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Researchers from the Netherlands Institute for Neuroscience have, for the first time, witnessed nerve plasticity in the axon in motion.

Our nerve cells communicate through rapid transmission of electrical signals known as action potentials. All action potentials in the brain start in one unique small area of the cell: the axon initial segment (AIS). This is the very first part of the axon, the long, thin extension of a nerve cell that transmits signals or impulses from one nerve cell to another. It acts as a control center where it is decided when an action potential is initiated before traveling further along the axon.

Previously, researchers made the surprising observation that plasticity also occurs at the AIS. Plasticity refers to the brain’s ability to create new connections and structures in order to scale the amount of electrical activity, which is crucial for learning and memory. AIS plasticity occurs during changes in brain network activity. The segment’s length can become shorter with excessive activity or longer with low activity. But how does this structure change, and how quickly does it happen? Amélie Fréal and Nora Jamann in the lab of Maarten Kole have, for the first time, observed in real-time how this adaptability functions within the axon and identified the molecular mechanisms behind this process.

A new review published in The Lancet Neurology by researchers at Mass General Brigham presents findings indicating that cardiovascular disease risk may be increased by traumatic brain injury (TBI). The review presented evidence of the long-term associations between TBI and cardiovascular disease noting that post-injury comorbidities, as well as neuroinflammation, and changes in the brain-gut connection may be culprits in the elevated risk compared to the general population.

“Despite decades of extensive traumatic brain-injury-focused research, surprisingly, there has been minimal progress in mitigating long-term outcomes and mortality following injuries. The cardiovascular effects of TBI may be a missing link in advancing our efforts to improve long-term quality of life and reducing mortality rates in TBI patients,” said first author Saef Izzy, MD, of the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital. “We have the opportunity to identify and improve targeted screening for high-risk populations, build preventative care strategies and improve outcomes for survivors of TBI.”

While past research has exhibited there is a strong link between TBI and neurodegenerative conditions such as Alzheimer’s disease and dementia, decades of research has failed to understand the mechanisms that occur after a TBI that drive these diseases. Izzy and review co-authors now suggest that there may be non-neurological effects of TBI, including cardiovascular, cardiometabolic, and endocrine dysfunction that may act as intermediaries that contribute to neurological disorders that may appear decades later.

A letter, signed by 124 scholars and posted online last week, has caused an uproar in the consciousness-research community. It argues that a prominent theory describing what makes someone or something conscious — called the integrated information theory (IIT) — should be labelled as pseudoscience. Since its publication on 15 September in the preprint repository PsyArXiv1, the letter has resulted in some researchers arguing over the label and others worrying that it will increase polarization in a field that has grappled with issues of credibility in the past.

Decades-long bet on consciousness ends — and it’s philosopher 1, neuroscientist 0

“I think it’s inflammatory to describe IIT as pseudoscience,” says neuroscientist Anil Seth, director of the Centre for Consciousness Science at the University of Sussex near Brighton, UK, adding that he disagrees with the label. “IIT is a theory, of course, and therefore may be empirically wrong,” says Christof Koch, a meritorious investigator at the Allen Institute for Brain Science in Seattle, Washington, and a proponent of the theory. But he says that it makes its assumptions — for example, that consciousness has a physical basis and can be mathematically measured — very clear.

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University of Basel.

People differ significantly in their memory performance. Researchers at the University of Basel have now discovered that certain brain signals are related to these differences.

While it is well known that certain brain regions play a crucial role in memory processes, so far it has not been clear whether these regions exhibit different activities when it comes to storing information in people with better or worse memory performance.

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New research hints at a few ways fatty foods affect cells in the brain, a finding that could help explain the link between a high-fat diet and impaired memory – especially as we age.

The Ohio State University study in cell cultures found the omega-3 fatty acid DHA may help protect the brain from an unhealthy diet’s effects by curbing fat-induced inflammation at the cellular source.

Separate experiments using brain tissue from aging mice showed a high-fat diet may lead specific brain cells to overdo cell-signaling management in a way that interferes with the creation of new memories.

An experimental neuroimaging study in Poland found that exposure to hate speech diminishes the brain’s response to stories about other people suffering. The effect was present irrespective of the group membership of the person suffering in the story – whether they were Polish, like the participants, or Arab. The study was published in Scientific Reports.

Hate speech is a form of communication that involves the expression of discriminatory, hostile, or prejudiced sentiments and ideas directed towards individuals or groups based on their race, ethnicity, religion, gender, sexual orientation, disability, or other characteristics.

Exposure to hate speech deteriorates neurocognitive mechanisms of the ability to understand others’ pain, was authored by Agnieszka Pluta, Joanna Mazurek, Jakub Wojciechowski, Tomasz Wolak, Wiktor Soral, and Michał Bilewicz.

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Scientists have identified two types of brain cell linked to a reduced risk of dementia in older people — even those who have brain abnormalities that are hallmarks of Alzheimer’s disease1.

The finding could eventually lead to new ways to protect these cells before they die. The results were published in Cell on 28 September.

Plaques in the brain.

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Restoration of lost memories.

Prof Bryce Vissel, who leads the Clinical Neuroscience and Regenerative Medicine Initiative (CNRM) at St Vincent’s Centre for Applied Medical Research, and his team, have identified a molecule in the brain that controls loss of nerve cell connections.

This molecule we are calling ‘the switch’ is decreased in the Alzheimer’s brain but no one really understands why, or what role it plays. When ‘encouraged’ or ‘forced’ to be expressed normally again, in our laboratory tests of a mouse model, this molecule can actually rescue its memory.

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In a Stanford Medicine study, scientists transplanted stem cells into mice and found reduction of brain abnormalities typical of Alzheimer’s disease.