Posts Tagged ‘psychiatry’

A study by scientists of the German Center for Neurodegenerative Diseases (DZNE) points to a novel potential approach against Alzheimer’s disease. In studies in mice, the researchers were able to show that blocking a particular receptor located on astrocytes normalized brain function and improved memory performance. Astrocytes are star-shaped, non-neuronal cells involved in the regulation of brain activity and blood flow. The findings are published in the Journal of Experimental Medicine (JEM).

Alzheimer’s disease is a common and currently incurable brain disorder leading to dementia, whose mechanisms remain incompletely understood. The disease appears to be sustained by a combination of factors that include pathological changes in blood flow, neuroinflammation and detrimental changes in brain cell activity.

“The brain contains different types of cells including neurons and astrocytes”, explains Dr. Nicole Reichenbach, a postdoc researcher at the DZNE and first author of the paper published in JEM. “Astrocytes support brain function and shape the communication between neurons, called synaptic transmission, by releasing a variety of messenger proteins. They also provide metabolic and structural support and contribute to the regulation of blood flow in the brain.”

Glitches in network activity

Similar to neurons, astrocytes are organized into functional networks that may involve thousands of cells. “For normal brain function, it is crucial that networks of brain cells coordinate their firing rates. It’s like in a symphony orchestra where the instruments have to be correctly tuned and the musicians have to stay in synchrony in order to play the right melody”, says Professor Gabor Petzold, a research group leader at the DZNE and supervisor of the current study. “Interestingly, one of the main jobs of astrocytes is very similar to this: to keep neurons healthy and to help maintain neuronal network function. However, in Alzheimer’s disease, there is aberrant activity of these networks. Many cells are hyperactive, including neurons and astrocytes. Hence, understanding the role of astrocytes, and targeting such network dysfunctions, holds a strong potential for treating Alzheimer’s.”

Astrocyte-targeted treatment alleviated memory impairment

Petzold and colleagues tested this approach in an experimental study involving mice. Due to a genetic disposition, these rodents exhibited certain symptoms of Alzheimer’s similar to those that manifest in humans with the disease. In the brain, this included pathological deposits of proteins known as “Amyloid-beta plaques” and aberrant network activity. In addition, the mice showed impaired learning ability and memory.

In their study, the DZNE scientists targeted a cell membrane receptor called P2Y1R, which is predominately expressed by astrocytes. Previous experiments by Petzold and colleagues had revealed that activation of this receptor triggers cellular hyperactivity in mouse models of Alzheimer’s. Therefore, the researchers treated groups of mice with different P2Y1R antagonists. These chemical compounds can bind to the receptor, thus switching it off. The treatment lasted for several weeks.

“We found that long-term treatment with these drugs normalized the brain’s network activity. Furthermore, the mice’s learning ability and memory greatly improved”, Petzold says. On the other hand, in a control group of wild type mice this treatment had no significant effect on astrocyte activity. “This indicates that P2Y1R inhibition acts quite specifically. It does not dampen network activity when pathological hyperactivity is absent.”

New approaches for research and therapies?

Petzold summarizes: “This is an experimental study that is currently not directly applicable to human patients. However, our results suggest that astrocytes, as important safeguards of neuronal health and normal network function, may hold the potential for novel treatment options in Alzheimer’s disease.” In future studies, the scientists intend to identify additional novel pathways in astrocytes and other cells as potential drug targets.

Reference:
Reichenbach, N., Delekate, A., Breithausen, B., Keppler, K., Poll, S., Schulte, T., . . . Petzold, G. C. (2018). P2Y1 receptor blockade normalizes network dysfunction and cognition in an Alzheimer’s disease model. The Journal of Experimental Medicine. doi:10.1084/jem.20171487

https://www.dzne.de/en/news/public-relations/press-releases/press/detail/the-brains-rising-stars-new-options-against-alzheimers/

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On the heels of one failed drug trial after another, a recent study suggests people with early Alzheimer’s disease could reap modest benefits from a device that uses magnetic fields to produce small electric currents in the brain.

Alzheimer’s is a degenerative brain disorder that afflicts more than 46 million people worldwide. At present there are no treatments that stop or slow its progression, although several approved drugs offer temporary relief from memory loss and other cognitive symptoms by preventing the breakdown of chemical messengers among nerve cells.

