examined whether nicotine could interrupt the effect.

In mice with the CHRNA5 gene variant, brain images confirmed hypofrontality, researchers reported. Behavioral tests further revealed that the mice shared key characteristics of people with schizophrenia, such as an inability to suppress a startle response and aversion to social interaction. The findings, they explained, suggest the CHRNA5 gene variant plays a role in schizophrenia by causing hypofrontality.

Nicotine, however, seemed to reverse hypofrontality. When researchers gave the mice daily nicotine, their sluggish brain activity improved within 2 days. Within a week, it was normal.

Researchers believe the nicotine corrected the impaired brain activity by acting on nicotinic receptors in regions important for healthy cognitive function.

Noting that hypofrontality is also linked with addiction, attention deficit hyperactivity disorder, bipolar disorder, and other psychiatric conditions, researchers believe the discovery could lead to new nonaddictive, nicotine-based medications.

“This defines a completely novel strategy for medication development,” said lead author Uwe Maskos, PhD, of Institut Pasteur, Paris, France.

—Jolynn Tumolo

References:

Koukouli F, Rooy M, Tziotis D, et al. Nicotine reverses hypofrontality in animal models of addiction and schizophrenia. Nature Medicine. 2017 January 23;[Epub ahead of print].

Nicotine normalizes brain deficits key to schizophrenia [press release]. Boulder, CO: University of Colorado Boulder; January 23, 2017.

Supplementation with taurine, the additive found in many energy drinks, may improve the symptoms in young people suffering a first episode of psychosis (FEP), according to a new study presented at the International Early Psychosis Association (IEPA) meeting.

Taurine, an amino acid naturally occurring in the body, exhibits an inhibitory neuro-modulatory effect in the nervous system and also functions as a neuroprotective agent. The authors devised a study to analyze the efficacy of taurine supplementation in improving symptoms and cognition in patients with FEP.

The study included 86 individuals with FEP between the ages of 18 and 25 years. It was conducted by Dr. Colin O’Donnell, Donegal Mental Health Service, Co. Donegal, Ireland, and Professor Patrick McGorry and Dr. Kelly Allott, Orygen, The National Centre of Excellence in Youth Mental Health, Australia, and colleagues. Each participant was taking a low dose antipsychotic medication and was attending Orygen.

Forty-seven participants received 4g of taurine daily, while 39 received placebo. Symptoms were assessed Using the scoring system called BPRS (Brief Psychiatric Rating Scale) and cognition was assessed with the MCCB tool (MATRICS consensus cognitive battery).

Results showed that taurine significantly improved symptoms on the BPRS scale, in overall score and in psychosis specific analysis, however, there was no difference between the treatment and placebo group regarding cognition. Depression symptoms (rated by the Calgary Depression Scale for Schizophrenia) and general overall functioning also improved in the taurine group.

“The use of taurine warrants further investigation in larger randomised studies, particularly early in the course of psychosis,” concluded the authors, who themselves, are planning to conduct further studies into the potential benefits of taurine in the treatment of psychosis.

http://www.empr.com/news/energy-drink-additive-could-potentially-improve-psychosis-symptoms/article/567497/?DCMP=EMC-MPR_Charts_rd&cpn=&hmSubId=&NID=&c_id=&dl=0&spMailingID=16159114&spUserID=MzI5NTMwMzQ0NDIyS0&spJobID=921765029&spReportId=OTIxNzY1MDI5S0


St. Jude Children’s Research Hospital scientists have linked disruption of a brain circuit associated with schizophrenia to an age-related decline in levels of a single microRNA in one brain region

St. Jude Children’s Research Hospital scientists have identified a small RNA (microRNA) that may be essential to restoring normal function in a brain circuit associated with the “voices” and other hallucinations of schizophrenia. The microRNA provides a possible focus for antipsychotic drug development. The findings appear today in the journal Nature Medicine.

The work was done in a mouse model of a human disorder that is one of the genetic causes of schizophrenia. Building on previous St. Jude research, the results offer important new details about the molecular mechanism that disrupts the flow of information along a neural circuit connecting two brain regions involved in processing auditory information. The findings also provide clues about why psychotic symptoms of schizophrenia are often delayed until late adolescence or early adulthood.

