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Tai chi, yoga, and jogging may be the best forms of exercise to improve sleep quality and ease insomnia, suggest the findings of a comparative pooled data analysis published in the online journal BMJ Evidence Based Medicine.

The study, which involved 1348 participants and 13 different treatment approaches to ease insomnia, found that these three exercise-based interventions showed promising results. Yoga likely resulted in a large increase in total sleep time of nearly 2 hours and may improve sleep efficiency by nearly 15%. Walking or jogging may result in a large reduction in insomnia severity of nearly 10 points, while Tai Chi may reduce poor sleep quality scores by more than 4 points, increase total sleep time by more than 50 minutes, and reduce time spent awake after falling asleep by over half an hour.

Further in-depth analyses revealed that Tai Chi performed significantly better on all subjectively and objectively assessed outcomes than existing treatments for up to 2 years. The researchers suggest that Tai Chi’s focus on body awareness, controlled breathing, and attentional training may alter brain activity, thereby alleviating anxiety and depressive symptoms which often interfere with a good night’s sleep.

The study also found that exercise-based interventions, including yoga, Tai Chi, and walking or jogging, have the potential to serve as viable primary treatment options for insomnia. The researchers conclude that these interventions are well-suited for integration into primary care and community health programs due to their low cost, minimal side effects, and high accessibility.

Overall, the findings of this study further underscore the therapeutic potential of exercise interventions in the treatment of insomnia, suggesting that their role may extend beyond adjunctive support to serve as viable primary treatment options.

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.

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.