Flying under the radar: TMEM106B(120–254) fibrils break out in diverse neurodegenerative disorders
Author(s) -
Katie E. Copley,
James Shorter
Publication year - 2022
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2022.03.032
Subject(s) - biology , frontotemporal lobar degeneration , fibril , amyloid fibril , neuroscience , disease , degeneration (medical) , neurodegeneration , frontotemporal dementia , amyloid β , biochemistry , pathology , medicine , dementia
Neurodegenerative diseases commonly exhibit aggregation of specific proteins that define each disease. Chang et al. (2022) establish that a C-terminal fragment of TMEM106B, a frontotemporal-lobar-degeneration risk factor, unexpectedly forms amyloid fibrils with similar structures in diverse neurodegenerative disorders. These unanticipated TMEM106B(120-254) fibrils may herald etiological shifts for several neurodegenerative diseases.
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