“In 2014, we identified the specific circuit in the brain that is targeted by antipsychotic drugs. However, the existing antipsychotics also cause devastating side effects,” said corresponding author Stanislav Zakharenko, M.D., Ph.D., a member of the St. Jude Department of Developmental Neurobiology. “In this study, we identified the microRNA that is a key player in disruption of that circuit and showed that depletion of the microRNA was necessary and sufficient to inhibit normal functioning of the circuit in the mouse models.

“We also found evidence suggesting that the microRNA, named miR-338-3p, could be targeted for development of a new class of antipsychotic drugs with fewer side effects.”

There are more than 2,000 microRNAs whose function is to silence expression of particular genes and regulate the supply of the corresponding proteins. Working in a mouse model of 22q11 deletion syndrome, researchers identified miR-338-3p as the microRNA that regulates production of the protein D2 dopamine receptor (Drd2), which is the prime target of antipsychotics.

Individuals with the deletion syndrome are at risk for behavior problems as children. Between 23 and 43 percent develop schizophrenia, a severe chronic disorder that affects thinking, memory and behavior. Researchers at St. Jude are studying schizophrenia and other brain disorders to improve understanding of how normal brains develop, which provides insights into the origins of diseases like cancer.

The scientists reported that Drd2 increased in the brain’s auditory thalamus when levels of the microRNA declined. Previous research from Zakharenko’s laboratory linked elevated levels of Drd2 in the auditory thalamus to brain-circuit disruptions in the mutant mice. Investigators also reported that the protein was elevated in the same brain region of individuals with schizophrenia, but not healthy adults.

Individuals with the deletion syndrome are missing part of chromosome 22, which leaves them with one rather than the normal two copies of more than 25 genes. The missing genes included Dgcr8, which facilitates production of microRNAs.

Working in mice, researchers have now linked the 22q11 deletion syndrome and deletion of a single Dgcr8 gene to age-related declines in miR-338-3p in the auditory thalamus. The decline was associated with an increase in Drd2 and reduced signaling in the circuit that links the thalamus and auditory cortex, a brain region implicated in auditory hallucination. Levels of miR-338-3p were lower in the thalamus of individuals with schizophrenia compared to individuals of the same age and sex without the diagnosis.

The miR-338-3p depletion did not disrupt other brain circuits in the mutant mice, and the findings offer a possible explanation. Researchers found that miR-338-3p levels were higher in the thalamus than in other brain regions. In addition, miR-338-3p was one of the most abundant microRNAs present in the thalamus.

Replenishing levels of the microRNA in the auditory thalamus of mutant mice reduced Drd2 protein and restored the circuit to normal functioning. That suggests that the microRNA could be the basis for a new class of antipsychotic drugs that act in a more targeted manner with fewer side effects. Antipsychotic drugs, which target Drd2, also restored circuit function.

The findings provide insight into the age-related delay in the onset of schizophrenia symptoms. Researchers noted that microRNA levels declined with age in all mice, but that mutant mice began with lower levels of miR-338-3p. “A minimum level of the microRNA may be necessary to prevent excessive production of the Drd2 that disrupts the circuit,” Zakharenko said. “While miR-338-3p levels decline as normal mice age, levels may remain above the threshold necessary to prevent overexpression of the protein. In contrast, the deletion syndrome may leave mice at risk for dropping below that threshold.”

The study’s first authors are Sungkun Chun, Fei Du and Joby Westmoreland, all formerly of St. Jude. The other authors are Seung Baek Han, Yong-Dong Wang, Donnie Eddins, Ildar Bayazitov, Prakash Devaraju, Jing Yu, Marcia Mellado Lagarde and Kara Anderson, all of St. Jude.

https://www.stjude.org/media-resources/news-releases/2016-medicine-science-news/small-rna-identified-that-offers-clues-for-quieting-the-voices-of-schizophrenia.html

A pair of new studies links childhood cat ownership and infection with the parasite Toxoplasma gondii (T. gondii) with later onset schizophrenia and other mental illness. Researchers published their findings in the online Schizophrenia Research and Acta Psychiatrica Scandinavica.

