1. Injury from contact sport has harmful, though temporary effect on memory

    November 22, 2017 by Ashley

    From the McMaster University press release:

    McMaster University neuroscientists studying sports-related head injuries have found that it takes less than a full concussion to cause memory loss, possibly because even mild trauma can interrupt the production of new neurons in a region of the brain responsible for memory.

    Though such losses are temporary, the findings raise questions about the long-term effects of repeated injuries and the academic performance of student athletes.

    The researchers spent months following dozens of athletes involved in high-contact sports such as rugby and football, and believe that concussions and repetitive impact can interrupt neurogenesis — or the creation of new neurons — in the hippocampus, a vulnerable region of the brain critical to memory.

    The findings were presented today (Tuesday, November 14th) at the Society for Neuroscience’s annual conference, Neuroscience 2017, in Washington D.C.

    “Not only are newborn neurons critical for memory, but they are also involved in mood and anxiety,” explains Melissa McCradden, a neuroscience postdoctoral fellow at McMaster University who conducted the work. “We believe these results may help explain why so many athletes experience difficulties with mood and anxiety in addition to memory problems.”

    For the study, researchers administered memory tests and assessed different types of athletes in two blocks over the course of two years. In the first block, they compared athletes who had suffered a concussion, uninjured athletes who played the same sport, same-sport athletes with musculoskeletal injuries, and healthy athletes who acted as a control group.

    Concussed athletes performed worse on the memory assessment called a mnemonic similarity test (MST), which evaluates a person’s ability to distinguish between images that are new, previously presented, or very similar to images previously presented.

    In the second study, rugby players were given the MST before the season started, halfway through the season, and one month after their last game. Scores for injured and uninjured athletes alike dropped midseason, compared to preseason scores, but recovered by the postseason assessment.

    Both concussed and non-concussed players showed a significant improvement in their performance on the test after a reprieve from their sport.

    For the concussed athletes, this occurred after being medically cleared to return to full practice and competition. For the rugby players, they improved after approximately a month away from the sport.

    If neurogenesis is negatively affected by concussion, researchers say, exercise could be an important tool in the recovery process, since it is known to promote the production of neurons. A growing body of new research suggests that gentle exercise which is introduced before a concussed patient is fully symptom free, is beneficial.

    “The important message here is that the brain does recover from injury after a period of reprieve,” says McCradden. “There is a tremendous potential for the brain to heal itself.”


  2. Study suggests brain activity buffers against worsening anxiety

    November 21, 2017 by Ashley

    From the Duke University press release:

    Boosting activity in brain areas related to thinking and problem-solving may also buffer against worsening anxiety, suggests a new study by Duke University researchers.

    Using non-invasive brain imaging, the researchers found that people at-risk for anxiety were less likely to develop the disorder if they had higher activity in a region of the brain responsible for complex mental operations. The results may be a step towards tailoring psychological therapies to the specific brain functioning of individual patients.

    “These findings help reinforce a strategy whereby individuals may be able to improve their emotional functioning — their mood, their anxiety, their experience of depression — not only by directly addressing those phenomena, but also by indirectly improving their general cognitive functioning,” said Ahmad Hariri, a professor of psychology and neuroscience at Duke. The results are published Nov. 17 in the journal Cerebral Cortex.

    Previous findings from Hariri’s group show that people whose brains exhibit a high response to threat and a low response to reward are more at risk of developing symptoms of anxiety and depression over time.

    In the current work, Hariri and Matthew Scult, a clinical psychology graduate student in the department of psychology and neuroscience at Duke, wanted to investigate whether higher activity in a region of the brain called the dorsolateral prefrontal cortex could help shield these at-risk individuals from future mental illness.

    “We wanted to address an area of understanding mental illness that has been neglected, and that is the flip side of risk,” Hariri said. “We are looking for variables that actually confer resiliency and protect individuals from developing problems.”

    The dorsolateral prefrontal cortex is our brain’s “executive control” center, helping us focus our attention and plan complex actions. It also plays a role in emotion regulation, and well-established types of psychotherapy, including cognitive behavioral therapy, engage this region of the brain by equipping patients with strategies to reframe or re-evaluate their emotions.

