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A new study from the Minichiello group, published recently in the journal Biology, has shown that dysfunction in BDNF-TrkB signalling, restricted to a specific subset of cerebellar granule cells, is sufficient to generate ataxic symptoms

Granule cells and Purkinje cells © Figure created in BioRender

While motor incoordination in patients suffering from ataxia disorders is primarily linked to the dysfunction and degeneration of cerebellar Purkinje cells (PCs), this study highlights how signalling dysfunction in a subset of cerebellar granule cells (GCs), which provide input to PCs, can trigger ataxia symptoms.

Brain-derived neurotrophic factor (BDNF)-TrkB signalling-activated pathways have been implicated in ataxia disorders. In spinocerebellar ataxia 6 (SCA6), for example, reduced BDNF-TrkB signalling has been linked to PC dysfunction and motor incoordination. However, the TrkB receptor is also present in GCs, which have extensive connections with PCs, suggesting that impaired BDNF-TrkB signalling in GCs would also negatively affect the function of PCs and possibly contribute to symptoms of motor incoordination in ataxia disorders.

Read the full story on the The Department of Pharmacology  website.

 

 

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