Meet our 2017 NARSAD Independent Investigator Grantees

Meet our 2017 NARSAD Independent Investigator Grantees

Posted: April 11, 2017
Meet our 2017 NARSAD Independent Investigator Grantees

We are proud to announce that 40 scientists from 36 institutions in 10 countries have received NARSAD Independent Investigator Grants totaling $3.9 million. These scientists were awarded to further their research in the following categories: basic research, new technologies, early intervention/diagnostic tools, and next-generation therapies for research into schizophrenia, depression, bipolar disorder, ADHD, autism, PTSD, and other serious mental illnesses.

Covering a broad spectrum of brain and behavior disorders, the NARSAD Independent Investigator Grants provide $50,000 per year for up to two years to support investigators during the critical period between the initiation of research and the receipt of sustained funding. Every year, applications are reviewed by members of the Foundation’s Scientific Council, which is comprised of 150 leading experts across disciplines in brain and behavior research who volunteer their time to select the most promising research ideas to fund. We are very grateful to all of our donors whose contributions make the awarding of these grants possible.

Read the full press release.

Below are the 40 Independent Investigators who received their grants in 2017. To see a comprehensive list of NARSAD Grantees visit our Grantee Database.


 

Attention Deficit Hyperactivity Disorder (ADHD)

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Sarah Elizabeth Medland, Ph.D., QIMR Berghofer Medical Research Institute, Australia, Dr. Medland will study the ways in which genetic variants contribute to ADHD. Her team will use an Australian database of families affected by ADHD to collect in-depth phenotypic data provided by the parents and combine the data with electronic medical records and pharmaceutical treatment details. The team plans to collect DNA samples from those with ADHD in this cohort to examine the genetic variants that have been previously linked to ADHD and map their effects.

Autism Spectrum Disorder (ASD)

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Christina Gross, Ph.D., Cincinnati Children's Hospital Medical Center, University of Cincinnati, Dr. Gross will work on connecting gene defects already associated with autism and schizophrenia to molecules that can be targeted by drugs. The work aims to bridge the gap between discovery of large number of gene defects underlying mental illnesses and the development of treatments tailored to target those defects, which will ultimately pave the way toward developing precision-medicine treatments for autism and schizophrenia.

Terunaga Nakagawa, M.D., Ph.D., Vanderbilt University, Dr. Nakagawa aims to understand the molecular mechanisms behind abnormal communication between neurons and how this leads to mental illnesses, such as autism and depression. He and his team will look at the AMPA receptor, which regulates the majority of excitatory synaptic transmission in our brain. The team will focus on a component of AMPA receptor, a membrane protein called GSG1La, the amount of which is linked to autism. Deciphering the basic biology of GSG1L may help develop novel drugs to treat abnormal neuronal communication in mental illnesses.

NEXT GENERATION THERAPIES: to reduce symptoms of mental illness and retrain the brain

Grainne M. McAlonan, M.B.B.S., Ph.D., Institute of Psychiatry/King's College London, UK-England, Dr. McAlonan will study the interplay between excitatory and inhibitory brain system in people with autism. The balance between these two systems influences the communication between brain networks controlling behavior and cognition. In people with autism, this balance seems to be altered, leading to a different brain communication pattern from that of controls. Dr. McAlonan’s team will explore the brain responses of people with autism to pharmacological activation of the inhibitory neurotransmitter GABA. Their aim is to determine whether shifting the balance through medication will restores brain communication patterns abnormalities in autism.

 

Bipolar Disorder

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Cynthia V. Calkin, M.D., Dalhousie University, Canada, Dr. Calkin will study the relationship between the progression of bipolar disorder and declining health of the blood-brain barrier, a thin web of small vessels that protect the brain from foreign molecules. Using their new method for assessing the functioning of blood-brain barrier, Dr. Calkin’s team plans to compare healthy controls and people with bipolar disorder, and also measure the corresponding brain electrical activity in both groups, while gauging the severity of individuals’ bipolar disorder.

Koko Ishizuka, M.D., Ph.D., Johns Hopkins University, Dr. Ishizuka will use olfactory neurons obtained from the nasal cavity (the brain’s olfactory bulb) to study bipolar disorder. Access to living human tissue will further the exploration of molecular changes in people with bipolar disorder. Dr. Ishizuka’s team has developed a novel, quick and non-invasive method to capture neurons from nasal tissue of participants who are given a local anesthetic spray. The team plans to study the link between neuronal markers and mood symptom severity in patients with bipolar disorder.

