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Neuroscientist: Brain Surgery Can Create “Two Conscious Entities”

Christof’s idea that split brain patients have split consciousness doesn’t really make sense and doesn’t correspond to the evidence. Consciousness is metaphysically simple — that is, my thoughts and sense of self can’t be split with a knife like the brain or a material thing can be split. What would it mean to say that I have “split” consciousness? Instead of Mike, there would be Mike and Joe, which wouldn’t be “split,” it would just be two people.

A category error

‘Split consciousness’ is an oxymoron, a category error. Consciousness is not the kind of thing that can be split, and there’s no evidence that one person can ever become two people. It’s science fiction, not science.

New IQ research shows why smarter people make better decisions

Smarter people don’t just crunch numbers better—they actually see the future more clearly. Examining thousands of over-50s, Bath researchers found the brightest minds made life-expectancy forecasts more than twice as accurate as those with the lowest IQs. By tying cognitive tests and genetic markers to real-world predictions, the study shows how sharp probability skills translate into wiser decisions about everything from crossing the road to planning retirement—and hints that clearer risk information could help everyone close the gap.

3D-printed magnetoelastic smart pen may help diagnose Parkinson’s

Every year, tens of thousands of people with signs of Parkinson’s disease go unnoticed until the incurable neurodegenerative condition has already progressed.

Motor symptoms, such as tremors or rigidity, often emerge only after significant neurological damage has occurred. By the time patients are diagnosed, more than half of their dopamine-producing neurons may already be lost. This kind of diagnostic delay can limit treatment options and slow progress on early-stage interventions.

While there are existing tests to detect biomarkers of Parkinson’s, including cell loss in the brain and inflammatory markers in blood, they typically require access to specialists and costly equipment at major medical centers, which may be out of reach for many.

Striking parallels between biological brains and AI during social interaction suggest fundamental principles

UCLA researchers have made a significant discovery showing that biological brains and artificial intelligence systems develop remarkably similar neural patterns during social interaction. This first-of-its-kind study reveals that when mice interact socially, specific brain cell types synchronize in “shared neural spaces,” and AI agents develop analogous patterns when engaging in social behaviors.

The study, “Inter-brain neural dynamics in biological and artificial intelligence systems,” appears in the journal Nature.

This new research represents a striking convergence of neuroscience and artificial intelligence, two of today’s most rapidly advancing fields. By directly comparing how biological brains and AI systems process social information, scientists reveal fundamental principles that govern across different types of intelligent systems.

Uncertainty—not just social context—drives brain activity when we ‘read the minds’ of others, psychologists find

Imagine you are about to confront a friend about a hurtful comment she made and are trying to predict her response. Depending on what you know about your friend, you might infer that she will understand where you’re coming from and apologize, get defensive, or respond with criticism of you.

This process of trying to predict other people’s beliefs, intentions, and emotions is known as mentalizing, and the dorsal medial prefrontal cortex (DMPFC) is one of the key brain regions that make up what is known as the “mentalizing network.” Studies have shown that the network is more engaged during mentalizing than when people make other kinds of inferences, such as about objects—like the comfort of a chair—or human physical traits.

But new research from psychologists at the University of Pennsylvania challenges the interpretation of these findings by highlighting a confounding variable in DMPFC activation: uncertainty.

Does a prospective father’s gut microbiota matter?

Germline cells play a key role in the transmission of phenotypes and physiological adaptations to subsequent generations (1). Over a century ago, August Weismann proposed that changes in somatic cells cannot be passed on to germ cells or offspring, a theory known as the Weismann barrier (2). Nevertheless, recent studies have proven that the Weismann barrier is permeable, and information can pass from soma to germline and modulate offspring phenotypes. In the past decade, there has been tremendous interest and progress in understanding how an altered microbiome (dysbiosis) affects different somatic cells that compose body tissues, such as brain, liver, heart, kidney, and lungs (3). Nevertheless, whether gut microbiome dysbiosis can exert an influence on the mammalian germline cells (i.e., gut to germline), and ultimately nonexposed offspring, remains unclear.

To tackle this research question, my colleagues and I established an inducible model of gut microbiota dysbiosis in isogenic male mice, using ad lib nonabsorbable antibiotics (nABX) that cannot cross the epithelial barrier of the gut (4). As expected, 6 weeks of low-dose nABX treatment led to a physiologically significant dysbiosis, which is reversible and gradually normalized to a physiologically healthy gut microbiota after 8 weeks of nABX withdrawal (6 weeks + 8 recovery). The induced dysbiosis after 6 weeks of nABX had no appreciable effects on male body weight, growth, or fertility. No nABx residues were detected in the serum or testes of treated males, which confirmed that any distal tissue responses are gut dysbiosis–induced rather than systemic drug effects.

We then examined physiological changes in the male reproductive system in response to 6 weeks of dysbiosis. Dysbiotic males had smaller testes, lower sperm count, and more abnormally shaped sperm. Histological analysis uncovered a wide range of anatomical abnormalities in testes of dysbiotic males, including increased number of abnormal seminiferous tubules, reduced epithelial thickness, and absence of mitotic compartments, which were not observed in control testes. Testicular metabolomic profiles revealed that testes clustered according to gut microbiota status and exhibited dysregulated sphingolipids, glycerophospholipids, and endocannabinoids, all known to play pivotal roles in germ cell function. Moreover, in dysbiotic male testes, spermatogenesis-regulating genes were misexpressed—most notably leptin, a reproductive hormone, was strongly down-regulated.

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