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People diagnosed with various mental health disorders can sometimes start engaging in intense political behavior, such as violent protests, civil disobedience and the aggressive expression of political views. So far, however, the link between political behavior and the brain has been rarely explored, as it was not viewed as central to the understanding of mental health disorders.

Researchers at Harvard Medical School, Stanford University School of Medicine and Northwestern University Feinberg School of Medicine recently carried out a study investigating the neural underpinnings of political behavior. Their findings, published in Brain, unveil the existence of a brain circuit that is associated with the intensity of people’s political involvement, irrespective of their ideology or party affiliation.

“This paper started out as a collaborative effort that focused on learning how to help people better come together and thrive, alongside Stephanie Balters at Stanford,” Shan H. Siddiqi, first author of the paper, told Phys.org.

Beijing Normal University-led researchers have identified specific high-order thalamic nuclei that drive human conscious perception by activating the prefrontal cortex. Their findings enhance understanding of how the brain forms conscious experience, offering new empirical support for theories that assign a central role to thalamic structures rather than cortical areas alone.

Consciousness has been described as existing in two distinct forms: the general state of being awake or asleep, and the specific contents of subjective awareness. Most studies investigating the neural basis of have focused on the cerebral cortex.

Subcortical structures, including high-order thalamic nuclei, remain comparatively unexplored, ill-accounting for how rapidly shifting becomes part of .

A recent study published in The Journal of Neuroscience has found evidence for a link between breathing patterns and brain activity during anxious states. Researchers found that rats experiencing anxiety-like behavior in a common behavioral test breathed more rapidly and that this change in breathing influenced brain rhythms in a key frontal brain area. The study highlights how shifts in respiration actively shape how the brain functions during emotional experiences.

Scientists have long known that feelings of anxiety can trigger physical changes in the body, including alterations in breathing. Previous research has shown that breathing influences brain activity, particularly in areas involved in processing smells and in the front part of the brain. This connection between breathing and brain function has been especially well-documented in relation to fear, where slow, steady breathing is often linked to freezing behavior in rodents. However, it remained unclear whether breathing plays a similar role in other negative emotional states like anxiety, which tends to involve faster breathing.

To investigate this, researchers set out to understand how breathing affects brain activity in situations that evoke anxiety. They used a widely accepted method for studying anxiety in rodents called the elevated plus maze. This maze is shaped like a plus sign and has two arms that are enclosed and two that are open and exposed. Because rats naturally prefer the safety of enclosed spaces, spending time in the open arms is considered an indication of anxiety-like behavior.

Damage to the mitochondria, the “power plants” of the cells, contributes to many diseases. Researchers from Heinrich Heine University Düsseldorf (HHU) and the University of Cologne led by HHU professor of medicine Dr David Pla-Martín, now describe in the scientific journal Science Advances how cells with defective mitochondria activate a special recycling system to eliminate damaged genetic material.

Damage to the genetic material of mitochondria – the mitochondrial DNA or mtDNA for short – can lead to diseases such as Parkinson’s, Alzheimer’s, amyotrophic lateral sclerosis (ALS), cardiovascular diseases and type 2 diabetes. Such damage also speeds up the ageing process. However, the cells are normally capable of identifying such damage and reacting.

Damage to the genetic material of mitochondria—the mitochondrial DNA or mtDNA for short—can lead to diseases such as Parkinson’s, Alzheimer’s, amyotrophic lateral sclerosis (ALS), cardiovascular diseases and type 2 diabetes. Such damage also speeds up the aging process. However, the cells are normally capable of identifying such damage and reacting.

Scientists from University Hospital Düsseldorf and HHU have—in collaboration with the University of Cologne and the Center for Molecular Medicine Cologne (CMMC)—discovered a mechanism which protects and repairs the mitochondria. The research team, headed by Professor Pla-Martín from the Institute of Biochemistry and Molecular Biology I at HHU, has identified a specialized recycling system, which cells activate when they identify damage to the mtDNA.

According to the authors in Science Advances, this mechanism relies on a known as retromer and the lysosomes—cell organelles containing digestive enzymes. These special cellular compartments act like recycling centers, eliminating the damaged genetic material.