Po-Hsiu Kuo, Ph.D., National Taiwan University, Taiwan, Dr. Kuo aims to understand the mechanisms behind varying response to treatment for bipolar disorder. Lithium medication is often the first treatment option for bipolar disorder but many patients do not fully respond to this treatment. Genetic markers that may be at play will be identified. Dr. Kuo’s team will explore the functional properties of identified genetic variants to uncover the underlying mechanisms of lithium response.

DIAGNOSTIC TOOLS / EARLY INTERVENTION: to recognize early signs of mental illness and treat as early as possible

Bradley John MacIntosh, Ph.D., Sunnybrook Health Sciences Centre, University of Toronto, Canada, Dr. MacIntosh will examine the link between cardiovascular health and bipolar disorder and test whether problems with small blood vessels relate to cognitive problems in people with bipolar disorder, who have a high rate of cardiovascular disease. The team will use non-invasive imaging-based biomarkers, such as stiffness of the arteries, and test for differences between adolescents with and without bipolar disorder.

NEXT GENERATION THERAPIES: to reduce symptoms of mental illness and retrain the brain

Christian Georg Schuetz, M.D., Ph.D., M.P.H., University of British Columbia, Canada, Dr. Schuetz is seeking to translate findings from brain imaging studies of bipolar disorder into a clinical intervention. He will use Theta Burst Stimulation (TBS) to activate and to modulate specific brain regions. The team will evaluate whether stimulating the brain can augment cognitive control and help individuals with bipolar disorder to stop urges, an ability that’s impaired in this disorder.

 

Depression

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Alexandre Bonnin, Ph.D., University of Southern California, Dr. Bonnin will investigate the risks of using antidepressants by women during pregnancy, specifically in regard to increasing the risk of autism for children. His team plans to characterize a new molecular pathway by which SSRIs antidepressants, such as citalopram, could reach the brain of the fetus brain and directly impact fetal brain development. By altering serotonin signaling, SSRI antidepressants could affect brain areas involved in social cognition and lead to life-long problems. Building on their previous research, Dr. Bonnin’s team plans to measure the molecular effects of exposure to citalopram before and after birth using pharmacological methods as well as 3D imaging techniques.

Gloria Choi, Ph.D., Massachusetts Institute of Technology, Dr. Choi will explore the pathways through which inflammation can cause depression. She and her team will study how inflammatory responses, as reflected in the increased blood concentrations of pro-inflammatory cytokines—signaling cells of the immune system--lead to depressive-like behaviors. The team plans to identify key immune cell types and molecules that result in depressive-like symptoms upon inflammation and potentially help provide additional biomarkers and treatment for depression caused by problems in the immune system.

Gabriel S. Dichter, Ph.D., University of North Carolina at Chapel Hill, Dr. Dichter plans to study the role of inflammation in developing deficits in motivation and pleasure, together known as anhedonia, which is seen in a number of psychiatric illnesses, including mood and anxiety disorders, substance-use disorders, schizophrenia, and attention-deficit/hyperactivity disorder. The team will evaluate relations between treatment-related changes in symptoms of anhedonia, inflammatory markers in the body, and brain functioning over time. The team will use several methods including individualized psychotherapy and functional magnetic resonance imaging (fMRI) scans.

Kristen C. Jacobson, Ph.D., University of Chicago, Dr. Jacobson will study how common, adverse daily experiences impact the developing brain of children and their risk of developing depression later on. The team will focus on investigating the effects of witnessing and experiencing community violence, which is a strong environmental risk factor for depression. Using brain imaging, the team will probe the link between exposure to violence and heightened sensitivity to threat and deficits in reward processing in the brain.

Pilyoung Kim, Ph.D., University of Denver, Dr. Kim aims to identify the neural signatures that precede the onset of postpartum depression, in order to elucidate what happens in the brain before mental illness becomes evident. The team will track neural responses to emotional stimuli in pregnant women and compare them in mothers who will go on to develop depression and mothers who will not. The study will also assess environmental, psychosocial, and hormonal measures. The findings could inform efforts to identify women who may be at high risk for developing depression.

Jose A. Moron-Concepcion, Ph.D., Washington University, Dr. Moron-Concepcion will examine the emotional component of pain and study the role of Kappa opioid receptors in comorbid (co-occurring) pain and depression. Some opioid receptors modulate both the sensory component of pain and the negative emotions associated with it. The team will determine whether pain reduces the activity of the same neural circuits that process motivation and reward, and whether manipulation of opioid receptors prevents pain from leading to depression.

