3/4 - Latest in Autism News

Oxytocin may enhance social function in psychiatric disorders

Researchers at the Yerkes National Primate Research Center, Emory University, have shown inducing the release of brain oxytocin may be a viable therapeutic option for enhancing social function in psychiatric disorders, including autism spectrum disorders and schizophrenia. The study results are published in the advance online edition of Neuropsychopharmacology.

The oxytocin system is well-known for creating a bond between a mother and her newborn baby, and oxytocin is a lead drug candidate for treating social deficits in autism. Getting synthetic oxytocin into the brain, however, is challenging because of a blood-brain barrier. In this new study, lead researchers Meera Modi, PhD, and Larry Young, PhD, demonstrated for the first time the potential of oxytocin-releasing drugs to activate the social brain, to create bonds and, they believe, to possibly treat social deficits in psychiatric disorders. Meera, who is now at Pfizer, was a graduate student at the Yerkes Research Center when she worked with Young on this research. Young is division chief of Behavioral Neuroscience and Psychiatric Disorders at the Yerkes National Primate Research Center, William P. Timmie professor in the Emory School of Medicine Department of Psychiatry, director of the Center for Translational Social Neuroscience at Emory and principal investigator and director of the NIH Silvio O. Conte Center at Emory.

The researchers used pair bonding in monogamous prairie voles as an index of prosocial effects. Normally mating in the voles is necessary for the release of brain oxytocin that leads to a monogamous bond. For the first time, however, the Yerkes researchers showed that a drug that activates melanocortin receptors stimulates release of oxytocin in the brain to affect social relationships. According to Young, a simple injection of the melanocortin drug quickly induced a pair bond in male and female prairie voles without mating, and that bond lasted long after the drug wore away. The researchers also showed the same drug activated oxytocin cells so the cells released oxytocin directly into the brain's reward centers responsible for generating bonds.

Young believes this new found ability to induce an enduring bond in voles means the drug can also enhance attention to and learning from social information in people who have social disorders.

"Our latest discovery opens a new avenue of research to harness the power of the brain's oxytocin system to enhance the ability to process social information that could profoundly affect treatment of social disorders, particularly when combined with behavioral therapies used to treat children on the autism spectrum," says Young.

The Yerkes Research Center, the National Institute of Mental Health and Autism Speaks funded this study, the publication of which comes less than two weeks after Young and co-author Catherine Barrett's "Perspective" titled "Can Oxytocin Treat Autism" appeared in Science magazine. Barrett is a postdoctoral researcher at Yerkes.

Their perspective details the great potential and important limitations of current oxytocin therapeutic strategies. Young and Barrett are most optimistic the next generation approaches targeting oxytocin will excite the social brain by inducing brain cells to release oxytocin. Young says, "Imagine a drug that could induce the social attention and motivation a mother feels when nursing her infant or the bond between new lovers. This is exactly what we have shown in our latest oxytocin-related research and the chemical's viability to be a therapeutic target for enhancing social function in psychiatric disorders, including autism spectrum disorders and schizophrenia."

March 4, 2015, Science Daily - The above story is based on materials provided by Emory Health SciencesNote: Materials may be edited for content and length.

2/25 - Latest in Autism News

Omega-3 fatty acids, vitamin D may control brain serotonin, affecting behavior and psychiatric disorders

Although essential marine omega-3 fatty acids and vitamin D have been shown to improve cognitive function and behavior in the context of certain brain disorders, the underlying mechanism has been unclear. In a new paper published in FASEB Journal, serotonin is explained as the possible missing link tying together why vitamin D and marine omega-3 fatty acids might ameliorate the symptoms associated with a broad array of brain disorders.

In a previous paper published last year, authors Patrick and Ames discussed the implications of their finding that vitamin D regulates the conversion of the essential amino acid tryptophan into serotonin, and how this may influence the development of autism, particularly in developing children with poor vitamin D status.