    The team drew on data from 120 undergraduate students who participated in the Duke Neurogenetics Study. Each participant completed a series of mental health questionnaires and underwent a type of non-invasive brain scan called functional Magnetic Resonance Imaging (fMRI) while engaged in tasks meant to activate specific regions of the brain.

    The researchers asked each participant to answer simple memory-based math problems to stimulate the dorsolateral prefrontal cortex. Participants also viewed angry or scared faces to activate a region of the brain called the amygdala, and played a reward-based guessing game to stimulate activity in the brain’s ventral striatum.

    Scult was particularly interested in “at-risk” individuals with the combination of high threat-related activity in the amygdala and low reward-related activity in the ventral striatum. By comparing participants’ mental health assessments at the time of the brain scans, and in a follow-up occurring on average seven months later, he found that these at-risk individuals were less likely to develop anxiety if they also had high activity in the dorsolateral prefrontal cortex.

    “We found that if you have a higher functioning dorsolateral prefrontal cortex, the imbalance in these deeper brain structures is not expressed as changes in mood or anxiety,” Hariri said.

    The dorsolateral prefrontal cortex is especially skilled at adapting to new situations, the researchers say. Individuals whose brains exhibit the at-risk signatures may be more likely to benefit from strategies that boost the brain’s dorsolateral prefrontal activity, including cognitive behavioral therapy, working memory training, or transcranial magnetic stimulation (TMS).

    But, the researchers warn, the jury is still out on whether many brain-training exercises improve the overall functioning of the dorsolateral prefrontal cortex, or only hone its ability to complete the specific task being trained. Additional studies on more diverse populations are also needed to confirm their findings.

    “We are hoping to help improve current mental health treatments by first predicting who is most at-risk so that we can intervene earlier, and second, by using these types of approaches to determine who might benefit from a given therapy,” Scult said.


  3. Study suggests declining sense of smell may help identify patients with mild cognitive impairment

    by Ashley

    From the Columbia University Medical Center press release:

    Researchers at Columbia University Medical Center (CUMC) and the New York State Psychiatric Institute (NYSPI) may have discovered a way to use a patient’s sense of smell to treat Alzheimer’s disease before it ever develops. Having an impaired sense of smell is recognized as one of the early signs of cognitive decline, before the clinical onset of Alzheimer’s disease. The researchers at CUMC and NYSPI have found a way to use that effect to determine if patients with mild cognitive impairment may respond to cholinesterase inhibitor drugs to treat Alzheimer’s disease.

    The findings were published online this week in the Journal of Alzheimer’s Disease.

    Cholinesterase inhibitors, such as donepezil, enhance cholinergic function by increasing the transmission of the neurotransmitter acetylcholine in the brain. Cholinergic function is impaired in individuals with Alzheimer’s disease. Cholinesterase inhibitors, which block an enzyme that breaks down acetylcholine, have shown some effectiveness in improving the cognitive symptoms of Alzheimer’s disease. However, they have not been proven effective as a treatment for individuals with mild cognitive impairment (MCI), a condition that markedly increases the risk of Alzheimer’s disease.

    “We know that cholinesterase inhibitors can make a difference for Alzheimer’s patients, so we wanted to find out if we could identify patients at risk for Alzheimer’s who might also benefit from this treatment,” said D.P. Devanand, MBBS, MD, professor of psychiatry, scientist in the Gertrude H. Sergievsky Center at CUMC, and co-director of the Memory Disorders Clinic and the Late Life Depression Clinic at NYSPI. “Since odor identification tests have been shown to predict progression to Alzheimer’s, we hypothesized that these tests would also allow us to discover which patients with MCI would be more likely to improve with donepezil treatment.”

    In this year-long study, 37 participants with MCI underwent odor identification testing with the University of Pennsylvania Smell Identification Test (UPSIT). The test was administered before and after using an atropine nasal spray that blocks cholinergic transmission.