Thomas M. Olino, Ph.D., Temple University, Dr. Olino studies the mechanisms that contribute to the onset of depression during adolescence. His team examines the heightened risk in children from depressed parents. The team will also study how a stressful life alters the development of reward responsiveness, ultimately leading to the emergence of depressive symptoms in youth. To do so, Dr. Olino and his team will collect blood samples from young participants to measure markers of inflammation.

DIAGNOSTIC TOOLS / EARLY INTERVENTION: to recognize early signs of mental illness and treat as early as possible

Thomas L. Rodebaugh, Ph.D., Washington University, Dr. Rodebaugh will examine the biological mechanism through which loneliness can lead to poor health and increased mortality, particularly among older adults. Social support reduces loneliness and shields against mood consequences of stress. The hormone oxytocin may play a role in the protective effects of social support. Dr. Rodebaugh’s team will measure circulating oxytocin levels in the biological samples of an ongoing longitudinal study of older adults to examine associations between this hormone and indices of social function and experience. The findings will also reveal whether oxytocin level can act as a potential biomarker for future vulnerability to loneliness and mental health symptoms.

NEXT GENERATION THERAPIES: to reduce symptoms of mental illness and retrain the brain

Matthew S. Milak, M.D., Columbia University, Dr. Milak will investigate the mechanisms by which the anesthetic drug ketamine treats depression. Unlike commonly prescribed “SSRI” antidepressants which take weeks to show effect, ketamine has been shown to quickly lift depression, often in a matter of hours, even in patients with treatment-resistant depression. However, ketamine at high doses also has serious side effects. Dr. Milak’s team will study the role of ketamine’s metabolites – molecules into which it breaks down once in the body -- with the goal of zeroing in on those that produce an antidepressant effect. This could pave the way for developing rapid-acting antidepressants that lack the undesirable side effects of ketamine.

 

Mental Illness - General

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Andrea Mele, Ph.D., Universita' di Roma La Sapienza, Italy, Dr. Mele will investigate the neurobiological basis of a brain training technique aimed at slowing cognitive decline. The technique is based on the spacing effect, a phenomenon whereby information that’s spread out over time is easier to learn and remember than information presented over and over in a short time. Spaced training can help with memory deficit and alter molecular process in mice. Dr. Mele’s team plans to study the cellular basis of distributed learning and identify the neural bases of the spacing effect. Understanding the mechanisms that underlay this effect could help identify new pharmacological approaches for memory enhancement.

NEXT GENERATION THERAPIES: to reduce symptoms of mental illness and retrain the brain

Irving Michael Reti, M.B.B.S., Johns Hopkins University, Dr. Reti plans to explore new treatments for reducing self-harm behaviors in people with intellectual and developmental disabilities. Such behaviors, which include self-directed slapping, punching and biting, can be extreme in some patients, leading to devastating consequences for the patient and their family. Currently, treatments include medications, behavioral therapy, and electroconvulsive therapy. In search of a better treatment for severe cases, Dr. Reti’s team will evaluate the feasibility of deep brain stimulation, using mouse models.

 

Post-Traumatic Stress Disorder (PTSD)

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

Timothy William Bredy, Ph.D., University of Queensland, Australia, Dr. Bredy will turn to the “dark matter” of the genome, which encode RNAs and not proteins, to elucidate their role in fear-related anxiety disorders such as PTSD. To understand how fear-related memories are made permanent, the team will study the gene-environment interactions and determine the mechanisms by which certain non-protein encoding RNAs regulate gene expression and influence fear-related learning. This will allow scientists to better understand how the brain changes across the lifespan and may lead to better therapies for phobia and PTSD.

Eric Matthew Morrow, M.D., Ph.D., Brown University, Dr. Morrow will investigate the role of mitochondrial metabolism in brain development of newborns. Mutations in a mitochondrial enzyme are found to be linked to a novel childhood disorder that involves intellectual disability and reduced brain growth after birth. Given the role of mitochondria in producing energy and regulating the metabolism of cells, including neurons, Dr. Morrow’s team will examine the metabolic pathways in the brain and their relationship to cognition and learning.

 

Schizophrenia

BASIC RESEARCH: to understand what happens in the brain to cause mental illness

James Andrew Bourne, Ph.D., Monash University, Australia, Dr. Bourne will study the role of a subcortical brain area known as the medial pulvinar, which connects strongly with the dorsolateral prefrontal cortex, a brain area implicated in schizophrenia. The medial pulvinar is thought to 'gate' the transfer of information across the brain. Therefore, it could be responsible for symptoms of sensory information overload, which is a frequent complaint of people with schizophrenia. Dr. Bourne’s team hopes to better understand the role of the medial pulvinar by defining the connectivity of this region from early life to adulthood in the marmoset monkey. The team will then also inactivate the medial pulvinar and its connectivity in early life, to see what consequence this has on the neurons of the DLPFC and behavior of the animal once it reaches adulthood.

