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Behavior

Groundbreaking Study Shows Vagus Nerve Stimulation Can Eliminate PTSD Symptoms for Up to Six Months

In a recent clinical study, patients with treatment-resistant post-traumatic stress disorder were symptom-free up to six months after completing traditional therapy paired with vagus nerve stimulation.

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Groundbreaking Study Shows Vagus Nerve Stimulation Can Eliminate PTSD Symptoms for Up to Six Months

A historic clinical trial conducted by researchers from The University of Texas at Dallas (UTD) and Baylor University Medical Center has demonstrated that patients with treatment-resistant post-traumatic stress disorder (PTSD) can experience significant long-term benefits when paired with vagus nerve stimulation (VNS). The results, published in Brain Stimulation, show that all nine participants remained symptom-free for up to six months after completing traditional therapy along with VNS.

Dr. Michael Kilgard, the Margaret Fonde Jonsson Professor of neuroscience at UTD’s School of Behavioral and Brain Sciences, expressed his excitement about the outcome, stating, “In a trial like this, some subjects usually do get better, but rarely do they lose their PTSD diagnosis. Typically, the majority will have this diagnosis for the rest of their lives.” Kilgard emphasized that the 100% loss of diagnosis among participants is “very promising.”

The study employed prolonged exposure therapy, a form of cognitive behavioral therapy, in conjunction with short bursts of VNS delivered via an implantable device. Assessments were conducted four times during the six months following the completion of the standard 12-session therapy course. The benefits persisted throughout this period for all nine participants.

This research represents the largest clinical trial to date utilizing an implanted device for PTSD treatment, according to Kilgard. Pioneering work by UTD researchers has previously demonstrated that VNS paired with physical rehabilitation can accelerate neuroplasticity – the rewiring of areas in the brain. Their 13-year effort to treat a wide variety of conditions using VNS has resulted in FDA approval for treating impaired upper-limb movement in stroke patients.

The National Center for PTSD estimates that 5% of adults in the U.S. have post-traumatic stress disorder in any given year, with women being twice as likely to develop PTSD at some point in their life. Many PTSD patients fail to respond to therapy or experience intolerable side effects or relapse, leaving them with no viable prospect for remission.

Kilgard emphasized that PTSD patients are not limited to military veterans but can also be found among average citizens who have faced traumatic events. “When you hear PTSD, you may picture a combat zone, but it’s much more prevalent than that,” he said. “It can stem from any event that inspires fear of death or bodily injury, or death of a loved one.”

The next step in the PTSD research – a double-blind, placebo-controlled Phase 2 pilot study – is ongoing in Dallas and Austin. Researchers hope that it will represent another step toward FDA approval of a treatment that doesn’t exist now, and it would be invented, tested, and delivered by UTD, as was the case for upper-limb recovery after stroke.

Licensed clinical psychologist Dr. Mark Powers, a research center director of the Trauma Research Center at Baylor University Medical Center, is the lead author of the study. He expressed his enthusiasm about VNS, stating that it has “changed the game” by improving both treatment efficacy and its tolerability.

Powers added that his collaboration with UTD has a multidisciplinary synergy that he regards as rare. “With this alliance, we have people doing the preclinical and the clinical work at the same time, giving each other feedback and ideas,” he said. “Neither one of our groups could do this alone.”

The research was funded by a grant from the Biological Technologies Office at the Defense Advanced Research Projects Agency.

Behavior

Unraveling the Mind: How a Scent Can Change Your Decisions

Mice taught to link smells with tastes, and later fear, revealed how the amygdala teams up with cortical regions to let the brain draw powerful indirect connections. Disabling this circuit erased the links, hinting that similar pathways in humans could underlie disorders like PTSD and psychosis, and might be tuned with future brain-modulation therapies.

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The human brain is a masterful machine that makes decisions based on associations between stimuli in our environment. But did you know that these decisions can also be influenced by indirect associations between seemingly unrelated events? A recent study by the Cellular Mechanisms in Physiological and Pathological Behavior Research Group at the Hospital del Mar Research Institute has shed new light on this process, revealing how a specific scent can alter our mind’s decision-making processes.

The research team, led by PhD student José Antonio González Parra and supervised by Dr. Arnau Busquets, conducted experiments with mice to understand the mechanisms behind indirect associations between different stimuli. They trained the mice to associate two distinct smells – banana and almond – with sweet and salty tastes respectively. Later, a negative stimulus was linked to the smell of banana, causing the mice to reject the sweet taste associated with it.

The researchers used genetic techniques to observe which brain areas were activated throughout this process. They found that the amygdala, a region linked to responses such as fear and anxiety, played a crucial role in encoding and consolidating these associations. Other brain areas also interacted with the amygdala, forming a brain circuit that controls indirect associations between stimuli.