    The patients were then treated with donepezil for 52 weeks, and were periodically reevaluated with the UPSIT and with memory and cognitive function tests. Those who had a greater decline in UPSIT scores, indicating greater cholinergic deficits in the brain, after using the anticholinergic nasal spray test saw greater cognitive improvement with donepezil.

    In addition, short-term improvement in odor identification from baseline to eight weeks tended to predict longer-term cognitive improvement with donepezil treatment over one year.

    “These results, particularly if replicated in larger populations, suggest that these simple inexpensive strategies have the potential to improve the selection of patients with mild cognitive impairment who are likely to benefit from treatment with cholinesterase inhibitors like donepezil,” said Dr. Devanand.


  4. Study suggests biomarker may predict early Alzheimer’s disease

    November 20, 2017 by Ashley

    From the Sanford-Burnham Prebys Medical Discovery Institute press release:

    Researchers at Sanford Burnham Prebys Medical Discovery Institute (SBP) have identified a peptide that could lead to the early detection of Alzheimer’s disease (AD). The discovery, published in Nature Communications, may also provide a means of homing drugs to diseased areas of the brain to treat AD, Parkinson’s disease, as well as glioblastoma, brain injuries and stroke.

    “Our goal was to find a new biomarker for AD,” says Aman Mann, Ph.D., research assistant professor at SBP who shares the lead authorship of the study with Pablo Scodeller, Ph.D., a postdoctoral researcher at SBP. “We have identified a peptide (DAG) that recognizes a protein that is elevated in the brain blood vessels of AD mice and human patients. The DAG target, connective tissue growth factor (CTGF) appears in the AD brain before amyloid plaques, the pathological hallmark of AD.”

    “CTGF is a protein that is made in the brain in response to inflammation and tissue repair,” explains Mann. “Our finding that connects elevated levels of CTGF with AD is consistent with the growing body of evidence suggesting that inflammation plays an important role in the development of AD.”

    The research team identified the DAG peptide using in vivo phage display screening at different stages of AD development in a mouse model. In young AD mice, DAG detected the earliest stage of the disease. If the early appearance of the DAG target holds true in humans, it would mean that DAG could be used as a tool to identify patients at early, pre-symptomatic stages of the disease when treatments already available may still be effective.

    “Importantly, we showed that DAG binds to cells and brain from AD human patients in a CTGF-dependent manner” says Mann. “This is consistent with an earlier report of high CTGF expression in the brains of AD patients.”

    “Our findings show that endothelial cells, the cells that form the inner lining of blood vessels, bind our DAG peptide in the parts of the mouse brain affected by the disease,” says Erkki Ruoslahti, M.D., Ph.D., distinguished professor at SBP and senior author of the paper. “This is very significant because the endothelial cells are readily accessible for probes injected into the blood stream, whereas other types of cells in the brain are behind a protective wall called the blood-brain barrier. The change in AD blood vessels gives us an opportunity to create a diagnostic method that can detect AD at the earliest stage possible.

    “But first we need to develop an imaging platform for the technology, using MRI or PET scans to differentiate live AD mice from normal mice. Once that’s done successfully, we can focus on humans,” adds Ruoslahti.

    “As our research progresses we also foresee CTGF as a potential therapeutic target that is unrelated to amyloid beta (Aß), the toxic protein that creates brain plaques,” says Ruoslahti. “Given the number of failed clinical studies that have sought to treat AD patients by targeting Aß, it’s clear that treatments will need to be given earlier — before amyloid plaques appear — or have to target entirely different pathways.

    DAG has the potential to fill both roles — identifying at risk individuals prior to overt signs of AD and targeted delivery of drugs to diseased areas of the brain. Perhaps CTGF itself can be a drug target in AD and other brain disorders linked to inflammation. We’ll just have to learn more about its role in these diseases.”


  5. Study identifies group of brain cells responsible for keeping us awake

    November 19, 2017 by Ashley

    From the Emory Health Sciences press release:

    Scientists have identified an additional group of cells in the brain responsible for keeping us awake: the supramammillary nucleus, part of the caudal hypothalamus.

