We know shockingly little about what goes on in a mother’s brain during pregnancy.

For example, we know only a handful of the hormones involved—out of hundreds scientists think may exist—and very little about how they might impact the brain. This gap in our understanding is one of the reasons we don’t have great treatments for pregnancy-related maladies, whether it’s extreme nausea, or anxiety and depression.

Closing this gap is the mission of the new Stanford Neuro-Pregnancy Initiative, part of the Wu Tsai Neurosciences Institute's Big Ideas in Neuroscience Program.

Today on the show, we speak with initiative leaders Nirao Shah, a neuroscientist who studies sex differences in animal behavior, and Katrin Svensson is an expert in how our tissues use hormones to communicate in health and disease. Together with Longzhi Tan, an expert in gene regulation and 3d genome structure, the team aims to chart the cellular and molecular transformation that occurs in a mother's brain during pregnancy, in hopes of better understanding this fundamental event in a person's life and improving health outcomes for both mothers and infants.

Learn more:

• Big Ideas in Neuroscience tackle brain science of everyday life and more (Wu Tsai Neuro, 2026)
• Nirao Shah lab
• Katrin Svensson lab
• Longzhi Tan lab

References

• Hoekzema, E., Barba-Müller, E., Pozzobon, C., ... Carmona, S., & Vilarroya, O. (2017). Pregnancy leads to long-lasting changes in human brain structure. Nature Neuroscience, 20(2), 287–296. https://doi.org/10.1038/nn.4458 This is the landmark neuroimaging study discussed in the episode that provided the first evidence of long-lasting, pregnancy-induced changes in the structure of the human brain.
• Fejzo, M., Sazonova, O., Sathira-Anuchit, S., ... & MacGibbon, K. (2023). GDF15 underlies nausea and vomiting of pregnancy. Nature, 624(7992), 639-646. https://doi.org/10.1038/s41586-023-06921-9 This recent breakthrough paper provides strong evidence that the hormone GDF15 acts on the brainstem to cause nausea and vomiting in pregnancy.
• Ishii, K. K., Osakada, T., Mori, H., & Shah, N. M. (2017). A Labeled-Line Hypothalamic Circuit for Intraspecific Social Behaviors. Cell, 171(3), 689-703.e15. https://doi.org/10.1016/j.cell.2017.09.018 This is the work from Dr. Shah’s lab mentioned in the episode, identifying a specific circuit in the hypothalamus that changes its connectivity across the estrous cycle to control female mating behavior.

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Here’s a question for you that may at first seem trivial, but is actually profound: Why do our minds drift?

If you have ever dabbled in mindfulness or meditation, you know this mind wandering has an almost gravitational pull. In fact, researchers now think we spend as much as 50 percent of our waking time in this state, which cognitive scientists have dubbed the brain’s “default mode.”

Today’s guest is Vinod Menon. He’s a giant in the field of cognitive science who played a central role in defining the brain “default mode network” back in 2003.

In our conversation, he argues our tendency to daydream may be at the core of our self-identities, our creativity – and also many of our most troubling psychiatric disorders, from Alzheimer’s to ADHD.

Vinod Menon is Rachel L. and Walter F. Nichols, MD., Professor of Psychiatry & Behavioral Science at Stanford Medicine, and an affiliate of the Wu Tsai Neurosciences Institute.

Learn More

• Menon's "Stanford Cognitive & Systems Neuroscience Laboratory"
• Stanford Medicine study identifies distinct brain organization patterns in women and men (Stanford Medicine, 2024)
• Children with autism have broad memory difficulties, Stanford Medicine-led study finds (Stanford Medicine, 2023)
• Interactions between attention-grabbing brain networks weak in ADHD (Stanford Medicine, 2015)

Send us a text!

Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience.

We want to hear from your neurons! Email us at at neuronspodcast@stanford.edu

Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

For decades, Alzheimer's research has focused on clearing amyloid plaques from the brain. But new drugs that successfully remove plaques have proven clinically "underwhelming", leaving the field searching for alternative approaches.

Stanford neurologist Katrin Andreasson has spent twenty years pursuing a different path—investigating how aging triggers an energy crisis in the brain's immune and support cells. Her work reveals that inflammation and metabolic dysfunction in microglia and astrocytes may be the real drivers of Alzheimer's pathology.

Most remarkably, her recent research—supported by the Knight Initiative for Brain Resilience here at the Wu Tsai Neurosciences Institute—shows that targeting inflammation in the peripheral immune system—outside the brain entirely—can restore memory in mouse models of the disease.

While human trials are still needed, Andreasson's findings offer fresh hope and demonstrate the critical importance of supporting curiosity-driven science, even when it challenges prevailing dogma.

Learn More:

• Alzheimer's Association honors Katrin Andreasson
• Research links age-related inflammation, microglia and Alzheimer’s Disease
• Q&A: How the aging immune system impacts brain health
• Rethinking Alzheimer's: Could it begin outside the brain?
• Why new Alzheimer's drugs may not work for patients
• Parkinson’s comes in many forms. New biomarkers may explain why.

Send us a text!

Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience.

We want to hear from your neurons! Email us at at neuronspodcast@stanford.edu

Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.