Brain Imaging Research Pinpoints Neurobiological Basis for Key Symptoms Associated with Post-Traumatic Stress Disorder Like Listlessness and Emotional Detachment in Trauma Victims

In a novel brain-imaging study among trauma victims, researchers at NYU Langone Medical Center have linked an opioid receptor in the brain — associated with emotions — to a narrow cluster of trauma symptoms, including sadness, emotional detachment and listlessness. The study, published online today in the journal JAMA Psychiatry, holds important implications for targeted, personalized treatment of post-traumatic stress disorder, or PTSD, a psychiatric condition affecting more than 8 million Americans that can cause a wide range of debilitating psychiatric symptoms.

“Our study points toward a more personalized treatment approach for people with a specific symptom profile that’s been linked to a particular neurobiological abnormality,” says lead author Alexander Neumeister, MD, director of the molecular imaging program in the Departments of Psychiatry and Radiology at NYU School of Medicine, and Co-Director of NYU Langone’s Steven and Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress Disorder and Traumatic Brain Injury. “Understanding more about where and how symptoms of PTSD manifest in the brain is a critical part of research efforts to develop more effective medications and treatment modalities.”

The new study confirms a growing body of evidence linking a particular set of symptoms to specific brain circuits and chemicals, and bolsters a shift within the field of psychiatry away from “one-size-fits-all treatments” and toward more individualized medication regimens that target highly specific neurobiological components. “We know from previous clinical trials that antidepressants, for example, do not work well for dysphoria and the numbing symptoms often found in PTSD,” Dr. Neumeister added. “Currently available antidepressants are just not linked specifically enough to the neurobiological basis of these symptoms in PTSD. Going forward, our study will help pave the way toward development of better options.”

“People with cancer have a variety of different treatment options available based on the type of cancer that they have,” adds Dr. Neumeister. “We aim to do the same thing in psychiatry. We’re deconstructing PTSD symptoms, linking them to different brain dysfunction, and then developing treatments that target those symptoms. It’s really a revolutionary step forward that has been supported by the National Institute of Mental Health (NIMH) over the past few years in their Research Domain Criteria Project.”

The study, funded by the National Institute of Mental Health (NIMH), compared the brain scans of healthy volunteers with those of clinically diagnosed trauma victims with PTSD, major depression, and generalized anxiety disorder whose symptoms ranged from emotional detachment to isolation. Participants received a harmless radioactive tracer that binds to and illuminates a class of opioid receptors, known as kappa, when exposed to high-resolution positron emission tomography (PET). Kappa opioid receptors bind a potent natural opioid known as dynorphin, which is released by the body during times of stress to help relieve dysphoria or numbing.

Chronic exposure to stress, such as the case with PTSD, taxes kappa opioid receptors, however, causing the receptors to retract inside cells, leaving dynorphin without a place to dock. As a result, patients can experience dysphoria, characterized by feelings of hopelessness, detachment and emotional unease.

Results showed that fewer available kappa opioid receptors in the brain regions believed to govern emotions were associated with more intense feelings of dysphoria, but not feelings of anxious arousal. The findings confirm previous studies in animals linking the opioid-receptor system expressed in these specific brain regions to symptoms of dysphoria. The study also found an association between lower levels of cortisol, a stress hormone, and unavailable kappa opioid receptors, suggesting a new role for cortisol as a biomarker for certain types of PTSD symptoms.

“This is the first brain-imaging study to explore any psychiatric condition using a protein that binds to the kappa opioid receptor system,” notes Dr. Neumeister, who says the data support clinical trials under way at NYU Langone and other institutions of new medications that target kappa opioid receptors and other brain systems that can be linked to specific symptoms in trauma survivors. Such medications could be widely available for the treatment of PTSD in the future if ongoing clinical trials yield encouraging results.

(Image: Alamy)

Brain Structure of Kidney Donors May Make Them More Altruistic

That’s the finding of a study published in today’s Proceedings of the National Academy of Sciences (PNAS) by Georgetown researchers.