    Neurologists had suspected that a component of the “ascending arousal system” could be found in this part of the brain for more than 100 years, but the precise location had been a mystery. In mice, activating this region using targeted chemical genetic techniques resulted in prolonged wakefulness during the animals’ normal sleep periods.

    The results are scheduled for publication in Nature Communications.

    In humans, this region could be a target for bringing some brain injury patients out of a comatose state via electrical stimulation, says lead author Nigel Pedersen, MD, assistant professor of neurology at Emory University School of Medicine and an epilepsy specialist at Emory Brain Health Center.

    The supramammillary nucleus was known for its connections to the hippocampus, important for memory formation, and parts of the frontal cortex involved in focused attention, Pedersen says.

    “Given these connections, this region may be important for the voluntary maintenance of wake and attention, but more work is needed to study this,” he says.

    Pedersen conducted the research with Clifford Saper, MD, PhD, and Patrick Fuller, PhD, at Harvard Medical School and Beth Israel Deaconess Medical Center. Pedersen is continuing work at Emory on the importance of the supramammillary nucleus in memory and learning, and studying its connections to the hippocampus in relation to epilepsy control.

    For decades, neurologists had known that damage to the hypothalamus — including that seen in the mysterious post-World War I epidemic encephalitis lethargica — resulted in marked sleepiness. Now that the location and identity of the wake-promoting neurons are precisely defined, the supramammillary region joins other parts of the brain known as being involved in keeping people awake, such as the nearby lateral hypothalamus, the upper brain stem and basal forebrain.

    In the current paper, Pedersen and his colleagues used genetic engineering techniques to selectively activate particular groups of cells in the brain. They did so with a combination of a designer drug (clozapine-N-oxide) and receptors engineered to be triggered only by that drug. They injected viral vectors carrying an activation switch into the hypothalami of mice, and then gave the mice clozapine-N-oxide.

    Investigators mapped precisely where their injections went and which ones promoted wakefulness; only those involving the supramammillary nucleus did. So what does having this part of the brain stimulated “feel like” for the mice?

    “It’s hard to say, but they display a normal repertoire of behavior,” Pedersen says. “They’re not as wound up, and they don’t show stereotyped repetitive behaviors, as they would with stimulants. The main difference between these and normal mice is that there is no ‘quiet’ wakefulness or napping during the normally sleep-enriched daytime period.”

    Inhibiting the same area of the brain with similar techniques increased the amount of time mice slept, especially non-REM (rapid eye movement) sleep, although sleep was not instant upon drug administration, as has been shown for other parts of the arousal system, Pedersen says.

    “The effects of inhibition of the supramammillary region is to increase sleep, but not dramatically,” he says. “Disruption of other components of the arousal system typically has relatively mild effects. This may amount to some redundancy in the arousal network, but may also relate to the way in which different components of the arousal system have a role in particular types or components of wakefulness. We are actively exploring this idea.”

    Genetic manipulations also allowed the scientists to determine that the brain chemical glutamate was critical for wake signals. When the gene for a glutamate transporter VGLUT2 was snipped out of the supramammillary nucleus, artificial stimulation had no effect on wake and sleep.

    The presence of the enzyme nitric oxide synthase was used to identify an especially potent wake-promoting group of neurons, but their functions still depend on glutamate release. The role of the gaseous neurotransmitter nitric oxide in this brain network is not yet known, Pedersen adds.


  6. Study investigates patterns of degeneration in Alzheimer’s disease

    November 18, 2017 by Ashley

    From the Brigham and Women’s Hospital press release:

    Alzheimer’s disease (AD) is known to cause memory loss and cognitive decline, but other functions of the brain can remain intact. The reasons cells in some brain regions degenerate while others are protected is largely unknown. In a paper to be published in Stem Cell Reports, researchers from Brigham and Women’s Hospital have found that factors encoded in the DNA of brain cells contribute to the patterns of degeneration, or vulnerability, in AD.

