Thank you Georg! Very happy to have worked on this.
Here is a short 🧵 on what ECT-triggered CSD looks like, and why we think it is going to help shape the future of ECT research.
(1/12)
Targeted mitochondrial delivery: Extracellular donor mitochondria are delivered specifically to neurons via bispecific protein binders.
💡What if we could reboot sick cells?
IOB scientists @timayupov.bsky.social, @vmorenojuan.bsky.social and collaborators led by Botond Roska have developed #MitoCatch, a system that delivers healthy mitochondria directly to diseased cells. A step toward precision mitochondrial medicine.
Pic©IOB
🧵👇
I've been waiting for this particular flavor of naysayer review (it's in Swedish). TL;DR: Brain research has failed to deliver on its big promises in the past; ergo, we must be wary now too.
Indeed. I was inspired to write Elusive Cures ... /1
lakartidningen.se/kultur/recen...
This work was a collaborative effort between our lab and clinical experts at UPK Basel. The parallel approach of using mouse circuit and human patient data is likely the most promising approach we have to understanding the mechanism of psychiatric treatments.
Full paper:
doi.org/10.64898/202...
If CSD is the primary driver of recovery, we can rethink ECT:
• Can we trigger CSD without a generalized seizure?
• Could we pharmacologically block CSD from entering the hippocampus to prevent amnesia?
• CSD is currently unmonitored in clinics, would it be a better predictor of treatment outcomes?
In our study, if a mouse hemisphere had a seizure but no CSD, there was no increase in Fos. The plasticity only happened where the CSD traveled.
We also saw that the EEG metrics clinicians use to predict patient success correlate with CSD in our mice.
By combining widefield calcium imaging with EEG in mice, we find, consistent with previous work (pubmed.ncbi.nlm.nih.gov/40383825/), that stimulation triggers a CSD.
Crucially, the CSD perfectly predicts the expression of Fos, a key marker of neuronal plasticity.
For nearly a century, we believed the therapeutic effect of ECT is the seizure. Our latest research suggests we may have been looking at the wrong event.
A thread on why cortical spreading depression (CSD) might be the driver of therapeutic benefit.
Work led by @therehugolad.bsky.social
In this interview, @juliabatki.bsky.social, FMI’s newest group leader, reflects on the early curiosity that drew her to science, why FMI is the right home for her lab, how studying cell clearance could help us understand disease, and her love of improv.
www.fmi.ch/news-events/...
“What if there is a parallel antipsychotic pathway via immunosuppressive D2 activation on glia?” in just a few years. Fascinating time to work in the field!
Beautiful work! After decades of focusing the development of antipsychotic drugs on D2 antagonism in striatum, we have gone from “Is it really D2 expressing striatal neurons? pubmed.ncbi.nlm.nih.gov/37443282/%E2... to
Finally, I am particularly excited about this paper as it is the first to come out of our lab since we pivoted entirely to studying the circuit mechanisms of psychiatric treatments.
If the therapeutic effect of the drug is a plasticity mechanism, rather than the acute effects of receptor occupancy, this could provide a mechanistic justification for further exploring extended interval dosing for antipsychotic treatments, with the hope of reducing side effects of the treatment.
Why might this be relevant? Based on receptor occupancy arguments, daily dosing is the default clinical choice. However, alternate-day regimens have only recently been explored
clinicaltrials.gov/study/NCT044...
pubmed.ncbi.nlm.nih.gov/20868639/
Very excited to share new work by Leonardo Lupori. In mice, a single dose of the antipsychotic clozapine results in changes to behavior and cortical activity patterns that remain detectable a week later.
www.biorxiv.org/content/10.6...
Truly beautiful work. The first good evidence that prediction error driven plasticity actually functions to reduce prediction errors!
Join us at TENSS 2026 to open black boxes, explain how things/brains work and debate the impact (or lack or it) of various new technologies on understanding of the brain and on society. tenss.ro Apply by: March 15th!
Deadline March 1. Join the new Dietschy Facility for Tissue Science.
www.biozentrum.unibas.ch/open-positio...
and the idea of internal models for motor control (Jordan, Rumelhart, Kawato, Wolpert) – combined with the beautiful music box spacetime attractor ideas coming out of @behrenstimb.bsky.social ’s lab are the most promising approach we currently have to try to understand how cortex works.
We suspect, a model that combines the self-supervised learning of JEPA (@yann-lecun.bsky.social and team), the credit assignment and capacity to work on arbitrary graphs of predictive processing (work of the lab of Rafal Bogacz),
We think cortex might function like a JEPA. It looks like prediction errors in layer 2/3 are not computed against input (as is the idea in predictive processing), but against a representation in latent space (i.e. like in a JEPA arxiv.org/abs/2301.08243 or RPL doi.org/10.1101/2025...).
The Neurobiology of Mental Health 2026 from May 17 – May 21 in Thun, Switzerland.
Join leading scientists for a 3.5-day #LakeConference discussion on: "The Neurobiology of Mental Health" at the level of genes, cell types, organoids, circuits, networks and brain systems. Learn more & apply by January 31: lakeconferences.org/conf/1ed63fdb-de0c-4a56-...
Join us this May to explore the biological mechanisms of mental health challenges and treatment strategies. Apply by January 31: lakeconferences.org
1/6 New preprint 🚀 How does the cortex learn to represent things and how they move without reconstructing sensory stimuli? We developed a circuit-centric recurrent predictive learning (RPL) model based on JEPAs.
🔗 doi.org/10.1101/2025...
Led by @atenagm.bsky.social @mshalvagal.bsky.social
One of the most promising approaches to making headway in understanding the cortical algorithm that I have seen in a long time! www.biorxiv.org/content/10.1...
In this first-person account, FMI’s senior communications manager describes taking part in an early human trial that adapts previous experiments in mice to explore how the human brain responds when visual and auditory information suddenly fall out of sync. www.fmi.ch/news-events/...
Applications are open for the #LakeConference on the Neurobiology of Mental Health in Lake Thun, Switzerland.
📆 May 17-21, 2026
🏔️ All career stages welcome
⏳ Apply by January 31, 2026
Learn more and apply: https://t.co/WcuXHdWnFa
@lakeconferences.bsky.social
Very much looking forward to this collaboration with @georgkeller.bsky.social at @fmiscience.bsky.social, using a cross-species approach in humans and mice to investigate the effects of antipsychotics on cortical circuit function.
Join us for the second Neurobiology of Mental Health conference (May 2026) that will explore the biological mechanisms underlying mental health challenges and their treatment. Information and application on: lakeconferences.org. The deadline for applications is January 31st, 2026.
Please share: Postdoc position available in a new collaborative SNSF project with @georgkeller.bsky.social at @fmiscience.bsky.social using a cross-species approach in humans and mice to investigate the cortical circuit mechanisms underlying schizophrenia. Apply at karriere.upk.ch/Postdoctoral...