Georgetown College psychology professor Abigail Marsh worked with John VanMeter, director of Center for Functional and Molecular Imaging at Georgetown University Medical Center, to scan the brains of 19 altruistic kidney donors.

More Sensitive to Distress

“The results of brain scans and behavioral testing suggests that these donors have some structural and functional brain differences that may make them more sensitive, on average, to other people’s distress,” Marsh explains.

The Georgetown researchers used functional MRI to record the neural activity of the kidney donors and 20 control subjects who had never donated an organ as they viewed faces with fearful, angry or neutral expressions.

Underlying Neural Basis

In the right amygdala, an emotion-sensitive brain region, altruists displayed greater neural activity while viewing fearful expressions than did control subjects.

When asked to identify the emotional expressions presented in the face images, altruists recognized fearful facial expressions relatively more accurately than the control subjects.

“The brain scans revealed that the right amygdala volume of altruists is larger than that of non-altruists,” Marsh says. “The findings suggest that individual differences in altruism may have an underlying neural basis.”

Opposite From Psychopaths?

These findings dovetail with previous research by the professor showing  structural and functional brain differences that appear to make people with psychopathic traits less sensitive to others’ fear and distress.

These differences include amygdalas that are smaller and less responsive to fearful expressions. People who are unusually altruistic may therefore be the opposite in some ways from people who are psychopathic.

To find kidney donors, the researchers reached out to the Washington Regional Transplant Community (WRTC), a federally designated organ procurement organizations.

A Donor’s Story

Harold Mintz, former northern Virginian who volunteered with WRTC and agreed to participate in the Georgetown study, donated a kidney to an anonymous stranger he later learned was an Ethiopian refugee who had settled in Washington, D.C.

Mintz, who now lives in California and speaks to high school students about his 2000 donation, says a series of events over time led him to supply the kidney, including his father dying of cancer diagnosed too late at the age of 56.

One Valentine’s Day in 1988, Mintz and his wife were shopping separately for presents and Mintz noticed parents in a mall with a sign saying “Please Save Our Daughter’s Life.” He walked past them, then turned around and asked what they needed. It turned out the daughter had leukemia and needed a bone marrow transplant.

The couple decided to forget about the holiday and donated blood to see if either of them were a match. But no match was found and Mintz later noticed the daughter’s obituary in the newspaper.

Stories Taken to Heart

Mintz also was surprised to hear that although the couple’s daughter had just died, they thanked everyone who tried to help and expressed hope that they might help someone else.

“All these stories just kind of stuck inside my head and every time I’d see a story about a medical story of distress, it would just kind of get put away in a file inside my heart,” Mintz says.

Marsh notes that kidney disease is now the eighth-leading cause of death in the U.S., and that living kidney donations are the best hope for restoring people to health who have kidney disease.

“Dr. Marsh’s work is a great example of how fMRI can be used to provide insight into how differences in the brain’s response can lead individuals to perform such magnanimous acts,” VanMeter says.

EEG Study Findings Reveal How Fear is Processed in the Brain

An estimated 8% of Americans will suffer from post traumatic stress disorder (PTSD) at some point during their lifetime. Brought on by an overwhelming or stressful event or events, PTSD is the result of altered chemistry and physiology of the brain. Understanding how threat is processed in a normal brain versus one altered by PTSD is essential to developing effective interventions. 

New research from the Center for BrainHealth at The University of Texas at Dallas published online today in Brain and Cognition illustrates how fear arises in the brain when individuals are exposed to threatening images. This novel study is the first to separate emotion from threat by controlling for the dimension of arousal, the emotional reaction provoked, whether positive or negative, in response to stimuli. Building on previous animal and human research, the study identifies an electrophysiological marker for threat in the brain.

“We are trying to find where thought exists in the mind,” explained John Hart, Jr., M.D., Medical Science Director at the Center for BrainHealth. “We know that groups of neurons firing on and off create a frequency and pattern that tell other areas of the brain what to do. By identifying these rhythms, we can correlate them with a cognitive unit such as fear.”

