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The field “touches on all the questions that humanity has asked since it was walking on this planet,” says Moshe Szyf, a professor of pharmacology at McGill University. “How much of our destiny is predetermined? How much of it do we control?”

For some people, the concept that we can carry a legacy of trauma makes sense because it validates their sense that they are more than the sum of their experiences.

“If you feel you have been affected by a very traumatic, difficult, life-altering experience that your mother or father has had, there’s something to that,” says Rachel Yehuda, professor of psychiatry and neuroscience of trauma at Mount Sinai in New York. Her research points to a small epigenetic “signal” that a life-altering experience “doesn’t just die with you,” she says. “It has a life of its own afterwards in some form.”

If you’ve heard of two of the brain’s chemical neurotransmitters, it’s probably dopamine and serotonin. Never mind that glutamate and GABA do most of the work—it’s the thrill of dopamine as the “pleasure chemical” and serotonin as a tender mood-stabilizer that attract all the headlines.

Of course, the headlines mostly get it wrong. Dopamine’s role in shaping behavior goes way beyond simple concepts like “pleasure” or even “reward”. And the fact that it takes weeks or months for serotonin-boosting SSRI antidepressants to work suggests that it’s not actually the immediate jump in serotonin levels that drum out the doldrums of depression, but some still-mysterious shift in downstream brain circuits.

A new study from Stanford’s Wu Tsai Neurosciences Institute reveals yet another new facet of these mood-managing molecules. The research, published November 25, 2024 in Nature, demonstrates for the first time exactly how dopamine and serotonin work together—or more precisely, in opposition—to shape our behavior.

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The central point made in this paper is this: human-level grounded meaning in an agent can only result from directly experiencing the world, which in turn can only be possible via embodiment (coupled with ‘embrainment’ — a suitable brain architecture).

A spatially resolved single-cell transcriptomics map of the mouse brain at different ages reveals signatures of ageing, rejuvenation and disease, including ageing effects associated with T cells and rejuvenation associated with neural stem cells.

Scientists at Neuro-Electronics Research Flanders (NERF), under the direction of Prof. Vincent Bonin, have released two innovative studies that provide fresh perspectives on the processing and distribution of visual information in the brain. These studies contest conventional beliefs regarding the straightforwardness of visual processing, instead emphasizing the intricate and adaptable nature of how the brain understands sensory information.

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Thanks to their genetic makeup, their ability to navigate mazes and their willingness to work for cheese, mice have long been a go-to model for behavioral and neurological studies.

In recent years, they have entered a new arena—virtual reality—and now Cornell researchers have built miniature VR headsets to immerse them more deeply in it.

The team’s MouseGoggles—yes, they look as cute as they sound—were created using low-cost, off-the-shelf components, such as smartwatch displays and tiny lenses, and offer visual stimulation over a wide field of view while tracking the mouse’s eye movements and changes in pupil size.

Summary: Researchers identified variants in the DDX53 gene, located on the X chromosome, as contributors to autism spectrum disorder (ASD). These genetic variants, found predominantly in males, provide critical insights into the biological mechanisms behind autism’s male predominance.

The study also uncovered another potential gene, PTCHD1-AS, near DDX53, linked to autism, emphasizing the complexity of ASD’s genetic architecture. This research highlights the importance of the X chromosome in ASD and opens avenues for more precise diagnostics and therapeutics.

The findings challenge current models, urging a re-evaluation of how autism is studied. These discoveries mark a significant step in understanding the genetic underpinnings of autism.