Alessandro Gozzi, Ph.D., Italian Institute of Technology, Italy, Dr. Gozzi will study how imbalances in regional excitatory and inhibitory functions may lead to abnormal communication between brain regions in schizophrenia or autism. The team will genetically alter inhibitory and excitatory cells in the mouse brain, and measure the ensuing brainwide network activity using functional magnetic resonance imaging (fMRI), to detect any connectivity alterations.

Christopher Martin Hammell, Ph.D., Cold Spring Harbor Laboratory, Dr. Hammell will study the function of hundreds of genes that are considered to be likely involved in schizophrenia. The team has developed a rapid and cost-effective strategy to ascribe and test putative functions to individual genes. The team plans to use the roundworm, C. elegans, as a model organism to explore the role of all known schizophrenia-risk genes in controlling the specification and shape of developing neurons.

Derek William Morris, Ph.D., National University of Ireland, Galway, Ireland, Dr. Morris aims to uncover the role of epigenetics in schizophrenia and cognitive ability. More specifically, he will focus on a group of newly identified genes that regulate the functions of other genes and are shown to both increase the risk for schizophrenia and affect cognitive function. Dr. Morris hopes to extend the list of known schizophrenia risk genes, and study their effects on educational attainment and direct measures of different cognitive functions.

Sergiu P. Pasca, M.D., Stanford University, Dr. Pasca studies the mechanisms causing brain abnormalities in people with 22q11.2 deletion syndrome. In this syndrome, the deletion of a small piece of chromosome 22 leads to abnormalities in the brain’s white matter and oligodendrocytes, and puts people at higher risk for developing mental illnesses such as schizophrenia, depression, anxiety, and bipolar disorder. Dr. Pasca and his team have developed a novel 3D model that allows them to investigate the development of oligodendrocytes in cultures derived from patients with 22q11.2 deletion syndrome.

Rebecca Ann Piskorowski, Ph.D., French National Institute of Health and Medical Research, INSERM, France, Dr. Piskorowski will take an integrative approach to decipher the complex relationships between environmental, genetic and epigenetic factors in numerous psychiatric diseases, including schizophrenia. She and her team focus on problems in social cognition, a core symptom of schizophrenia. The team will study how environmental factors alter social memory formation by affecting certain neurons in the hippocampus, which appear critical for social memory.

Amar Sahay, Ph.D., Massachusetts General Hospital, Dr. Sahay will study the neurobiology of a group of hippocampal neurons and their role in schizophrenia. Through communication with the dentate gyrus, CA3 neurons play a critical role in how the hippocampus faithfully stores and retrieves memories. A problem in this network may not only contribute to episodic memory impairments but also underlie negative bias perception in depression and psychosis in schizophrenia. Dr. Sahay and his team will use their optimized method to rapidly generate CA3 neurons from human fibroblasts to study how physiological properties and connectivity of CA3 neurons are altered in schizophrenia.

Patrick David Skosnik, Ph.D., Yale University, Dr. Skosnik will examine the interaction between cannabinoid and glutamatergic receptors and their role in psychosis. Drugs acting on these receptors can bring about a disruption in the activity of neurons and lead to psychotic symptoms. Dr. Skosnik and his team will administer ketamine and THC, two drugs that act on cannabinoid and glutamatergic systems, in order to evaluate the interactive contributions of these two systems to psychosis in people using both EEG and behavioral measures.

Deepak Prakash Srivastava, Ph.D., Institute of Psychiatry/King's College London, UK-England, Dr. Srivastava plans to study the molecular mechanisms underlying the beneficial effects of estrogen-based treatments in schizophrenia. The team will grow neurons from patient’s own samples to test whether estrogen-based compounds can increase the number of synapses in the brain, which are thought to be reduced in schizophrenia. The team will also determine the molecular changes that estrogenic-compounds induce in these cells, which will inform attempt to develop new medications with fewer side effects.

Duje Tadin, Ph.D., University of Rochester, Dr. Tadin will explore whether sensory noise underlies working-memory problems, a core feature of schizophrenia. Although working memory abilities are linked to the frontal regions of the brain, it is possible that abnormalities in sensory processing also contribute to working memory deficits. Dr. Tadin’s team will focus on neural noise, a fundamental limitation in neural processing. The team will use electrical brain stimulation to manipulate the level of internal noise and test the effects on working memory performance.