Utilizing electroencephalography (EEG), Dr. Hart’s research team identified theta and beta wave activity that signifies the brain’s reaction to visually threatening images. 

“We have known for a long time that the brain prioritizes threatening information over other cognitive processes,” explained Bambi DeLaRosa, study lead author. “These findings show us how this happens. Theta wave activity starts in the back of the brain, in it’s fear center – the amygdala – and then interacts with brain’s memory center - the hippocampus – before traveling to the frontal lobe where thought processing areas are engaged. At the same time, beta wave activity indicates that the motor cortex is revving up in case the feet need to move to avoid the perceived threat.” 

For the study, 26 adults (19 female, 7 male), ages 19-30 were shown 224 randomized images that were either unidentifiably scrambled or real pictures. Real pictures were separated into two categories: threatening (weapons, combat, nature or animals) and non-threatening (pleasant situations, food, nature or animals). 

While wearing an EEG cap, participants were asked to push a button with their right index finger for real items and another button with their right middle finger for nonreal/scrambled items. Shorter response times were recorded for scrambled images than the real images. There was no difference in reaction time for threatening versus non-threatening images. 

EEG results revealed that threatening images evoked an early increase in theta activity in the occipital lobe (the area in the brain where visual information is processed), followed by a later increase in theta power in the frontal lobe (where higher mental functions such as thinking, decision-making, and planning occur). A left lateralized desynchronization of the beta band, the wave pattern associated with motor behavior (like the impulse to run), also consistently appeared in the threatening condition.

This study will serve as a foundation for future work that will explore normal versus abnormal fear associated with an object in other atypical populations including individuals with PTSD.

Tipping the Balance of Behavior

Humans with autism often show a reduced frequency of social interactions and an increased tendency to engage in repetitive solitary behaviors. Autism has also been linked to dysfunction of the amygdala, a brain structure involved in processing emotions. Now Caltech researchers have discovered antagonistic neuron populations in the mouse amygdala that control whether the animal engages in social behaviors or asocial repetitive self-grooming. This discovery may have implications for understanding neural circuit dysfunctions that underlie autism in humans.

This discovery, which is like a “seesaw circuit,” was led by postdoctoral scholar Weizhe Hong in the laboratory of David J. Anderson, the Seymour Benzer Professor of Biology at Caltech and an investigator with the Howard Hughes Medical Institute. The work was published online on September 11 in the journal Cell. 

"We know that there is some hierarchy of behaviors, and they interact with each other because the animal can’t exhibit both social and asocial behaviors at the same time. In this study, we wanted to figure out how the brain does that," Anderson says.

Anderson and his colleagues discovered two intermingled but distinct populations of neurons in the amygdala, a part of the brain that is involved in innate social behaviors. One population promotes social behaviors, such as mating, fighting, or social grooming, while the other population controls repetitive self-grooming—an asocial behavior.

Interestingly, these two populations are distinguished according to the most fundamental subdivision of neuron subtypes in the brain: the “social neurons” are inhibitory neurons (which release the neurotransmitter GABA, or gamma-aminobutyric acid), while the “self-grooming neurons” are excitatory neurons (which release the neurotransmitter glutamate, an amino acid).

To study the relationship between these two cell types and their associated behaviors, the researchers used a technique called optogenetics. In optogenetics, neurons are genetically altered so that they express light-sensitive proteins from microbial organisms. Then, by shining a light on these modified neurons via a tiny fiber optic cable inserted into the brain, researchers can control the activity of the cells as well as their associated behaviors.

Using this optogenetic approach, Anderson’s team was able to selectively switch on the neurons associated with social behaviors and those linked with asocial behaviors.

With the social neurons, the behavior that was elicited depended upon the intensity of the light signal. That is, when high-intensity light was used, the mice became aggressive in the presence of an intruder mouse. When lower-intensity light was used, the mice no longer attacked, although they were still socially engaged with the intruder—either initiating mating behavior or attempting to engage in social grooming.