The new study tested a regimen that combines computerized cognitive training with a procedure known as repetitive transcranial magnetic stimulation (rTMS). The U.S. Food and Drug Administration has cleared rTMS devices for some migraine sufferers as well as for people with depression who have not responded to antidepressant medications.

Israel-based Neuronix reported results of a phase III clinical trial of its therapy system, known as neuroAD, in Alzheimer’s patients. More than 99 percent of Alzheimer’s drug trials have failed. The last time a phase III trial for a wholly new treatment succeeded (not just a combination of two already approved drugs) was about 15 years ago. The recent study did not test a drug but rather a device, which usually has an easier time gaining FDA clearance. NeuroAD has been approved for use in Europe and the U.K., where six weeks of therapy costs about $6,700. The system is not commercially available in the U.S., but based on the latest results the company submitted an application for FDA clearance last fall.

The neuroAD setup resembles a dental chair fitted with a touch screen and flexible arms, which generate magnetic fields from metal coils positioned near the person’s scalp. The magnetic fields produce electric currents within the brain that influence the activity of neurons. The procedure can reportedly speed up learning by strengthening synaptic connections between neurons while the person performs tasks that engage those particular brain cells. In the cognitive training that accompanies rTMS, when study participants see a picture of a strawberry and touch the screen to identify it as “fruit” or “furniture,” for instance, the system stimulates Wernicke’s area, the brain region responsible for language comprehension.

For its latest rTMS trial, the company enrolled about 130 people with mild to moderate Alzheimer’s at 10 sites—nine in the U.S. and one in Israel. Four out of five participants were already taking symptom-relieving therapies. At the start of the trial, each person took a cognitive battery—a 30-minute paper-and-pencil test commonly used to gauge mental function in Alzheimer’s studies—and was randomly assigned to receive the rTMS-cognitive therapy or a sham treatment for six weeks. The sessions lasted about an hour each day, five days per week.

A week after the six-week regimen, and again five weeks later, participants retook the paper-and-pencil test to see if their cognition improved. Despite the elaborate protocol, study adherence was high. More than 90 percent of participants completed at least 90 percent of their visits, says Babak Tousi, who heads the Clinical Trials Program at Cleveland Clinic Lou Ruvo Center for Brain Health and reported the trial’s results at the Vienna meeting.

Based on past studies of the neuroAD system in smaller groups (none had more than 30 participants), the company expected to see a cognitive benefit after six weeks of treatment. Curiously, though, the recent study revealed no significant difference in test scores between active and sham groups at the seven-week time point. (The sham group sat in the chair and saw pictures on the screen but received no cognitive training or exposure to magnetic fields.) At week 12—six weeks after the therapy ended—the active group did show an 1.8-point test score advantage over the sham group. “That is a pretty small effect,” says Lon Schneider, who directs the State of California Alzheimer’s Disease Center at the University of Southern California in Los Angeles and heard the study results presented in Vienna. By comparison, he says, drugs currently approved to treat Alzheimer’s symptoms have shown a 2.5- to 3-point improvement in six-month clinical trials. And in a study reported last fall, a leading pharmaceutical candidate tested in more than 2,100 people seemed to work about as well (a roughly 1.5-point improvement) but failed to achieve statistical significance.

Plus, the modest effect seen with the new rTMS trial only turned up in participants with mild Alzheimer’s, Tousi reported. People with more advanced cases did not improve on the therapy. “We’ve got that typical problem of a small study that does seem to give outcomes, but the outcomes are either unclear or not fully evaluable,” Schneider says, adding it is unclear, for instance, if the test scores improved because of the cognitive training or resulted from possible mood-enhancing effects of the rTMS, because some Alzheimer’s patients have depression or other psychiatric symptoms.

John-Paul Taylor, a neuropsychiatrist at Newcastle University in England who was not involved with the study and researches TMS’s prospects for treating visual hallucinations in dementia, agrees that it is hard to tell if the cognitive improvement was indeed “a real TMS effect.” He says, however, this technology is “ripe for more investigation.”

