Source: Why Inflammation is good and bad…

http://news.sciencemag.org/health/2015/11/steroid-eye-drops-reverse-cataracts-mice

I know this is not about mental health, but this is very big! Cataracts, a condition for which one has to have eye surgery, can be treated by steroid drops, at least in mice! Cataracts, if left untreated, can cause blindness! Also eye surgery is not a minor thing, so if it can be avoided, well that would be wonderful! Really, this is huge. Read the article below.

“More than half of Americans over the age of 70 have cataracts, caused by clumps of proteins collecting in the eye lens. The only way to remove them is surgery, an unavailable or unaffordable option for many of the 20 million people worldwide who are blinded by the condition. Now, a new study in mice suggests eye drops made with a naturally occurring steroid could reverse cataracts by teasing apart the protein clumps.

“This is a game changer in the treatment of cataracts,” says Roy Quinlan, a molecular biologist at Durham University in the United Kingdom who was not part of the study. “It takes decades for the cataracts to get to that point, so if you can reverse that by a few drops in the eye over a couple of weeks, that’s amazing.”
The proteins that make up the human lens are among the oldest in the body, forming at about 4 weeks after fertilization. The majority are crystallins, a family of proteins that allow the eye to focus and keep the lens clear. Two of the most abundant crystallins, CRYAA and CRYAB, are produced in response to stress or injury. They act as chaperones, identifying and binding to damaged and misfolded proteins in the lens, preventing them from aggregating. But over the years, as damaged proteins accumulate in the lens, these chaperones become overwhelmed. The mutated proteins then clump together, blocking light and producing the tell-tale cloudiness of cataracts.
To treat the condition without surgery—which is out of reach for many patients in developing nations—researchers have looked to drug treatments. Although boosting the function of CRYAA and CRYAB seems to be a good target, developing a therapeutic has been challenging. Most drugs that act on disease-related proteins work by changing how the protein functions, something scientists can measure by monitoring the protein’s enzymatic activity. CRYAA, CRYAB, and similar proteins are known as “undruggable” because their activity can’t be measured, says Jason Gestwicki, a biochemist at the University of California (UC), San Francisco, and a senior author of the new study, published online today in Science.
Gestwicki’s team decided to use a technology called differential scanning fluorimetry, which allows scientists to measure the temperature at which a target protein begins to melt. They analyzed CRYAA and CRYAB and discovered that in one type of hereditary cataract, CRYAB takes on a mutant form with a much higher melting temperature than its normal version. If they could find a molecule that would bind to the mutant CRYAB protein and lower its melting temperature back to that of a healthy CRYAB, they speculated, CRYAB should function normally and prevent damaged proteins from clumping in the lens. The researchers turned to a bank of 2450 molecules that exhibited similar properties to CRYAA and CRYAB. They added molecules to the mutant CRYAB, looking for one that would stabilize their target. They settled on compound 29, a steroid found naturally in the bloodstream but not in the lens, which has no blood supply. Mice with age-related and hereditary cataracts received drops in the right eye, whereas the left eye went untreated. After just a few weeks, the treated eye was visibly clearer, says Gestwicki, who conducted the work while at the University of Michigan. Cataract severity is measured on a scale of zero to four, with four being the worst case. On average, mice in the study had about a one-grade improvement in cataract severity after 4 weeks of treatment.
This is the second study this year to find that eye drops made from a class of steroids called sterols can successfully reverse cataracts. In July, researchers from UC San Diego reported that lanosterol, a steroid found in the human eye, reversed cataracts in dogs.
“It’s a me-too paper in the sense that this new study also treated cataracts with a sterol,” Quinlan says. “But they arrived at the same conclusion by completely different routes. That’s the way excellent science is done, and [it’s] something that should get philanthropists and pharma excited.”
One key difference between the two studies is the way the different steroids were administered. The dog study administered the drug both by injection into the eye and eye drops. The new study used only eye drops.
There’s still a lot to uncover before either study can move into clinical trials, Quinlan notes. The lens in the human eye is very different from those in mice or dogs, and neither study explains how the steroids work on cataracts. “Mechanistically, we really don’t know what’s going on here. It’s a black box.”
Figuring out how the treatment reverses cataracts is the team’s next task, a key step toward clinical trials, which Gestwicki hopes to launch in the next year. ViewPoint Therapeutics, a biotech company he co-founded in San Francisco, California, holds the license to the technology and will launch more animal studies soon.”

http://www.sciencealert.com/early-treatment-for-brain-inflammation-could-prevent-schizophrenia-study-finds
The disorder may be a side effect of our immune response.

PETER DOCKRILL 20 OCT 2015

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There’s no shortage of research identifying the possible root causes of schizophrenia, but a new study published this week is the first to demonstrate that the brains of people with schizophrenia – or at risk of developing it – have significantly higher levels of immune cell activity than those with no sign of the disorder.