When the neurons associated with asocial behavior were turned on, the mouse began self-grooming behaviors such as paw licking and face grooming while completely ignoring all intruders. The self-grooming behavior was repetitive and lasted for minutes even after the light was turned off.

The researchers could also use the light-activated neurons to stop the mice from engaging in particular behaviors. For example, if a lone mouse began spontaneously self-grooming, the researchers could halt this behavior through the optogenetic activation of the social neurons. Once the light was turned off and the activation stopped, the mouse would return to its self-grooming behavior.

Surprisingly, these two groups of neurons appear to interfere with each other’s function: the activation of social neurons inhibits self-grooming behavior, while the activation of self-grooming neurons inhibits social behavior. Thus these two groups of neurons seem to function like a seesaw, one that controls whether mice interact with others or instead focus on themselves. It was completely unexpected that the two groups of neurons could be distinguished by whether they were excitatory or inhibitory. “If there was ever an experiment that ‘carves nature at its joints,’” says Anderson, “this is it.”

This seesaw circuit, Anderson and his colleagues say, may have some relevance to human behavioral disorders such as autism.

"In autism," Anderson says, "there is a decrease in social interactions, and there is often an increase in repetitive, sometimes asocial or self-oriented, behaviors"—a phenomenon known as perseveration. "Here, by stimulating a particular set of neurons, we are both inhibiting social interactions and promoting these perseverative, persistent behaviors."

Studies from other laboratories have shown that disruptions in genes implicated in autism show a similar decrease in social interaction and increase in repetitive self-grooming behavior in mice, Anderson says. However, the current study helps to provide a needed link between gene activity, brain activity, and social behaviors, “and if you don’t understand the circuitry, you are never going to understand how the gene mutation affects the behavior.” Going forward, he says, such a complete understanding will be necessary for the development of future therapies.

But could this concept ever actually be used to modify a human behavior?

"All of this is very far away, but if you found the right population of neurons, it might be possible to override the genetic component of a behavioral disorder like autism, by just changing the activity of the circuits—tipping the balance of the see-saw in the other direction," he says.

New Study Examines Impact of Violent Media on the Brain

With the longstanding debate over whether violent movies cause real world violence as a backstop, a study published today in PLOS One found that each person’s reaction to violent images depends on that individual’s brain circuitry, and on how aggressive they were to begin with.

The study, which was led by researchers at the Icahn School of Medicine at Mount Sinai and the NIH Intramural Program, featured brain scans which revealed that both watching and not watching violent images caused different brain activity in people with different aggression levels. The findings may have implications for intervention programs that seek to reduce aggressive behavior starting in childhood.

“Our aim was to investigate what is going on in the brains of people when they watch violent movies,” said lead investigator Nelly Alia-Klein, PhD, Associate Professor of Neuroscience and Psychiatry at the Friedman Brain Institute and Icahn School of Medicine at Mount Sinai. “We hypothesized that if people have aggressive traits to begin with, they will process violent media in a very different way as compared to non-aggressive people, a theory supported by these findings.”

After answering a questionnaire, a group of 54 men were split by the research team into two groups—one with individuals possessing aggressive traits, including a history of physical assault, and a second group without these tendencies. The participants’ brains were then scanned as they watched a succession of violent scenes (shootings and street fights) on day one, emotional, but non-violent scenes (people interacting during a natural disaster) on day two, and nothing on day three.

The scans measured the subjects’ brain metabolic activity, a marker of brain function. Participants also had their blood pressure taken every 5 minutes, and were asked how they were feeling at 15 minute intervals.

Investigators discovered that during mind wandering, when no movies were presented, the participants with aggressive traits had unusually high brain activity in a network of regions that are known to be active when not doing anything in particular. This suggests that participants with aggressive traits have a different brain function map than non-aggressive participants, researchers said.