Taylor is working with colleagues who are trying to use computational modeling to get a better idea how rTMS works. “That’s where it’s going to get really interesting,” he says. “I suspect you’ll have to tailor the stimulation to individual patients.” Consistent with that idea, earlier this year researchers reported using brain imaging to identify different types of depression—and patients in one of those subgroups responded especially well to rTMS.

With the computational modeling, one could imagine feeding in a person’s brain scan “and the computer would say, you need to be in this position at this stimulation intensity to equal what another person would receive,” Taylor says. “That’s not that far off.” Ultimately, though, “we want a therapeutic that still works across everybody to some degree,” he says. “There’s a hint of that in this trial. I’m cautiously optimistic.”

https://www.scientificamerican.com/article/could-magnetic-brain-stimulation-help-people-with-alzheimer-rsquo-s/


Pinpoint stimulation of a cluster of nerve cells in the brains of mice encouraged timid responses to a perceived threat, whereas stimulation of an adjacent cluster induced boldness and courage.

Researchers at the Stanford University School of Medicine have identified two adjacent clusters of nerve cells in the brains of mice whose activity level upon sighting a visual threat spells the difference between a timid response and a bold or even fierce one.

Located smack-dab in the middle of the brain, these clusters, or nuclei, each send signals to a different area of the brain, igniting opposite behaviors in the face of a visual threat. By selectively altering the activation levels of the two nuclei, the investigators could dispose the mice to freeze or duck into a hiding space, or to aggressively stand their ground, when approached by a simulated predator.

People’s brains probably possess equivalent circuitry, said Andrew Huberman, PhD, associate professor of neurobiology and of ophthalmology. So, finding ways to noninvasively shift the balance between the signaling strengths of the two nuclei in advance of, or in the midst of, situations that people perceive as threatening may help people with excessive anxiety, phobias or post-traumatic stress disorder lead more normal lives.

“This opens the door to future work on how to shift us from paralysis and fear to being able to confront challenges in ways that make our lives better,” said Huberman, the senior author of a paper describing the experimental results. It was published online May 2 in Nature. Graduate student Lindsey Salay is the lead author.

Perilous life of a mouse
There are plenty of real threats in a mouse’s world, and the rodents have evolved to deal with those threats as best they can. For example, they’re innately afraid of aerial predators, such as a hawk or owl swooping down on them. When a mouse in an open field perceives a raptor overhead, it must make a split-second decision to either freeze, making it harder for the predator to detect; duck into a shelter, if one is available; or to run for its life.

To learn how brain activity changes in the face of such a visual threat, Salay simulated a looming predator’s approach using a scenario devised some years ago by neurobiologist Melis Yilmaz Balban, PhD, now a postdoctoral scholar in Huberman’s lab. It involves a chamber about the size of a 20-gallon fish tank, with a video screen covering most of its ceiling. This overhead screen can display an expanding black disc simulating a bird-of-prey’s aerial approach.

Looking for brain regions that were more active in mice exposed to this “looming predator” than in unexposed mice, Salay pinpointed a structure called the ventral midline thalamus, or vMT.

Salay mapped the inputs and outputs of the vMT and found that it receives sensory signals and inputs from regions of the brain that register internal brain states, such as arousal levels. But in contrast to the broad inputs the vMT receives, its output destination points were remarkably selective. The scientists traced these outputs to two main destinations: the basolateral amygdala and the medial prefrontal cortex. Previous work has tied the amygdala to the processing of threat detection and fear, and the medial prefrontal cortex is associated with high-level executive functions and anxiety.

Further inquiry revealed that the nerve tract leading to the basolateral amygdala emanates from a nerve-cell cluster in the vMT called the xiphoid nucleus. The tract that leads to the medial prefrontal cortex, the investigators learned, comes from a cluster called the nucleus reuniens, which snugly envelopes the xiphoid nucleus.

Next, the investigators selectively modified specific sets of nerve cells in mice’s brains so they could stimulate or inhibit signaling in these two nerve tracts. Exclusively stimulating xiphoid activity markedly increased mice’s propensity to freeze in place in the presence of a perceived aerial predator. Exclusively boosting activity in the tract running from the nucleus reuniens to the medial prefrontal cortex in mice exposed to the looming-predator stimulus radically increased a response seldom seen under similar conditions in the wild or in previous open-field experiments: The mice stood their ground, right out in the open, and rattled their tails, an action ordinarily associated with aggression in the species.

