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Category: neuroscience – Page 98

Health during pregnancy does not cause autism, according to a study of 1.1M pregnancies. Genetics and fetal complications play a much larger role, challenging long-held assumptions about autism risk factors. +.

Summary: A large study analyzing over 1.1 million pregnancies found no strong evidence that maternal health conditions during pregnancy cause autism. Instead, nearly all previously reported associations between maternal diagnoses and autism could be explained by genetic or environmental factors.

Researchers found that only fetal complications remained statistically linked to autism, suggesting these issues might be early signs rather than causes. By analyzing sibling and paternal health records, the study further ruled out many maternal conditions as contributing factors.

The findings emphasize that autism likely begins before birth due to genetic influences rather than maternal health conditions. This research may help alleviate guilt for parents and shift focus toward early diagnosis and support.

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Summary: Scientists have used advanced X-ray phase-contrast tomography (XPCT) to uncover how gut health may influence Alzheimer’s disease. The study found structural changes in the gut of Alzheimer’s-affected mice, revealing abnormalities in intestinal cells, neurons, and mucus secretion.

This supports the hypothesis that harmful gut bacteria may escape into circulation, triggering brain inflammation and neurodegeneration. The findings highlight the gut-brain connection and provide a new tool for detecting early disease markers.

Researchers aim to further explore how the enteric nervous system communicates with the brain in Alzheimer’s. The study paves the way for potential new therapeutic targets based on gut health.

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Random noise, such as background hubbub on a phone call, is usually thought of as unwanted interference. Now researchers at Columbia Engineering find the brain may harness unavoidable random fluctuations of its activity to perform useful computations, particularly in tasks relying on memory.

These findings not only deepen our understanding of how the brain works, but also may provide a blueprint for building smarter, more resilient technologies, the research team says.

They detailed their findings Jan. 16 in the Proceedings of the National Academy of Sciences.

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A major trial in frontotemporal dementia patients has found that oxytocin can help improve symptoms of apathy. A new study led by Western researchers suggests that frequent treatment with intranasal oxytocin—a hormone linked to empathy—may help reduce apathy in patients with frontotemporal dementia (FTD).

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Carboncopies mind uploading workshop 🧠 🤖 2/22/25 $55 online.

https://www.eventbrite.com/e/brain-emulation-challenge-works…4113147839

A Two-Part Series of Workshops.
This workshop is the first in a two-part series designed to result in hands-on experience for a community of innovators driving progress in brain emulation. While this session focuses on knowledge-sharing, it also serves as an invitation to join a pioneering movement. Attendees will connect with peers and experts, engage in discussions on emerging research, and explore ways to collaborate and support this transformative work.

Join us as we lay the foundation for a rigorous, standardized, and open approach to brain emulation and related goals.

Eventbrite Page.

Continue reading “The Brain Emulation Challenge Workshop Part 1 Teaser” | >

It is commonly believed that there is a mind-body problem because we can give an explanation of matter but not of the mind. But according to John Collins, we don’t understand matter either. Materialism was refuted by Newton in the 17th century, and the physicalism which has replaced it is not a substantive doctrine. There are gaps in our understanding of the mental – we still do not have a good theory of what the mind is – but after Newton, there is no ‘mind-body problem’

Minds are problematic. We don’t quite know what they are. If one has a mind, let us agree, then one is sentient and sapient, able to be self-aware and to think and reason about things. But both of these qualities are opaque, not least because they have no apparent analogy in the non-mental world. What, exactly, does one need to add to a body to get a mind? How is a thing that is merely subject to physical laws self-aware and able to think about dinosaurs and the afterlife? This conundrum is invariably depicted in terms of there being a mind-body problem. I’ll try in what follows to give you reasons to think that this label is at best misleading. There are lots of mind problems and lots of body problems, but no mind-body problem, because there is no realm of bodies in some general sense from which minds are excluded. Before you call for an intervention, let me explain.

A potted history.

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A significant advancement in knowledge of the link between cognition and genetics has been made thanks to a study led by Université de Montréal graduate students Guillaume Huguet and Thomas Renne, working under the supervision of medical geneticist Sébastien Jacquemont, an associate professor of pediatrics and a researcher at the UdeM-affiliated CHU Saint-Justine.

Published in Cell Genomics, the research explored how the copy number variation, or CNV, of certain DNA segments can influence cognitive abilities.

Analyzing the CNV of nearly 260,000 people in the general population, the scientists were able to compare each individual’s CNV and cognition to define a reference model—a kind of “map” of the effects of CNV on cognition, such as the intelligence quotient and memory—and to establish links between these CNVs and achievements within the brain, as well as in other organs and tissues.

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Common genetic variants may underlie autism spectrum disorder and schizophrenia across human populations, according to a study appearing September 11th in the journal Cell Reports. In line with previous studies in Caucasians, the researchers found that Japanese individuals with autism spectrum disorder and schizophrenia have overlapping copy number variations (CNVs)—inter-individual variations in the number of copies of a particular gene.

“The strength of our study is the systematic head-to-head comparison of pathogenic CNVs and biological pathways between and ,” says senior study author Norio Ozaki of Nagoya University Graduate School of Medicine. “Previous studies in Caucasian populations found overlap in pathogenic CNVs between the two disorders, but their analyses were limited to a small number of genes and CNV loci.”

Autism spectrum disorder and schizophrenia have complex inheritance patterns, with multiple genetic and environmental factors influencing disease risk. Available evidence points to genetic overlap between the two clinically distinct disorders. For example, they tend to co-occur at a higher rate than would be expected in the general population, and a large epidemiological study showed that a family history of schizophrenia in first-degree relatives is a risk factor for spectrum disorder. In particular, previous studies have revealed that these two disorders are associated with an increased burden of CNVs, and that rare CNVs in specific loci are shared risk factors for both disorders.

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