Interestingly, while watching scenes from violent movies, the aggressive group had less brain activity than the non-aggressive group in the orbitofrontal cortex, a brain region associated by past studies with emotion-related decision making and self-control. The aggressive subjects described feeling more inspired and determined and less upset or nervous than non-aggressive participants when watching violent (day 1) versus just emotional (day 2) media. In line with these responses, while watching the violent media, aggressive participants’ blood pressure went down progressively with time while the non-aggressive participants experienced a rise in blood pressure.

“How an individual responds to their environment depends on the brain of the beholder,” said Dr. Alia-Klein. “Aggression is a trait that develops together with the nervous system over time starting from childhood; patterns of behavior become solidified and the nervous system prepares to continue the behavior patterns into adulthood when they become increasingly coached in personality. This could be at the root of the differences in people who are aggressive and not aggressive, and how media motivates them to do certain things. Hopefully these results will give educators an opportunity to identify children with aggressive traits and teach them to be more aware of how aggressive material activates them specifically.”

(Image credit)

Scientists Link Alcohol-Dependence Gene to Neurotransmitter

Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence.

This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.

“This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence,” said TSRI Associate Professor Marisa Roberto, a co-author of the paper. “Importantly, the study also offers a correlation between rodent and human data.”

In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.

Pietro Paolo Sanna, associate professor at TSRI and the study’s corresponding author, was optimistic about the long-term clinical implications of the work. “A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy,” he said.

A Genetic Culprit

Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. “Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood,” said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.

This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren’t sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.

“As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption,” said Herman.

The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.

Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.

In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.

The team sees the new findings as “pieces to the puzzle.” Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

(Image caption: This image depicts the injection sites and the expression of the viral constructs in the two areas of the brain studied: the Dentate Gyrus of the hippocampus (middle) and the Basolateral Amygdala (bottom corners). Image courtesy of the researchers)

Neuroscientists reverse memories’ emotional associations

Most memories have some kind of emotion associated with them: Recalling the week you just spent at the beach probably makes you feel happy, while reflecting on being bullied provokes more negative feelings.

A new study from MIT neuroscientists reveals the brain circuit that controls how memories become linked with positive or negative emotions. Furthermore, the researchers found that they could reverse the emotional association of specific memories by manipulating brain cells with optogenetics — a technique that uses light to control neuron activity.

The findings, described in the Aug. 27 issue of Nature, demonstrated that a neuronal circuit connecting the hippocampus and the amygdala plays a critical role in associating emotion with memory. This circuit could offer a target for new drugs to help treat conditions such as post-traumatic stress disorder, the researchers say.

“In the future, one may be able to develop methods that help people to remember positive memories more strongly than negative ones,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, director of the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory, and senior author of the paper.

The paper’s lead authors are Roger Redondo, a Howard Hughes Medical Institute postdoc at MIT, and Joshua Kim, a graduate student in MIT’s Department of Biology.

Shifting memories

Memories are made of many elements, which are stored in different parts of the brain. A memory’s context, including information about the location where the event took place, is stored in cells of the hippocampus, while emotions linked to that memory are found in the amygdala.

Previous research has shown that many aspects of memory, including emotional associations, are malleable. Psychotherapists have taken advantage of this to help patients suffering from depression and post-traumatic stress disorder, but the neural circuitry underlying such malleability is not known.

In this study, the researchers set out to explore that malleability with an experimental technique they recently devised that allows them to tag neurons that encode a specific memory, or engram. To achieve this, they label hippocampal cells that are turned on during memory formation with a light-sensitive protein called channelrhodopsin. From that point on, any time those cells are activated with light, the mice recall the memory encoded by that group of cells.

Last year, Tonegawa’s lab used this technique to implant, or “incept,” false memories in mice by reactivating engrams while the mice were undergoing a different experience. In the new study, the researchers wanted to investigate how the context of a memory becomes linked to a particular emotion. First, they used their engram-labeling protocol to tag neurons associated with either a rewarding experience (for male mice, socializing with a female mouse) or an unpleasant experience (a mild electrical shock). In this first set of experiments, the researchers labeled memory cells in a part of the hippocampus called the dentate gyrus.

