TMEM106B C‐terminal fragments drive a distinct neurodegenerative proteinopathy in C<i>. elegans</i>.

Taken together, our data suggest expression of TMEM CT in C. elegans neurons provides a useful model for the functional characterization of TMEM106B proteinopathy in neurodegenerative disease. Comparison with other proteinopathy models will inform potential disease mechanisms.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2024-12-01
DOI
https://doi.org/10.1002/alz.088591
Primary Topic
Genetic Neurodegenerative Diseases
Type
article
Field-Weighted Citation Impact
0.00
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article

TMEM106B C‐terminal fragments drive a distinct neurodegenerative proteinopathy in C. elegans.

Ruben Riordan, Brian C. Kraemer
Alzheimer s & Dementia
Genetic Neurodegenerative Diseases
article

TMEM106B C‐terminal fragments drive a distinct neurodegenerative proteinopathy in C. elegans.

Ruben Riordan, Brian C. Kraemer
article en

Abstract

Taken together, our data suggest expression of TMEM CT in C. elegans neurons provides a useful model for the functional characterization of TMEM106B proteinopathy in neurodegenerative disease. Comparison with other proteinopathy models will inform potential disease mechanisms.

Alzheimer s & DementiaVol. 20(S1)
University of Washington (US), VA Puget Sound Health Care System (US), Geriatric Research Education and Clinical Center (US)
Openalex Percentile: Top 74%
Genetic Neurodegenerative Diseases
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