Thumping tails

This “courageous” behavior was unmistakable, and loud, Huberman said. “You could hear their tails thumping against the side of the chamber. It’s the mouse equivalent of slapping and beating your chest and saying, ‘OK, let’s fight!’” The mice in which the nucleus reuniens was stimulated also ran around more in the chamber’s open area, as opposed to simply running toward hiding places. But it wasn’t because nucleus reuniens stimulation put ants in their pants; in the absence of a simulated looming predator, the same mice just chilled out.

In another experiment, the researchers showed that stimulating mice’s nucleus reuniens for 30 seconds before displaying the “looming predator” induced the same increase in tail rattling and running around in the unprotected part of the chamber as did vMT stimulation executed concurrently with the display. This suggests, Huberman said, that stimulating nerve cells leading from the nucleus reunions to the prefrontal cortex induces a shift in the brain’s internal state, predisposing mice to act more boldly.

Another experiment pinpointed the likely nature of that internal-state shift: arousal of the autonomic nervous system, which kick-starts the fight, flight or freeze response. Stimulating either the vMT as a whole or just the nucleus reuniens increased the mice’s pupil diameter — a good proxy of autonomic arousal.

On repeated exposures to the looming-predator mockup, the mice became habituated. Their spontaneous vMT firing diminished, as did their behavioral responses. This correlates with lowered autonomic arousal levels.

Human brains harbor a structure equivalent to the vMT, Huberman said. He speculated that in people with phobias, constant anxiety or PTSD, malfunctioning circuitry or traumatic episodes may prevent vMT signaling from dropping off with repeated exposure to a stress-inducing situation. In other experiments, his group is now exploring the efficacy of techniques, such as deep breathing and relaxation of visual fixation, in adjusting the arousal states of people suffering from these problems. The thinking is that reducing vMT signaling in such individuals, or altering the balance of signaling strength from their human equivalents of the xiphoid nucleus and nucleus reuniens may increase their flexibility in coping with stress.

Reference:
Salay, L. D., Ishiko, N., & Huberman, A. D. (2018). A midline thalamic circuit determines reactions to visual threat. Nature. doi:10.1038/s41586-018-0078-2

http://med.stanford.edu/news/all-news/2018/05/scientists-find-fear-courage-switches-in-brain.html

A research team at University of Copenhagen including a researcher from the Faculty of Health and Medical Sciences has discovered a circuit in the brains of mice connecting circadian rhythm to aggressive behaviour. The discovery is particularly interesting to Alzheimer’s patients who experience increased aggression at night. The researchers have developed special protein tools capable of turning off the cells in the brain causing the behaviour.

Each year around 8,000 Danes are diagnosed with a form of dementia. Alzheimer’s disease is one of them. The disease manifests itself in memory difficulties in particular, but can also result in personality changes and mood swings.

When the sun sets 20 per cent of all Alzheimer’s patients experience increased bewilderment, anxiety, unease, disorientation, irritation and aggression. This phenomenon is called ‘sundowning’ or sundown syndrome. At worst, the condition can mean that the patient must be left in professional care, as it can be difficult for family members to handle. The cause of the condition is unknown, but previous research has suggested that it is connected to the circadian rhythm.

A research team including a researcher from the Department of Drug Design and Pharmacology at the University of Copenhagen is now able to confirm this connection. The researchers have identified and mapped a circuit between the part of the brain containing the circadian clock or circadian rhythm and a part of the brain controlling aggression.

’We have shown that the circadian clock in mice is closely linked to an aggression centre in the mouse brain by a cell circuit. The human brain has those same groups of cells that the circuit goes through. With this knowledge, we are now enabled to target this circuit pharmacologically and target cells that make people aggressive at the end of the day’, says Assistant Professor Timothy Lynagh from the Department of Drug Design and Pharmacology at the University of Copenhagen.

Turn off the Aggression
The inner clock or circadian rhythm is located in the part of the brain called suprachiasmatic nucleus. One of the parts of the brain that control aggressive behaviour is called the ventromedial hypothalamus. Researchers have previously observed a connection between the two parts of the brain, though none have had knowledge of the specific circuit connecting them.