Here they discuss the relevance of these micronutrients for neuropsychiatric illness. Serotonin affects a wide-range of cognitive functions and behaviors including mood, decision-making, social behavior, impulsive behavior, and even plays a role in social decision-making by keeping in check aggressive social responses or impulsive behavior.

Many clinical disorders, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, and depression share as a unifying attribute low brain serotonin. "In this paper we explain how serotonin is a critical modulator of executive function, impulse control, sensory gating, and pro-social behavior," says Dr. Patrick. "We link serotonin production and function to vitamin D and omega-3 fatty acids, suggesting one way these important micronutrients help the brain function and affect the way we behave."

Eicosapentaenoic acid (EPA) increases serotonin release from presynaptic neurons by reducing inflammatory signaling molecules in the brain known as E2 series prostaglandins, which inhibit serotonin release and suggests how inflammation may negatively impact serotonin in the brain. EPA, however, is not the only omega-3 that plays a role in the serotonin pathway. Docosahexaenoic acid (DHA) also influences the action of various serotonin receptors by making them more accessible to serotonin by increasing cell membrane fluidity in postsynaptic neurons.

Their paper illuminates the mechanistic links that explain why low vitamin D, which is mostly produced by the skin when exposed to sun, and marine omega-3 deficiencies interacts with genetic pathways, such as the serotonin pathway, that are important for brain development, social cognition, and decision-making, and how these gene-micronutrient interactions may influence neuropsychiatric outcomes. "Vitamin D, which is converted to a steroid hormone that controls about 1,000 genes, many in the brain, is a major deficiency in the US and omega-3 fatty acid deficiencies are very common because people don't eat enough fish," said Dr. Ames.

This publication suggests that optimizing intakes of vitamin D, EPA, and DHA would optimize brain serotonin concentrations and function, possibly preventing and ameliorating some of the symptoms associated with these disorders without side effects.

 UCSF Benioff Children's Hospital OaklandNote: Materials may be edited for content and length.

 

2/15 - Latest in Autism News

How mindfulness training affects health

Over the past decade, there have been many encouraging findings suggesting that mindfulness training can improve a broad range of mental and physical health problems. Yet, exactly how mindfulness positively impacts health is not clear.

Carnegie Mellon University's J. David Creswell -- whose cutting-edge work has shown how mindfulness meditation reduces loneliness in older adults and alleviates stress -- and his graduate student Emily K. Lindsay have developed a model suggesting that mindfulness influences health via stress reduction pathways. Their work, published in "Current Directions in Psychological Science," describes the biological pathways linking mindfulness training with reduced stress and stress-related disease outcomes.

"If mindfulness training is improving people's health, how does it get under the skin to affect all kinds of outcomes?" asked Creswell, associate professor of psychology in CMU's Dietrich College of Humanities and Social Sciences. "We offer one of the first evidence-based biological accounts of mindfulness training, stress reduction and health."

Creswell and Lindsay highlight a body of work that depicts the biological mechanisms of mindfulness training's stress reduction effects. When an individual experiences stress, activity in the prefrontal cortex -- responsible for conscious thinking and planning -- decreases, while activity in the amygdala, hypothalamus and anterior cingulate cortex -- regions that quickly activate the body's stress response -- increases. Studies have suggested that mindfulness reverses these patterns during stress; it increases prefrontal activity, which can regulate and turn down the biological stress response.

Excessive activation of the biological stress response increases the risk of diseases impacted by stress (like depression, HIV and heart disease). By reducing individuals' experiences of stress, mindfulness may help regulate the physical stress response and ultimately reduce the risk and severity of stress-related diseases.

Creswell believes by understanding how mindfulness training affects different diseases and disorders, researchers will be able to develop better interventions, know when certain treatments will work most effectively and identify people likely to benefit from mindfulness training.

