Schweighauser M, Shi Y, Tarutani A, Kametani F, Murzin AG, Ghetti B, Matsubara T, Tomita T, Ando T, Hasegawa K, Murayama S, Yoshida M, Hasegawa M, Scheres SH, Goedert M. Structures of α-synuclein filaments from multiple system atrophy. bioXriv, February 6, 2020
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National Institute on Aging
As the authors indicate, this has important implications for lab modelling of synucleinopathies. It would seem relatively important to be able to show whether the types of assemblies we use in the lab are at all related structurally to those extracted from brain, because processes such as cellular uptake or signaling to immune cells might be different depending on the physical fold the assemblies take.
One other thing that I think would also be helpful to know is how much of each assembly is present in brain at any given time—I think that understanding not just what we put into model systems but also how much will help us have more confidence that our models are as relevant to the human disease as we can possibly make them.
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