Using electrophysiology and microscopy, the researchers measured the activity of the brain cells at main author Clifford Saper’s laboratory in Boston. They also turned off parts of the cell circuit in the brains of mice to map the circuit and to identify the cells connecting the two parts of the brain. To map circuits in the brain you need a protein tool that can turn off the various cells to determine their function. Assistant Professor Timothy Lynagh has designed precisely such a tool.

‘We take a receptor and mutate it, so that it is not sensitive to anything in the brain, but very sensitive to a particular drug. The tool works like an on/off switch. When you put the protein tool in the mouse brain, under normal circumstances, nothing will happen. But when you give the animal the drug, the cells that have the receptor on them will be turned off’, Timothy Lynagh explains.

Using this tool, the researchers can thus in theory turn off the cells that cause people suffering from sundown syndrome to become more aggressive at night.

May Be Used on Humans 20 Years into the Future
The tool can also be used in other contexts than sundown syndrome. In other studies, Tim Lynagh’s tool has been used to turn off cells in rats linked to anxiety and fear.

‘If you can start understanding which cells in the brain lead to which problems, you can then put this tool into any of those parts of the brain. The person who takes the drug will then have the cells causing the problem turned off’, Timothy Lynagh says.

Even though the study was conducted on mice, the tool and the knowledge the research has generated can potentially be used in the treatment of humans.

‘Because of the huge advances that are coming along with CRISPR, I would be tempted to say that based on a recent demonstration of gene therapy for brain disease, potentially, it could be used in the human brain in 20 years’ time. Of course it needs a lot more research’, he says.

Reference:
Todd, W. D., Fenselau, H., Wang, J. L., Zhang, R., Machado, N. L., Venner, A., … & Lowell, B. B. (2018). A hypothalamic circuit for the circadian control of aggression. Nature neuroscience, 1.

http://healthsciences.ku.dk/news/2018/05/researchers-discover-connection-between-circadian-rhythm-and-aggression/


The study simulated long-term consumption of three cups of coffee a day.

It is well known that memory problems are the hallmarks of Alzheimer’s disease. However, this dementia is also characterized by neuro-psychiatric symptoms, which may be strongly present already in the first stages of the disorder. Known as Behavioural and Psychological Symptoms of Dementia (BPSD), this array of symptoms — including anxiety, apathy, depression, hallucinations, paranoia and sundowning (or late-day confusion) — are manifested in different manners depending on the individual patient, and are considered the strongest source of distress for patients and caregivers.


Coffee and caffeine: good or bad for dementia?

Caffeine has recently been suggested as a strategy to prevent dementia, both in patients with Alzheimer’s disease and in normal ageing processes. This is due to its action in blocking molecules — adenosine receptors — which may cause dysfunctions and diseases in old age. However, there is some evidence that once cognitive and neuro-psychiatric symptoms develop, caffeine may exert opposite effects.

To investigate this further, researchers from Spain and Sweden conducted a study with normal ageing mice and familial Alzheimer’s models. The research, published in Frontiers in Pharmacology, was conducted from the onset of the disease up to more advanced stages, as well as in healthy age-matched mice.

“The mice develop Alzheimer’s disease in a very close manner to human patients with early-onset form of the disease,” explains first author Raquel Baeta-Corral, from Universitat Autònoma de Barcelona, Spain. “They not only exhibit the typical cognitive problems but also a number of BPSD-like symptoms. This makes them a valuable model to address whether the benefits of caffeine will be able to compensate its putative negative effects.”

“We had previously demonstrated the importance of the adenosine A1 receptor as the cause of some of caffeine’s adverse effects,” explains Dr. Björn Johansson, a researcher and physician at the Karolinska University Hospital, Sweden.

“In this study, we simulated a long oral treatment with a very low dose of caffeine (0.3 mg/mL) — equivalent to three cups of coffee a day for a human — to answer a question which is relevant for patients with Alzheimer’s, but also for the ageing population in general, and that in people would take years to be solved since we would need to wait until the patients were aged.”

Worsened Alzheimer’s symptoms outweigh cognition benefits

The results indicate that caffeine alters the behavior of healthy mice and worsens the neuropsychiatric symptoms of mice with Alzheimer’s disease. The researchers discovered significant effects in the majority of the study variables — and especially in relation to neophobia (a fear of everything new), anxiety-related behaviors, and emotional and cognitive flexibility.

