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Behavior

Running with a Safer Beat: Marathon Cardiac Deaths Plummet

New findings indicate that while the rate of marathon runners who suffer cardiac arrests remained unchanged, their chance for survival is twice what it was in the past. Now, far fewer marathon runners who suffer cardiac arrest are dying of it.

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Running with a Safer Beat: Marathon Cardiac Deaths Plummet

In recent years, an increasing number of people have taken up running as a sport. While this trend has many benefits, it also poses certain risks, particularly when it comes to cardiac health. However, according to a new study published in JAMA, the risk of dying from a heart attack during a marathon has dramatically decreased over the past decade.

Jonathan Kim, an associate professor at Emory School of Medicine, led the research and followed up on his 2012 study into unexpected cardiac arrests during long-distance running events. The new findings indicate that while the rate of marathon runners who suffer cardiac arrests remained unchanged, their chance for survival is twice what it was in the past.

What’s behind this significant decline? Kim attributes it to the growing awareness within the sport about the risks and the need for emergency services to be available to runners. He notes that a vast majority of survivors received immediate access to an automated external defibrillator (AED) after experiencing cardiac arrest, which significantly improved their chances of survival.

This trend is comparable to other public places where AEDs are routinely made available, such as airports and casinos. These locations have also seen declines in deaths due to cardiac arrests. Kim emphasizes that making CPR training available to race participants and strategically placing defibrillators along the racecourse can further reduce the risk of cardiac arrest during marathons.

The study also highlights the importance of identifying vulnerable individuals before they participate in a marathon, particularly older runners with unrecognized cardiovascular risk factors. By doing so, primary preventive cardiovascular care can be improved, potentially reducing the risk of cardiac arrest even further.

As recreational running continues to grow in popularity, it’s reassuring to know that efforts are being made to ensure that participants have access to the necessary medical support and training to minimize risks. With continued research and improvements in emergency response, running with a safer beat is becoming an increasingly achievable reality.

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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