Neuroscientist studying the mechanisms of psychiatric treatments.
apredictiveprocessinglab.org
Georg Keller
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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.
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...