In mice with Alzheimer’s disease, the increase in neophobia and anxiety-related behaviours exacerbates their BPSD-like profile. Learning and memory, strongly influenced by anxiety, got little benefit from caffeine.

“Our observations of adverse caffeine effects in an Alzheimer’s disease model, together with previous clinical observations, suggest that an exacerbation of BPSD-like symptoms may partly interfere with the beneficial cognitive effects of caffeine. These results are relevant when coffee-derived new potential treatments for dementia are to be devised and tested,” says Dr. Lydia Giménez-Llort, researcher from the INc-UAB Department of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, and lead researcher of the project.

The results of the study form part of the PhD thesis of Raquel Baeta-Corral, first author of the article, and are the product of a research led by Lydia Giménez-Llort, Director of the Medical Psychology Unit, Department of Psychiatry and Legal Medicine and researcher at the UAB Institute of Neuroscience, together with Dr Björn Johansson, Researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet and the Department of Geriatrics, Karolinska University Hospital, Sweden, under the framework of the Health Research Fund project of the Institute of Health Carlos III.

Long-term caffeine worsens symptoms associated with Alzheimer’s disease

By Elizabeth Bernstein

You’re feeling depressed. What have you been eating?

Psychiatrists and therapists don’t often ask this question. But a growing body of research over the past decade shows that a healthy diet—high in fruits, vegetables, whole grains, fish and unprocessed lean red meat—can prevent depression. And an unhealthy diet—high in processed and refined foods—increases the risk for the disease in everyone, including children and teens.

Now recent studies show that a healthy diet may not only prevent depression, but could effectively treat it once it’s started.

Researchers, led by epidemiologist Felice Jacka of Australia’s Deakin University, looked at whether improving the diets of people with major depression would help improve their mood. They chose 67 people with depression for the study, some of whom were already being treated with antidepressants, some with psychotherapy, and some with both. Half of these people were given nutritional counseling from a dietitian, who helped them eat healthier. Half were given one-on-one social support—they were paired with someone to chat or play cards with—which is known to help people with depression.

After 12 weeks, the people who improved their diets showed significantly happier moods than those who received social support. And the people who improved their diets the most improved the most. The study was published in January 2017 in BMC Medicine. A second, larger study drew similar conclusions and showed that the boost in mood lasted six months. It was led by researchers at the University of South Australia and published in December 2017 in Nutritional Neuroscience.

And later this month in Los Angeles at the American Academy of Neurology’s annual meeting, researchers from Rush University Medical Center in Chicago will present results from their research that shows that elderly adults who eat vegetables, fruits and whole grains are less likely to develop depression over time.

The findings are spurring the rise of a new field: nutritional psychiatry. Dr. Jacka helped to found the International Society for Nutritional Psychiatry Research in 2013. It held its first conference last summer. She’s also launched Deakin University’s Food & Mood Centre, which is dedicated to researching and developing nutrition-based strategies for brain disorders.

The annual American Psychiatric Association conference has started including presentations on nutrition and psychiatry, including one last year by chef David Bouley on foods that support the peripheral nervous system. And some medical schools, including Columbia University’s Vagelos College of Physicians and Surgeons, are starting to teach psychiatry residents about the importance of diet on mental health.

Depression has many causes—it may be genetic, triggered by a specific event or situation, such as loneliness, or brought on by lifestyle choices. But it’s really about an unhealthy brain, and too often people forget this. “When we think of cardiac health, we think of strengthening an organ, the heart,” says Drew Ramsey, a psychiatrist in New York, assistant clinical professor of psychiatry at Columbia and author of “Eat Complete.” “We need to start thinking of strengthening another organ, the brain, when we think of mental health.”

A bad diet makes depression worse, failing to provide the brain with the variety of nutrients it needs, Dr. Ramsey says. And processed or deep-fried foods often contain trans fats that promote inflammation, believed to be a cause of depression. To give people evidenced-based information, Dr. Ramsey created an e-course called “Eat to Beat Depression.”

