Join our webinar to see how early synaptic dysfunction can be captured with long-term organoid electrophysiology using Mesh MEA.

Prion diseases are fatal neurodegenerative disorders marked by progressive synaptic dysfunction long before widespread neuronal loss becomes evident. Using both mouse models and human brain organoids, researchers are uncovering how prion replication disrupts synaptic transmission and connectivity at the earliest stages of disease, often well before significant prion accumulation or clinical symptoms appear.

In this webinar, we explore how these models reveal early synaptic deficits in both infectious and genetic prion disease, including during the prodromal phase. We'll also discuss why capturing these gradual, long-term changes requires electrophysiological approaches and technologies like Mesh MEA that are capable of monitoring neuronal activity over extended timeframes, providing critical insights into disease progression and new opportunities for early detection.

Key Topics:

• Early synaptic dysfunction is a shared hallmark of prion disease across mouse and human models.


• Disease-associated prion protein mutations drive early synaptic abnormalities in inherited prion disorders.


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  Advanced electrophysiology technology, like Mesh MEA, helps track synaptic damage and understand prion neurodegeneration mechanisms.