    AD is characterized by plaques composed of amyloid ?-protein (A?) and tangles composed of Tau protein; accumulation of A? protein leads to disruption of Tau and, eventually, neurodegeneration which affects brain regions in a variety of ways. The front, rostral, portion of the brain is generally more damaged by plaque build-up while the back, caudal, portion is generally spared.

    Though there are several mechanisms that could cause these differences, the team focused on the potential contributions of cell-autonomous factors among neuronal subtypes that could affect both the generation of and the responses to A?. In a novel application of human induced-pluripotent stem cell (iPSC) technology, the team generated powerful culture systems that represent different areas of the brain. The systems were developed by taking skin cells from patients with a familial Alzheimer’s disease mutation and turning these skin cells into stem cells. Stem cells divide to make more stem cells, providing an unlimited supply of cells. Stem cells also can be turned into any type of cell in the body, including brain cells. In this study, the authors showed that vulnerable brain cells made more toxic A? protein compared to brain cells from more protected regions of the brain.

    In addition, the researchers found that brain cells in the protected, caudal portion of the brain have a less toxic response to A? than their rostral counterparts. Though early-onset, familial Alzheimer’s disease (fAD) accounts for a small number of AD cases, the study of fAD patients, or samples in this case, can reveal important aspects of the cell and molecular mechanisms underlying all types of AD. The team is currently using this information to investigate exactly why caudal neurons are protected and what differences in cell type cause neurons to be protected from AD.

    “These findings illuminate our understanding of why some neurons are spared and why others are not spared in AD,” said Christina Muratore, PhD, of the Department of Neurology. “If we can find out more information about why these subtypes of cells are protected, we may be able to use this information to tailor therapies to protect the vulnerable cells.”


  7. How challenges change the way you think

    November 17, 2017 by Ashley

    From the Frontiers press release:

    Research published today in Frontiers in Behavioral Neuroscience shows that challenging situations make it harder to understand where you are and what’s happening around you. A team of researchers showed participants video clips of a positive, a negative and a neutral situation. After watching the challenging clips — whether positive or negative — the participants performed worse on tests measuring their unconscious ability to acquire information about where and when things happen. This suggests that challenging situations cause the brain to drop nuanced, context-based cognition in favor of reflexive action.

    Previous research suggests that long-term memories formed under stress lack the context and peripheral details encoded by the hippocampus, making false alarms and reflexive reactions more likely. These context details are necessary for situating yourself in space and time, so struggling to acquire them has implications for decision-making in the moment as well as in memory formation.

    The research team, led by Thomas Maran, Marco Furtner and Pierre Sachse, investigated the short-term effects of challenging experiences on acquiring these context details. The team also investigated whether experiences coded as positive produced the same response as those coded as negative.

    “We aimed to make this change measurable on a behavioral level, to draw conclusions on how behavior in everyday life and challenging situations is affected by variations in arousal,” Thomas Maran explains.

    The researchers predicted that study participants would be less able to acquire spatial and sequential context after watching challenging clips, and that their performance would worsen the same way faced with either a positive or a negative clip. To test this, they used clips of film footage used previously to elicit reactions in stress studies: one violent scene (which participants experienced as negative), one sex scene (which participants experienced as positive), and one neutral control scene.

    Immediately after watching the clips, two groups of participants performed tasks designed to test their ability to acquire either spatial or sequential context. Both the sex scene and violent scene disrupted participants’ ability to memorize where objects had been and notice patterns in two different tasks, compared to the neutral scene. This supports the hypothesis that challenging situations — positive or negative — cause the brain to drop nuanced, context-based cognition in favor of reflexive action.

    So if challenging situations decrease the ability to pick up on context cues, how does this happen? The researchers suggest that the answer may lie in the hippocampus region of the brain — although they caution that since no neurophysiological techniques were applied in this study, this can’t be proven. Since existing evidence supports the idea that the hippocampus is deeply involved in retrieving and reconstructing spatial and temporal details, downgrading this function when faced with a potentially dangerous situation could stop this context acquisition and achieve the effect seen in this behavioral study. Reflexive reactions are less complex and demanding, and might stop individuals from making decisions based on unreliable information from unpredictable surroundings.