A bad diet also affects our microbiome—the trillions of micro-organisms that live in our gut. They make molecules that can alter the production of serotonin, a neurotransmitter found in the brain, says Lisa Mosconi, a neuroscientist, nutritionist and associate director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College in New York. The good and bad bacteria in our gut have complex ways to communicate with our brain and change our mood, she says. We need to maximize the good bacteria and minimize the bad.

So what should we eat? The research points to a Mediterranean-style diet made up primarily of fruits and vegetables, extra-virgin olive oil, yogurt and cheese, legumes, nuts, seafood, whole grains and small portions of red meat. The complexity of this diet will provide the nutrition our brain needs, regulate our inflammatory response and support the good bacteria in our gut, says Dr. Mosconi, author of “Brain Food: The Surprising Science of Eating for Cognitive Power.”

Can a good diet replace medicine or therapy? Not for everyone. But people at risk for depression should pay attention to the food they eat. “It really doesn’t matter if you need Prozac or not. We know that your brain needs nutrients,” Dr. Ramsey says. A healthy diet may work even when other treatments fail. And at the very least, it can serve as a supplemental treatment—one with no bad side effects, unlike antidepressants—that also has a giant upside. It can prevent other health problems, such as heart disease, obesity and diabetes.

Loretta Go, a 60-year-old mortgage consultant in Ballwin, Mo., suffered from depression for decades. She tried multiple antidepressants and cognitive behavioral therapy, but found little relief from symptoms including insomnia, crying jags and feelings of hopelessness. About five years ago, after her doctor wanted to prescribe yet another antidepressant, she refused the medicine and decided to look for alternative treatments.

Ms. Go began researching depression and learned about the importance of diet. When she read that cashews were effective in reducing depression symptoms, she ordered 100 pounds, stored them in the freezer, and started putting them in all her meals.

She also ditched processed and fried foods, sugar and diet sodas. In their place, she started to eat primarily vegetables and fruits, eggs, turkey and a lot of tofu. She bought a Vitamix blender and started making a smoothie with greens for breakfast each morning.

Within a few months, Ms. Go says she noticed a difference in her mood. She stopped crying all the time. Her insomnia went away and she had more energy. She also began enjoying activities again that she had given up when she was depressed, such as browsing in bookstores and volunteering at the animal shelter.

Ms. Go’s depression has never come back. “This works so well,” she says. “How come nobody else talks about this?”

https://www.wsj.com/articles/the-food-that-helps-battle-depression-1522678367

By Jane Ridley

Four years ago, Lillyth Quillan cowered behind a padlocked door as her teenage son, taller and stronger than she is, paced back and forth in a rage.

Suddenly he went quiet. “Don’t let me hurt you, Mom,” he said, his voice sounding chillingly calm.

It was the first time the high school freshman had used that particular tone, but he continued to deploy it as he menaced his mom and dad.

“He used the kind of language of abusive husbands — manipulating and controlling,” says Quillan, who had installed locks on every door in her house except her son’s bedroom. “I was terrified of what he was going to do next.”

The boy — whom Quillan chooses to call Kevin in her interview with The Post in reference to the unnerving Lionel Shriver novel “We Need To Talk About Kevin” about a school shooter in upstate New York — was out of control.

After years of cruel and violent behavior plus multiple suspensions and expulsions from school, psychiatrists finally diagnosed the then-14-year-old Kevin with “conduct disorder,” which, in its most extreme form, can be a precursor to psychopathy.

Psychopathy, which is often used interchangeably with the term sociopathy, is believed to affect 1 percent of adults. Key attributes that sociopaths and psychopaths have in common include a disregard for laws, social mores and the rights of others, a failure to feel remorse or guilt and, in some but not all cases, a tendency to violence.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) dictates that people under the age of 18 cannot be labelled psychopaths. However, in 2013 the American Psychiatric Association decided to include the condition “conduct disorder with callous and unemotional traits” for children ages 12 and over.

According to a 2001 report published in the journal American Family Physician, approximately 6 to 16 percent of boys and 2 to 9 percent of girls meet the diagnostic criteria for conduct disorder — only a fraction of which have the “callous and unemotional” label that can potentially lead to psychopathy in adulthood.

More than 50 studies have found that kids with the latter diagnosis are more likely to become criminals or display aggressive, psychopathic traits later in life. It has been reported that Nikolas Cruz, the 19-year-old who allegedly shot and killed 17 people at Marjory Stoneman Douglas High School in Parkland, Fla., last month showed classic signs of the disorder as a child, including abusing animals.

