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Category: neuroscience

Moral inconsistency is based on the vmPFC’s insufficient representation across tasks and connectedness

A new Cell Reports study looked at why people sometimes judge others harshly for dishonest behavior while excusing similar behavior in themselves. The researchers call this moral inconsistency: a mismatch between the moral standards someone uses to judge others and the standards they apply to their own behavior. The study used an honesty-versus-profit task, where participants could gain money by being dishonest, and then judged both their own behavior and other people’s behavior.

The main finding was that people who were more morally inconsistent showed weaker involvement of the ventromedial prefrontal cortex, or vmPFC, a brain region involved in value-based decision-making, social judgment, emotion regulation, and moral evaluation. In morally consistent participants, the vmPFC seemed to represent moral judgment more similarly across “judging myself” and “judging others.” In morally inconsistent participants, that cross-task representation was weaker, especially when they were making choices for themselves.

Liu. V, et al. find that moral inconsistency arises from a reduced ability of the vmPFC to form a cross-task representation of moral principles and its connectedness during the moral behavior task. This indicates that individuals with higher moral inconsistency consider moral principles less often to guide their own behavior.

Brain enzyme caught doing something unexpected—it builds polysialic acid on itself

A chance discovery at Nagoya University in Japan has shown that a well-known brain enzyme has a hidden ability: It builds a sugar chain on itself, becomes secreted from the cell and deactivates, then switches on outside the cell once the chain is removed. The finding, published in the Journal of Biological Chemistry, overturns a decades-old assumption about how polysialic acid, a sugar chain critical for brain development and function, is produced and shows a new way an enzyme can regulate its own activity.

The human brain is covered in sugar chains, or glycans, molecular structures that coat cells and regulate how they communicate. One of the most important is polysialic acid, a long chain found mainly in the brain.

Polysialic acid keeps brain cells from adhering too tightly to each other and binds to growth factors and neurotrophins to regulate the presentation of their receptors. Through this, it plays a key role in learning, memory and neural development. Importantly, these sugar chains change rapidly in response to brain activity. The ability to restore them quickly is thought to be essential for normal brain function.

Before tangles kill neurons, tau-linked transport defects may be reversible

Neurons, specialized cells that transmit information across the nervous system, communicate with each other via projections known as axons. These microscopic, cable-like structures are also used to deliver proteins, signaling molecules and other cargo across different areas of the brain.

Past studies have found that this transfer of cargo, also known as axonal transport, is impaired in models of diseases known as tauopathies. Tauopathies include Alzheimer’s disease (AD), frontotemporal dementia and other neurodegenerative diseases associated with the pathological accumulation of a protein called tau inside neurons, which forms structures known as tau tangles.

Researchers at the UK Dementia Research Institute at University College London (UK DRI, UCL) and the UCL Queen Square Institute of Neurology recently carried out a study in mice aimed at investigating the link between tauopathies and axonal transport. Their findings, published in Nature Neuroscience, show that axonal transport defects prompted by the aggregation of pathological tau could be reversible, identifying a possible strategy for reversing this damage during the early stages of neurodegeneration.

Restless legs syndrome—zebrafish reveal a cerebellar connection

An irresistible urge to move the legs or other areas, often accompanied by unpleasant sensations at night or during rest: Restless Legs Syndrome (RLS) affects millions of people worldwide. Despite being one of the most common sleep-related disorders, its biological causes remain poorly understood.

Researchers led by Professor Alex Schier at the Biozentrum of the University of Basel have discovered new clues about the underlying brain regions and mechanisms. Surprisingly, their findings come from an unlikely model organism: larval zebrafish.

“Studies in humans have implicated many different brain regions, but it remains unclear how they relate to RLS,” says Schier. “Our work highlights possible contributions from the cerebellum, a brain region crucial for coordinating movement.”

Scientists Let People Play Video Games Using Only Their Thoughts

Researchers developed a brain-controlled gaming system that learns from the brain’s natural wiring, enabling fast BCI training and potentially transforming medicine, mental health, and human-computer interaction. It may not be long before video game controllers become optional. Researchers at

The APOE-R136S mutation protects against APOE4-driven Tau pathology, neurodegeneration and neuroinflammation

Nelson et al. present a detailed biomolecular study of how the APOE-R136S mutation protects against Alzheimer’s disease (AD) in mice and in patient-derived cells. Lots of data on glial contributions and transcriptomic changes. I see this as an excellent target for gene therapies aiming to combat AD. So do the folks at Lexeo Therapeutics (an exciting company you should check out!)

Nelson et al. report that the APOE-R136S mutation protects against APOE4-promoted Alzheimer’s disease pathologies, including phosphorylated Tau accumulation, neuroinflammation and neurodegeneration, in mouse and human neuron models.

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