Elisabet Vilella, Ph.D., Institute Pre Mata (IISPV -HPU), Spain, Dr. Vilella will investigate the role of gene variants affecting the integrity of myelin, the protective sheath around the axons that connect neurons. Myelin alterations, in addition to causing multiple sclerosis, have been shown in psychiatric diseases such as schizophrenia and bipolar disorder. Dr. Vilella and her team have identified a receptor, DDR1, present in the cells that produce brain myelin. The team aims to study the impact of DDR1 variants on processing speed and myelin volume in patients with schizophrenia and bipolar disorder.

James T.R. Walters, M.D., Ph.D., Cardiff University, United Kingdom, Dr. Walters will investigate why some people who are at high genetic risk for schizophrenia do not develop the condition. Numerous genetic variants have been found to increase risk of schizophrenia. However, many healthy individuals carry these variants with minimal detrimental effects. Dr. Walters and his team seek to identify factors that lead to resistance to developing schizophrenia. They will compare people at the highest genetic risk to those without such genetic risk factors to determine whether the high-risk individuals also have protective genetic factors or lower levels of environmental risk such as cannabis use, social deprivation and adverse childhood events.

DIAGNOSTIC TOOLS / EARLY INTERVENTION: to recognize early signs of mental illness and treat as early as possible

Clare L. Beasley, Ph.D., University of British Columbia, Canada, Dr. Beasley aims to uncover the role of microglial cells in altering the communications between neurons in bipolar disorder and schizophrenia. Her recent postmortem studies have uncovered changes in the shape and density of microglial cells in the brains of people with bipolar disorder and schizophrenia. Dr. Beasley’s team plans to focus on the signaling protein fractalkine, which is produced by neurons and plays a major role in communication between neurons and microglial cells. The team will quantify fractalkine in postmortem brain tissue and measure its blood levels in the same subjects, in order to examine the potential of this protein as a biomarker of microglial function.

NEXT GENERATION THERAPIES: to reduce symptoms of mental illness and retrain the brain

Simon McCarthy-Jones, Ph.D., Trinity College, Dublin, Ireland, Dr. McCarthy-Jones will study the potential of neurofeedback training for diminishing auditory hallucination in schizophrenia. Hearing voices is a common symptom experienced by the people with schizophrenia, which causes major distress and is hard to treat. McCarthy-Jones and his team will employ a brain-computer interface to present participants' neural activity to them in real time, and help them alter this activity through reinforcement learning. Brain activity readings will be based on EEG, which is an inexpensive and accessible method to use in outpatient clinics.

Oded Meiron, Ph.D., Sarah Herzog Memorial Hospital, Hebrew University, Israel, Dr. Meiron plans to examine whether executive functioning can be improved in people with schizophrenia by using a noninvasive method to electrically stimulate the brain, known as Transcranial Direct Current Stimulation or tDCS. Schizophrenia patients suffer from impaired brain communication across widely dispersed brain regions. Building on promising early results, Dr. Meiron’s team plans to use tDCS to stimulate the frontal regions of the brain to enhance working memory in people with schizophrenia, and determine the right amount of stimulation and duration for optimal results.

Vijay Anand Mittal, Ph.D., Northwestern University, Dr. Mittal will probe the effects of brain stimulation for improving verbal working memory in people with psychosis. The ability to hold verbal information in mind is central to achieving everyday goals but can be impaired in psychosis. Dr. Mittal’s team will use transcranial direct current stimulation or tDCS, a noninvasive method, to temporarily stimulate parts of the brain, to determine if cerebellar tDCS can improve verbal working memory in psychosis, while keeping track of brain responses via fMRI scans.

Laura M. Rowland, Ph.D., University of Maryland School of Medicine, Dr. Rowland studies the underlying neurobiological mechanisms responsible for learning and memory deficits in schizophrenia. An important element of learning is the brain’s ability to alter the strength of connections between neurons, known as plasticity. Research has suggested plasticity is impaired in schizophrenia. Dr. Rowland’s team will test whether repetitive transcranial magnetic stimulation (rTMS) will enhance plasticity in the brain’s visual areas in people with schizophrenia.

Bryan Andrew Strange, M.B.B.S., Ph.D., Technical University of Madrid, Spain, Dr. Strange will use deep-brain stimulation (DBS) to investigate abnormal activity in the dopamine system in schizophrenia. The team will collect electrophysiological recordings through DBS in a patient to study the firing pattern of dopaminergic neurons, which is thought to be impaired in schizophrenia. Secondly, the team will test patients in behavioral tasks such as working memory, in order to determine the cognitive effects of DBS treatment.