The Progression of Prion Diseases Is Not Altered in the Absence of TMEM106B
Abstract
Transmembrane protein 106B (TMEM106B) is a type II transmembrane glycoprotein localized in late endosomes and lysosomes. This protein has been attributed to relevant roles in disease risk and progression of multiple neurodegenerative disorders. In experimental models, TMEM106B has been linked with the prion-like spread of misfolded tau proteins responsible for Alzheimer's disease and other tauopathies. The role of this protein in the spread of other misfolded proteins, like prions, has not been explored. Here, we tested whether the removal of TMEM106B altered the progression of prion diseases using animal mouse models (male and female). This was carefully tested using different prion dosages, strains, and routes of administration. Our results demonstrate that the absence of TMEM106B does not alter the progression of prion diseases in any of the tested conditions. This data provides supportive evidence on the specificity of TMEM106B in neurodegenerative conditions.
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BibTeX
@article{bravorisi2026progression,
title = {{The Progression of Prion Diseases Is Not Altered in the Absence of TMEM106B}},
author = {Francisca Bravo-Risi and Gabriela Alburquerque Orta and Peter J. Kim and Hannah Wylie-Young and Tucker H. Stimming and Paulina Soto and Lisbell Estrada and Joanna L. Jankowsky and Rodrigo Morales},
journal = {eneuro},
year = {2026},
month = oct,
doi = {10.1523/eneuro.0043-26.2026},
url = {https://www.eneuro.org/lookup/doi/10.1523/ENEURO.0043-26.2026},
note = {CC BY-NC-SA 4.0},
}
RIS
TY - JOUR
TI - The Progression of Prion Diseases Is Not Altered in the Absence of TMEM106B
AU - Francisca Bravo-Risi
AU - Gabriela Alburquerque Orta
AU - Peter J. Kim
AU - Hannah Wylie-Young
AU - Tucker H. Stimming
AU - Paulina Soto
AU - Lisbell Estrada
AU - Joanna L. Jankowsky
AU - Rodrigo Morales
PY - 2026
DA - 2026/10/01
JO - eneuro
DO - 10.1523/eneuro.0043-26.2026
UR - https://www.eneuro.org/lookup/doi/10.1523/ENEURO.0043-26.2026
AB - Transmembrane protein 106B (TMEM106B) is a type II transmembrane glycoprotein localized in late endosomes and lysosomes. This protein has been attributed to relevant roles in disease risk and progression of multiple neurodegenerative disorders. In experimental models, TMEM106B has been linked with the prion-like spread of misfolded tau proteins responsible for Alzheimer's disease and other tauopathies. The role of this protein in the spread of other misfolded proteins, like prions, has not been explored. Here, we tested whether the removal of TMEM106B altered the progression of prion diseases using animal mouse models (male and female). This was carefully tested using different prion dosages, strains, and routes of administration. Our results demonstrate that the absence of TMEM106B does not alter the progression of prion diseases in any of the tested conditions. This data provides supportive evidence on the specificity of TMEM106B in neurodegenerative conditions.
SN - 2373-2822
ER -