Dr. Busquets explained that if amygdala activity was inhibited while the mice were exposed to the stimuli, they were unable to form these indirect associations. This finding has significant implications for treating mental disorders linked to amygdala activity, such as PTSD and psychosis.

The researchers believe that the brain circuits involved in decision-making processes in humans are similar to those in mice. Therefore, understanding these complex cognitive processes can help us design therapeutic strategies for humans, including brain stimulation or modulation of activity in specific areas.

In conclusion, this study has revealed how a scent can change our mind’s decisions by altering indirect associations between stimuli. By exploring the neural mechanisms behind this process, we may be able to develop innovative treatments for mental disorders that affect millions of people worldwide.

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Autism

Unpacking the Gene That Hijacks Fear: How PTEN Rewires the Brain’s Anxiety Circuit

Deleting a gene called PTEN in certain brain cells disrupts the brain’s fear circuitry and triggers anxiety-like behavior in mice — key traits seen in autism. Researchers mapped how this genetic tweak throws off the brain’s delicate balance of excitation and inhibition in the amygdala, offering deep insights into how one gene can drive specific ASD symptoms.

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The gene PTEN has emerged as one of the most significant autism risk genes. Variations in this gene are found in a significant proportion of people with autism who also exhibit brain overgrowth. Researchers at the Max Planck Florida Institute for Neuroscience have discovered how loss of this gene rewires circuits and alters behavior, leading to increased fear learning and anxiety in mice – core traits seen in ASD.

PTEN has been linked to alterations in the function of inhibitory neurons in the development of ASD. The researchers focused on the changes in the central lateral amygdala driven by loss of PTEN in a critical neuronal population – somatostatin-expressing inhibitory neurons. They found that deleting PTEN specifically in these interneurons disrupted local inhibitory connectivity in the amygdala by roughly 50% and reduced the strength of the remaining inhibitory connections.

This diminished connectivity between inhibitory connections within the amygdala was contrasted by an increase in the strength of excitatory inputs received from the basolateral amygdala, a nearby brain region that relays emotionally-relevant sensory information to the amygdala. Behavioral analysis demonstrated that this imbalance in neural signaling was linked to heightened anxiety and increased fear learning, but not alterations in social behavior or repetitive behavior traits commonly observed in ASD.

The results confirm that PTEN loss in this specific cell type is sufficient to induce specific ASD-like behaviors and provide one of the most detailed maps to date of how local inhibitory networks in the amygdala are affected by genetic variations associated with neurological disorders. Importantly, the altered circuitry did not affect all ASD-relevant behaviors – social interactions remained largely intact – suggesting that PTEN-related anxiety and fear behaviors may stem from specific microcircuit changes.

By teasing out the local circuitry underlying specific traits, researchers hope to differentiate the roles of specific microcircuits within the umbrella of neurological disorders, which may one day help in developing targeted therapeutics for specific cognitive and behavioral characteristics. In future studies, they plan to evaluate these circuits in different genetic models to determine if these microcircuit alterations are convergent changes that underlie heightened fear and anxiety expression across diverse genetic profiles.

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Amyotrophic Lateral Sclerosis

“Reviving Memories: Gene Therapy Shows Promise in Reversing Alzheimer’s Disease in Mice”

UC San Diego scientists have created a gene therapy that goes beyond masking Alzheimer’s symptoms—it may actually restore brain function. In mice, the treatment protected memory and altered diseased brain cells to behave more like healthy ones.

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The field of neuroscience has made significant strides in understanding the complex mechanisms behind Alzheimer’s disease. A recent study by researchers at the University of California San Diego School of Medicine offers a glimmer of hope for those affected by this debilitating condition. By developing a gene therapy that targets the root cause of Alzheimer’s, these scientists may have found a way to not only slow down but also potentially reverse memory loss.

Alzheimer’s disease is a progressive disorder that affects millions worldwide. It occurs when abnormal proteins build up in the brain, leading to the death of brain cells and declines in cognitive function and memory. While existing treatments can manage symptoms, they do little to halt or reverse the progression of the disease. This new gene therapy, however, promises to address the underlying issue by influencing the behavior of brain cells themselves.

The researchers conducted their study using mice as models for human Alzheimer’s patients. They found that delivering the treatment at the symptomatic stage of the disease preserved hippocampal-dependent memory – a critical aspect of cognitive function often impaired in Alzheimer’s patients. Moreover, the treated mice had a similar pattern of gene expression compared to healthy mice of the same age, suggesting that the treatment has the potential to alter diseased cells and restore them to a healthier state.

While further studies are required to translate these findings into human clinical trials, this gene therapy offers a unique and promising approach to mitigating cognitive decline and promoting brain health. As researchers continue to refine and develop this technology, we may soon see a future where Alzheimer’s patients can experience a significant reversal of memory loss – a truly remarkable prospect that could revolutionize the way we understand and treat this devastating disease.

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