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Bassoon proteinopathy drives neurodegeneration in multiple sclerosis.

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Title: Bassoon proteinopathy drives neurodegeneration in multiple sclerosis.
Authors: Schattling, Benjamin (AUTHOR), Engler, Jan Broder (AUTHOR), Volkmann, Constantin (AUTHOR), Rothammer, Nicola (AUTHOR), Woo, Marcel S. (AUTHOR), Petersen, Meike (AUTHOR), Winkler, Iris (AUTHOR), Kaufmann, Max (AUTHOR), Rosenkranz, Sina C. (AUTHOR), Fejtova, Anna (AUTHOR), Thomas, Ulrich (AUTHOR), Bose, Aparajita (AUTHOR), Bauer, Simone (AUTHOR), Träger, Simone (AUTHOR), Miller, Katharine K. (AUTHOR), Brück, Wolfgang (AUTHOR), Duncan, Kent E. (AUTHOR), Salinas, Gabriela (AUTHOR), Soba, Peter (AUTHOR), Gundelfinger, Eckart D. (AUTHOR)
Source: Nature Neuroscience. Jun2019, Vol. 22 Issue 6, p887-896. 10p. 6 Color Photographs, 1 Diagram.
Abstract: Multiple sclerosis (MS) is characterized by inflammatory insults that drive neuroaxonal injury. However, knowledge about neuron-intrinsic responses to inflammation is limited. By leveraging neuron-specific messenger RNA profiling, we found that neuroinflammation leads to induction and toxic accumulation of the synaptic protein bassoon (Bsn) in the neuronal somata of mice and patients with MS. Neuronal overexpression of Bsn in flies resulted in reduction of lifespan, while genetic disruption of Bsn protected mice from inflammation-induced neuroaxonal injury. Notably, pharmacological proteasome activation boosted the clearance of accumulated Bsn and enhanced neuronal survival. Our study demonstrates that neuroinflammation initiates toxic protein accumulation in neuronal somata and advocates proteasome activation as a potential remedy. The authors report that the presynaptic protein bassoon forms toxic aggregates in neuronal somata in multiple sclerosis. Stimulation of proteasomal activity reduces bassoon aggregates, neuroaxonal loss and disability during CNS inflammation. [ABSTRACT FROM AUTHOR]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Bassoon proteinopathy drives neurodegeneration in multiple sclerosis.
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  Data: <searchLink fieldCode="JN" term="%22Nature+Neuroscience%22">Nature Neuroscience</searchLink>. Jun2019, Vol. 22 Issue 6, p887-896. 10p. 6 Color Photographs, 1 Diagram.
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  Data: Multiple sclerosis (MS) is characterized by inflammatory insults that drive neuroaxonal injury. However, knowledge about neuron-intrinsic responses to inflammation is limited. By leveraging neuron-specific messenger RNA profiling, we found that neuroinflammation leads to induction and toxic accumulation of the synaptic protein bassoon (Bsn) in the neuronal somata of mice and patients with MS. Neuronal overexpression of Bsn in flies resulted in reduction of lifespan, while genetic disruption of Bsn protected mice from inflammation-induced neuroaxonal injury. Notably, pharmacological proteasome activation boosted the clearance of accumulated Bsn and enhanced neuronal survival. Our study demonstrates that neuroinflammation initiates toxic protein accumulation in neuronal somata and advocates proteasome activation as a potential remedy. The authors report that the presynaptic protein bassoon forms toxic aggregates in neuronal somata in multiple sclerosis. Stimulation of proteasomal activity reduces bassoon aggregates, neuroaxonal loss and disability during CNS inflammation. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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