    Changes in cognition during high arousal states play an important role in psychopathology,” Thomas Maran explains, outlining his hopes for the future use of this research. He considers that the evidence provided by this study may have important therapeutic and forensic applications. It also gives a better basis for understanding reactions to challenging situations — from witnessing a crime to fighting on a battlefield — and the changes in the brain that make those reactions happen.


  8. Study uses stem cells to explore the causes of autism

    by Ashley

    From the Elsevier press release:

    Using human induced pluripotent stem cells (iPSCs) to model autism spectrum disorder (ASD), researchers at the University of São Paulo, Brazil and University of California, San Diego have revealed for the first time that abnormalities in the supporting cells of the brain, called astrocytes, may contribute to the cause of the disorder. The findings, published in Biological Psychiatry, help explain what happens at a biological level to produce ASD behavior, and may help researchers identify new treatments for patients with the disorder.

    Astrocytes play an important role in the development and function of the nervous system. But until now, iPSC models of autism have neglected their contribution. The new study, led by Dr. Patricia Beltrão-Braga and Dr. Alysson Muotri, used iPSCs to generate neurons and astrocytes to model the interaction between these brain cells and better understand how the brain forms in the disorder.

    “This new use of pluripotent stem cells suggests that neurobiological approaches to autism based solely on abnormal neuronal development may fail to account for complex interplay of neurons and astrocytes that may be an underappreciated component of the biology of this disorder,” said Dr. John Krystal, Editor of Biological Psychiatry.

    Induced pluripotent stem cell technology allows researchers to reprogram human cells into any cell in the body. In the study, first authors Dr. Fabiele Russo and Beatriz Freitas and colleagues used cells from three patients diagnosed with ASD and three healthy individuals to generate neurons and astrocytes. Neurons derived from ASD patients had less complex structure than healthy neurons, but adding healthy astrocytes to the ASD neurons improved their poorly developed structure. In reverse, pairing ASD astrocytes with healthy neurons interfered with their development, making them look more like the neurons from ASD patients.

    “The article highlights for the first time the influence of astrocytes in ASD, revealing that astrocytes play a fundamental role in neuronal structure and function,” said Beltrão-Braga.

    The researchers further investigated how the astrocytes exert their influence, and pegged a substance that astrocytes produce called IL-6, already suggested as a player in ASD, as the culprit for the defects. Astrocytes from the patients with ASD appeared to be producing too much of the substance, and the findings suggest that reducing IL-6 could be a beneficial treatment for neurons in ASD.

    Importantly, ASD has been a challenging disease to model using iPSCs because of its complexity. Several genes have been linked to ASD, but their contributions remain unknown, and genetic differences between patients have made it difficult to understand the cause and develop treatments for the disorder. But in this study, the ASD subjects were selected because they shared similar behaviors, rather than similar genes. According to Beltrão-Braga, this means the findings could provide a new alternative strategy for treating ASD symptoms, independent of the patient’s genotype.


  9. Brain imaging study suggests ADHD is a collection of different disorders

    by Ashley

    From the Elsevier press release:

    Researchers have found that patients with different types of attention-deficit/hyperactivity disorder (ADHD) have impairments in unique brain systems, indicating that there may not be a one-size-fits-all explanation for the cause of the disorder. Based on performance on behavioral tests, adolescents with ADHD fit into one of three subgroups, where each group demonstrated distinct impairments in the brain with no common abnormalities between them.

    The study, published in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, has the potential to radically reframe how researchers think about ADHD. “This study found evidence that clearly supports the idea that ADHD-diagnosed adolescents are not all the same neurobiologically,” said first author Dr. Michael Stevens, of the Olin Neuropsychiatry Research Center, Hartford, CT, and Yale University. Rather than a single disorder with small variations, the findings suggest that the diagnosis instead encompasses a “constellation” of different types of ADHD in which the brain functions in completely different ways.