Two days later, the mice were placed into a large rectangular arena. For three minutes, the researchers recorded which half of the arena the mice naturally preferred. Then, for mice that had received the fear conditioning, the researchers stimulated the labeled cells in the dentate gyrus with light whenever the mice went into the preferred side. The mice soon began avoiding that area, showing that the reactivation of the fear memory had been successful.

The reward memory could also be reactivated: For mice that were reward-conditioned, the researchers stimulated them with light whenever they went into the less-preferred side, and they soon began to spend more time there, recalling the pleasant memory.

A couple of days later, the researchers tried to reverse the mice’s emotional responses. For male mice that had originally received the fear conditioning, they activated the memory cells involved in the fear memory with light for 12 minutes while the mice spent time with female mice. For mice that had initially received the reward conditioning, memory cells were activated while they received mild electric shocks.

Next, the researchers again put the mice in the large two-zone arena. This time, the mice that had originally been conditioned with fear and had avoided the side of the chamber where their hippocampal cells were activated by the laser now began to spend more time in that side when their hippocampal cells were activated, showing that a pleasant association had replaced the fearful one. This reversal also took place in mice that went from reward to fear conditioning.

Altered connections

The researchers then performed the same set of experiments but labeled memory cells in the basolateral amygdala, a region involved in processing emotions. This time, they could not induce a switch by reactivating those cells — the mice continued to behave as they had been conditioned when the memory cells were first labeled.

This suggests that emotional associations, also called valences, are encoded somewhere in the neural circuitry that connects the dentate gyrus to the amygdala, the researchers say. A fearful experience strengthens the connections between the hippocampal engram and fear-encoding cells in the amygdala, but that connection can be weakened later on as new connections are formed between the hippocampus and amygdala cells that encode positive associations.

“That plasticity of the connection between the hippocampus and the amygdala plays a crucial role in the switching of the valence of the memory,” Tonegawa says.

These results indicate that while dentate gyrus cells are neutral with respect to emotion, individual amygdala cells are precommitted to encode fear or reward memory. The researchers are now trying to discover molecular signatures of these two types of amygdala cells. They are also investigating whether reactivating pleasant memories has any effect on depression, in hopes of identifying new targets for drugs to treat depression and post-traumatic stress disorder.

David Anderson, a professor of biology at the California Institute of Technology, says the study makes an important contribution to neuroscientists’ fundamental understanding of the brain and also has potential implications for treating mental illness.

“This is a tour de force of modern molecular-biology-based methods for analyzing processes, such as learning and memory, at the neural-circuitry level. It’s one of the most sophisticated studies of this type that I’ve seen,” he says.

Our connection to content

Using neuroscience tools, Innerscope Research explores the connections between consumers and media.

It’s often said that humans are wired to connect: The neural wiring that helps us read the emotions and actions of other people may be a foundation for human empathy.

But for the past eight years, MIT Media Lab spinout Innerscope Research has been using neuroscience technologies that gauge subconscious emotions by monitoring brain and body activity to show just how powerfully we also connect to media and marketing communications.

“We are wired to connect, but that connection system is not very discriminating. So while we connect with each other in powerful ways, we also connect with characters on screens and in books, and, we found, we also connect with brands, products, and services,” says Innerscope’s chief science officer, Carl Marci, a social neuroscientist and former Media Lab researcher.

With this core philosophy, Innerscope — co-founded at MIT by Marci and Brian Levine MBA ’05 — aims to offer market research that’s more advanced than traditional methods, such as surveys and focus groups, to help content-makers shape authentic relationships with their target consumers.

“There’s so much out there, it’s hard to make something people will notice or connect to,” Levine says. “In a way, we aim to be the good matchmaker between content and people.”

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