As the birthplace of artificial intelligence and cognitive psychology, Carnegie Mellon has been a leader in the study of brain and behavior for more than 50 years. The university has created some of the first cognitive tutors, helped to develop the Jeopardy-winning Watson, founded a groundbreaking doctoral program in neural computation, and completed cutting-edge work in understanding the genetics of autism. Building on its strengths in biology, computer science, psychology, statistics and engineering, CMU recently launched BrainHubSM, a global initiative that focuses on how the structure and activity of the brain give rise to complex behaviors.

By Shilo Rea,  Carnegie Mellon University. The original article was written by Shilo Rea. Note: Materials may be edited for content and length.

2/3- Latest in Autism News

Protective brain protein reveals gender implications for autism, Alzheimer's research

For parents of children struggling with autism, the dearth of information is heartbreaking. Medical professionals are hard put to answer the primary questions: Who is autistic? What causes autism? What treatments are available? The situation is similar for Alzheimer's patients and relatives, who are helpless before the aggressive disease devouring a sufferer's identity.

A new study by Tel Aviv University's Prof. Illana Gozes, published in Translational Psychiatry, may offer insight into the pathology of both autism and Alzheimer's by revealing that different activities of certain proteins in males and females cause gender-specific tendencies toward these diseases. While the three-to-one ratio of autism in boys to girls is well known, as is the greater number of female Alzheimer's patients, the reasons for these phenomena are less clear.

According to Prof. Gozes, "If we understand how ADNP, an activity-related neuroprotective protein which is a major regulatory gene, acts differently in males and females, we can try to optimize drugs for potential future therapeutics to treat both autism and Alzheimer's disease."

Prof. Gozes is the incumbent of the Lily and Avraham Gildor Chair for the Investigation of Growth Factors, Head of the Elton Laboratory for Molecular Neuroendocrinology at TAU's Sackler Faculty of Medicine, a member of TAU's Adams Super Center for Brain Studies and the Sagol School of Neuroscience. Research for the study was conducted by graduate students Anna Malishkevich, Noy Amram, and Gal Hacohen-Kleiman, in collaboration with post-doctoral fellow Dr. Iddo Magen, and staff scientist Dr. Eliezer Giladi, all of TAU.

The gender factor

For the purpose of the new study, Prof. Gozes and her team examined the behavioral response of male and female mice, both ADNP-altered and normal, to different cognitive challenges and social situations. To do so, they removed one copy of the ADNP gene -- which regulates over 400 proteins involved in development -- from some mice, and then examined their respective responses to unfamiliar objects, odors, and other mice.

Their results revealed sex-specific learning and memory differences in the mice, reflecting hippocampal expression changes in ADNP, resulting in ADNP-controlled autism and in genes which indicate a risk for Alzheimer's disease. For example, ADNP-deficient male mice exhibited deficiencies in object recognition and social memory, whereas ADNP-altered female mice were more socially deficient compared to the non-altered females.

Providing new hope?

"ADNP may be new to the world of autism, but I have been studying it for 15 years," said Prof. Gozes. "Its gender-dependent expression changes male and female chemical tendencies toward different neurological disorders. Male and female mice may look the same and their brains may look the same, but they are not. When the expression of ADNP is different, it may cause different behaviors and different cognitive abilities.

"This study emphasizes the need to analyze men and women separately in clinical trials to find cures for diseases because they may respond differently," she concludes.

Prof. Gozes hopes the new study will prompt further research into the drug Davunetide (NAP) as a means of treating social and cognitive deficits with special attention to gender differences. Prof. Gozes discovered Davunetide (NAP), a snippet of ADNP, by looking at the nerve cell protective activity of ADNP fragments. Proof-of-concept clinical studies performed in adults have shown that Davunetide protects memory in patients suffering from the mild cognitive impairment that precedes Alzheimer's disease as well as functional activity in schizophrenia patients.

The above story is based on materials provided by American Friends of Tel Aviv UniversityNote: Materials may be edited for content and length.