    The researchers tested 117 adolescents with ADHD to assess different types of impulsive behavior — a typical feature of ADHD. Three distinct groups emerged based on the participants’ performance. One group demonstrated impulsive motor responses during fast-moving visual tasks (a measure of executive function), one group showed a preference for immediate reward, and the third group performed relatively normal on both tasks, compared to 134 non-ADHD adolescents.

    “These three ADHD subgroups were otherwise clinically indistinguishable for the most part,” said Dr. Stevens. “Without the specialized cognitive testing, a clinician would have had no way to tell apart the ADHD patients in one subgroup versus another.” Dr. Stevens and colleagues then used functional magnetic resonance imaging (fMRI), a technique that allows researchers to make connections between behavior and brain function, to investigate how these different impulsivity-related test profiles related to brain dysfunction.

    “Far from having a core ADHD profile of brain dysfunction, there was not a single fMRI-measured abnormality that could be found in all three ADHD subgroups,” said Dr. Stevens. Instead, each subgroup had dysfunction in different brain regions related to their specific type of behavioral impairment.

    “The results of this study highlight that there are different neural systems related to executive functions and reward processing that may contribute independently to the development of ADHD symptoms,” said Dr. Cameron Carter, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.

    It will take more research to prove that ADHD is a collection of different disorders, but this study provides a big step in that direction. “Ultimately, by being open to the idea that psychiatric disorders like ADHD might be caused by more than one factor, it might be possible to advance our understanding of causes and treatments more rapidly,” said Dr. Stevens.

    According to Dr. Carter, the findings suggest that future approaches using clinical assessments to identify the specific type of brain dysfunction contributing to a patient’s symptoms may allow a more targeted approach to treatment. For example, medications that may not appear to work well in a group of ADHD patients as a whole, may be effective for one particular subgroup that arises from a specific causal pathway.


  10. Researchers develop way to stimulate formation of new neural connections in adult brain

    November 16, 2017 by Ashley

    From the University of Idaho press release:

    A team led by University of Idaho scientists has found a way to stimulate formation of new neural connections in the adult brain in a study that could eventually help humans fend off memory loss, brain trauma and other ailments in the central nervous system.

    Peter G. Fuerst, an associate professor in the College of Science’s Department of Biological Sciences and WWAMI Medical Education Program, and a team that included lead author doctoral student Aaron Simmons, were able to stimulate growth of new neural connections in mice that are needed to connect the cells into neural circuits. Their study, which included scientists from the University of Louisville and University of Puerto Rico-Humacao, is titled “DSCAM-Mediated Control of Dendritic and Axonal Arbor Outgrowth Enforces Tiling and Inhibits Synaptic Plasticity.” It was published today in the Journal Proceedings of the National Academy of Sciences.

    “The paper is a study into factors that prevent adult neurons from making new connections,” Fuerst said. “Regulation of this process is important to prevent several disorders, such as autism, but is also related to the inability of the adult nervous system to readily recover from damage.”

    Researchers studied a cell population that has the unusual ability to make new connections into adulthood, but under normal conditions does not grow the needed axons or dendrites. The team was able to genetically manipulate the cell population in the mice to induce axon and dendrite outgrowth. They found this induced the formation of stable, functional connections with new cells.

    “The idea is that one could stimulate the nervous system to make new connections if there was some kind of trauma,” Fuerst said. “Maybe this is the way to reactivate the cell to build those new connections that we can take advantage of clinically.”

    Their efforts included research through the regional WWAMI Medical Education Program at the University of Washington and could have wide ramifications for other adult neurological conditions that prevent human brains from making those needed connections as an adult.

    “In children in early development it’s very easy to make new connections, but adults lose that ability, and we want to see why that is,” he said.

    The genetic manipulation used in mice as part of the study wouldn’t work in humans. Instead, Fuerst and his team would next like to test small-molecule drugs that regulate these central nervous system processes — currently used to combat cancer in humans — to see if they can help the nervous system make new connections in mice.

    “These contributions by Peter and his team right here at the University of Idaho are helping advance global neurological research,” said Janet Nelson, vice president for research and economic development. “I’m excited by the potential impact of this research on the understanding of the brain and in advancing human health.”