“Psychopaths don’t just appear when they are 20. They are always different from an early age,” Kent Kiehl, a psychology professor at the University of New Mexico and the author of “The Psychopath Whisperer,” tells The Post.

Characteristics to look for — as detailed in the widely used Hare Psychopathy Checklist Youth Version considered by clinicians and researchers to be the “gold standard” in assessing psychopathy — include lack of empathy, lack of guilt and regret, pathological lying, grandiose self-worth and failure to accept responsibility for actions such as fighting and bullying.

“Individuals who score high on those traits are more likely to produce further violence,” adds Kiehl. “If they are sanctioned but continue on the same path, it’s not a perfect indicator, but it’s enough to cause concern.”

Kiehl notes that research has shown that psychopathy is hereditary roughly half of the time. But his own breakthrough was the discovery that the psychopathic brain has a different structure than a “normal” one.

In 2014, he conducted a major study that found at least two abnormalities in the brains of adult psychopaths. There was a lack of gray matter in the section involved in processing emotions, while the area that reacts to excitement and thrills is overactive. Although the research has not been carried out yet, the pattern is likely to also occur in the brains of “callous and unemotional” children. “Brain science has helped us understand what is different about these kids,” adds Kiehl.

At the moment, there is no such thing as a “cure” for psychopathy or conduct disorder. But early intervention can be key for harm reduction, even with children as young as 2 or 3.

Paul Frick, a psychology professor at Louisiana State University and the author of “Conduct Disorder and Severe Antisocial Behavior,” recommends a range of therapies, most of which revolve around rewards systems rather than punishments.

“There are so-called ‘emotion coaching’ techniques that parents and therapists can employ to help children pay attention to the feelings of others,” he explains. “We find that they miss the cues that another child is upset.

“By saying: ‘Can you see how Johnny is feeling?’ [when a toy is snatched from him] and getting them to respond correctly, you can motivate them. You give them a star or a sticker as an incentive.

“Even though it doesn’t come naturally to them, they can learn others’ perspectives.”

Experts can identify a callous and unemotional child when they are as young as 3 or 4. Faced with a crying peer, typically developing children either try to comfort them or take flight. But those with the mental condition remain in place, showing apathy and coldness.

Remarkably, the psychology department at King’s College London has been able to trace the characteristics back to infancy. They tested more than 200 babies at 5 months old, tracking whether they preferred looking at a person’s face or at a red ball. The tots who favored the ball displayed more callous traits two and a half years later.

For Quillan, hindsight is 20/20, but she distinctly recalls the first signs that Kevin had behavioral issues at the age of just 8 months.

“He had teeth and would bite me while he was breast-feeding and he would laugh. He thought it was hilarious. I tried looking very sad and mimicking crying to show it was hurting me, but he would only laugh,” says Quillan, who ended up having to put him on formula.

“It didn’t occur to me until much later that this was a child for whom the amusement of my reaction when he bit me was a greater reward than food.”

Now 18, Kevin, who has had numerous run-ins with police, including for shoplifting, was made a ward of state and no longer lives with his parents. He lives in a residential school for “at-risk” youth in California, where he is on a waiting list to receive treatment, such as therapy, to build empathy.

“Because there is no real treatment for conduct disorder. All you can do is wait for your child to be arrested and enter the juvenile system and hope they get better,” says his 40-year-old homemaker mom.

“Luckily, Kevin is no longer violent and is actually cooperative.”

He is doing so well that he is about to receive his high school diploma, recently won an award for wrestling and has encouraged his mother to tell his story.

Now Quillian, who has no other kids, is focusing on advocacy and encouraging parents facing similar nightmares to hers. Three years ago, she formed a support group for families with kids with CD that has 420 members worldwide. More recently, she launched the Society for Treatment Options for Potential Psychopaths to bring awareness and to campaign for treatment for these children before they cause serious harm.

Adds Quillan: “As every news article came out about Parkland and Nikolas Cruz, I thought: ‘My God, this could easily be one of our kids.’”

https://nypost.com/2018/03/07/how-to-tell-if-your-child-is-a-future-psychopath/