Not only does the finding point to new avenues of research so we can better understand how immune cells contribute to schizophrenia, it might one day lead to treatments that could prevent the progression of the disease altogether, based on early warning signs related to inflammation in the brain.
“Schizophrenia is a potentially devastating disorder and we desperately need new treatments to help sufferers, and ultimately to prevent it,” said Oliver Howes, head of the psychiatric imaging group at the Medical Research Council (MRC) Clinical Sciences Centre in the UK. “This is a promising study as it suggests that inflammation may lead to schizophrenia and other psychotic disorders. We now aim to test whether anti-inflammatory treatments can target these. This could lead to new treatments or even prevention of the disorders altogether.”
Immune cells in the brain, called microglia, serve to repair damage to the brain and defend against infections, but the researchers hypothesised that one consequence of their activity could be triggering the progression of schizophrenia. To test this idea, they used positron emission tomography (PET) scans to compare the levels of microglial activity in a group of participants.
Among those tested, some were patients already diagnosed with schizophrenia, some were at risk of developing the disease, and others showed no symptoms. The researchers found that the activity levels of microglia in the brain corresponded to the severity of schizophrenia symptoms in those diagnosed with the disorder.
“Our findings are particularly exciting because it was previously unknown whether these cells become active before or after onset of the disease,” said one of the team, Peter Bloomfield. “Now we have shown this early involvement, mechanisms of the disease and new medications can hopefully be uncovered.”
It’s early days yet. While the results are definitely promising, the sample size used in this particular study (just 56 participants) is small. But the findings also amount to the latest evidence that inflammation – in the form of potential over-activity of our immune response system – lies at the heart of a host of modern medical problems.
“This study adds to a growing body of research that inflammation in the brain could be one of the factors contributing to a range of disorders – including Alzheimer’s, schizophrenia and depression,“ said Hugh Perry, chair of the Neuroscience and Mental Health Board at the MRC, ”and with this new knowledge comes the hope of life-changing treatments.”
The findings are published in The American Journal of Psychiatry.

http://m.livescience.com/52674-prenatal-choline-schizophrenia-risk.html
Can Prenatal Choline Cut Schizophrenia Risk in Kids?by Sara G. Miller

In an update to a recent study, researchers say they are continuing to find evidence that women who take supplements containing choline when they’re pregnant may lower the risk of schizophrenia in their children.

The children in the study are now 4 years old, and are already showing fewer early signs of schizophrenia — such as certain attention and social problems — than expected, said Dr. Robert Freedman at a talk in New York City on Oct. 23. Half of the children in the study had an increased risk for schizophrenia because their mothers had depression, anxiety or psychosis.

Freedman, the chairman of the department of psychiatry at the University of Colorado School of Medicine and editor in chief of The American Journal of Psychiatry, gave attendees at the Brain and Behavior Research Foundation symposium an update on the participants in his study, which was originally published in 2013 in The American Journal of Psychiatry.

In the 2013 study, Freedman and his team looked at the brains of the babies when they were newborns. They found that those whose mothers took a supplement containing phosphatidylcholine (a version of the nutrient choline) during the second or third trimester of pregnancy showed improvements in how well nerve cells could block certain signals, compared to a group whose moms were given a placebo. In people with schizophrenia, this ability to block these signals does not fully develop.
This means that people with schizophrenia are unable to block out certain sensory signals, making it difficult to focus their attention, Freedman said at the research meeting last month.

Schizophrenia — which affects about 1 percent of American adults — is characterized by an inability to distinguish some aspects of reality from the imagination, Freedman told Live Science. People with the condition may hear voices that aren’t there, hallucinate and have delusions, he said. And they are less able to function in their daily lives, he said. [Schizophrenia: Symptoms and Treatments]

However, because the symptoms of schizophrenia usually don’t become apparent until late adolescence or early adulthood, studying the disease in infants and children is challenging, he said.

To do so, Freedman and his team turned their attention to neurons in infants’ brains. In the study, the researchers played clicking sounds for the babies, and measured how well the infants’ brain inhibited certain signals. 

In infants whose mothers had taken the choline supplement, the researchers observed more signal inhibition than those whose mothers had taken a placebo, Freedman said at the meeting.

Choline’s potential

It isn’t clear whether choline may actually lower children’s risk of developing schizophrenia later in life; much more research is needed to look at the question. But research has shown that choline turns on receptors in the brain that help promote the development of inhibitory nerve cells.

Many people with schizophrenia — and other mental illnesses as well — have fewer of these receptors to begin with, due to genetics, Freedman said. That means these people could benefit from making sure all of the receptors that are present are turned on, Freedman said.

Choline is necessary for other reasons too, during the development of a fetus, because it is used to make cell membranes, the researchers wrote in their study. However, higher levels than those that are usually recommended are needed to turn on the receptors, they wrote. The current recommended dosage for pregnant women is 450 milligrams of choline daily, according to the National Institutes of Health; foods that are rich in choline include egg yolks, meat and soybeans.

Four years later, the newborns whose moms took choline in the study are already doing better, Freedman said. Those whose moms took choline are less likely to have problems with attention and social interactions, he said. People with schizophrenia often have problems in these two areas as children.

Still, because the typical age at which schizophrenia begins is still many years off — and because the number of children in the study is low — researchers won’t have a definitive answer for some time.

Even without final results, Freedman said he believes that all women (and by implication, their children) could benefit from taking choline during pregnancy.

There are no risks to women at the doses we’re recommending, Freedman told Live Science. In the study, the women took the equivalent of 900 milligrams of choline daily. He did note, however, that if women take much more of the nutrient, they could have some problems digesting it.

Still, Freedman stressed that women should always check with their obstetrician before taking any nutritional supplement. 

http://m.scotsman.com/news/scotland/top-stories/breakthrough-eye-test-to-diagnose-mental-health-disorders-1-3932670#axzz3qQwFwCrR
A SIMPLE eye test which could help diagnose mental health disorders or spot them before they arise is a step closer to being available on the NHS.

The award-winning test developed by Aberdeen University scientists uses a specialised, ultrafast camera to track patterns in eye movement and early results suggest that it is nearly 100 per cent effective in detecting mental health disorders such as schizophrenia, bipolar disorder and depression.
“We hope that as many people as possible come along to the open meeting to hear about what were are doing and what they can do to help in our research.” Professor David St Clair.

People with conditions such as schizophrenia did not explore images as fully as those without as they would rest their gaze on certain points for longer, according to the original research published in 2012 in the scientific journal Biological Psychiatry

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