In the Schizophrenia Research study, investigators compared two previous studies that suggested childhood cat ownership could be a possible risk factor for schizophrenia or another serious mental illness with a third, even earlier survey on mental health to see if the finding could be replicated.

“The results were the same,” researchers reported, “suggesting that cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill.”

If accurate, the researchers expect the culprit to be infection with T. gondii, a parasite commonly carried by cats. At this point, though, they are urging others to conduct further studies to clarify the apparent link between cat ownership and schizophrenia.

The Acta Psychiatrica Scandinavica study was a meta-analysis of 50 previously published studies to investigate the prevalence of t. gondii infection in people diagnosed with psychiatric disorders compared with healthy controls.

In cases of schizophrenia, researchers said evidence of an association with T. gondii was “overwhelming,” CBS News reported. Specifically, people infected with T. gondii were nearly twice as likely to be diagnosed with schizophrenia as people never infected with the parasite, according to the report.

The meta-analysis also suggested associations between T. gondii infection and bipolar disorder, obsessive-compulsive disorder, and addiction. No association, however, was found for major depression.

—Jolynn Tumolo

References

1. Fuller Torrey E, Simmons W, Yolken RH. Is childhood cat ownership a risk factor for schizophrenia later in life? Schizophrenia Research. 2015 April 18. [Epub ahead of print].

2. Sutterland AL, Fond G, Kuin A, et al. Beyond the association. Toxoplasma gondii in schizophrenia, bipolar disorder, and addiction: systematic review and meta-analysis. Acta Psychiatrica Scandinavica. 2015 April 15. [Epub ahead of print].

http://www.psychcongress.com/article/studies-link-cat-ownership-schizophrenia-other-mental-illness

katharine-thakkar

People with schizophrenia have different levels of the neurotransmitters glutamate and gamma-aminobutyric acidergic (GABA) than healthy people do, and their relatives also have lower glutamate levels, according to a study published online in Biological Psychiatry.

Using magnetic resonance spectroscopy, researchers discovered reduced levels of glutamate — which promotes the firing of brain cells — in both patients with schizophrenia and healthy relatives. Patients also showed reduced levels of GABA, which inhibits neural firing. Healthy relatives, however, did not.

Researchers are unsure why healthy relatives with altered glutamate do not show symptoms of schizophrenia or how they maintain normal GABA levels despite a predisposition to the illness.

“This finding is what’s most exciting about our study,” said lead investigator Katharine Thakkar, PhD, assistant professor of clinical psychology at Michigan State University, East Lansing. “It hints at what kinds of things have to go wrong for someone to express this vulnerability toward schizophrenia. The study gives us more specific clues into what kinds of systems we want to tackle when we’re developing new treatments for this very devastating illness.”

The study included 21 patients with chronic schizophrenia, 23 healthy relatives of other people with schizophrenia not involved in the study, and 24 healthy nonrelatives who served as controls.

Many experts believe there are multiple risk factors for schizophrenia, including dopamine and glutamate-GABA imbalance. Drugs that regulate dopamine do not work for all patients with schizophrenia. Dr. Thakkar believes magnetic resonance spectroscopy may help clinicians target effective treatments for specific patients.

“There are likely different causes of the different symptoms and possibly different mechanisms of the illness across individuals,” said Dr. Thakkar.

“In the future, as this imaging technique becomes more refined, it could conceivably be used to guide individual treatment recommendations. That is, this technique might indicate that one individual would benefit more from treatment A and another individual would benefit more from treatment B, when these different treatments have different mechanisms of action.”

—Jolynn Tumolo

References

Thakkar KN, Rösler L, Wijnen JP, et al. 7T proton magnetic resonance spectroscopy of GABA, glutamate, and glutamine reveals altered concentrations in schizophrenia patients and healthy siblings [publisehd online ahead of print April 19, 2016]. Biological Psychiatry.
Study uncovers clue to deciphering schizophrenia [press release]. Washington, DC: EurekAlert!; June 7, 2016.