Autophagy induction enhances TDP43 turnover and survival in neuronal ALS models
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have distinct clinical features but a common pathology--cytoplasmic inclusions rich in transactive response element DNA-binding protein of 43 kDa (TDP43). Rare TDP43 mutations cause ALS or FTD, but abnormal TDP43 levels and localization may cause disease even if TDP43 lacks a mutation. Here we show that individual neurons vary in their ability to clear TDP43 and are exquisitely sensitive to TDP43 levels. To measure TDP43 clearance, we developed and validated a single-cell optical method that overcomes the confounding effects of aggregation and toxicity and discovered that pathogenic mutations shorten TDP43 half-life. New compounds that stimulate autophagy improved TDP43 clearance and localization and enhanced survival in primary murine neurons and in human stem cell-derived neurons and astrocytes harboring mutant TDP43. These findings indicate that the levels and localization of TDP43 critically determine neurotoxicity and show that autophagy induction mitigates neurodegeneration by acting directly on TDP43 clearance.
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Autophagy protects cells from death, especially motor neurons.
“Autophagy could protect cells from death (Hara et al., 2006; Komatsu et al., 2006), especially in the case of motor neurons (Barmada et al., 2014).”
From Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells (2017) · cites this paper as Barmada et al., 2014
Autophagy could protect cells from death, especially in motor neurons.
“Autophagy could protect cells from death (Hara et al., 2006; Komatsu et al., 2006), especially in motor neurons (Barmada et al., 2014).”
From Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells (2017) · cites this paper as Barmada et al., 2014
Inducing autophagy using benzoxazine compounds including 10-NCP enhances TARDBPM337V degradation and extends survival in rodent and human neurons.
“inducing autophagy using novel compounds belonging to the benzoxazine class of molecules, including 10-NCP, enhance TARDBPM337V degradation and extend survival in rodent and human neurons [357].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [357]
Benzoxazines are sufficient to reduce TARDBPM337V-associated toxicity in iPSC-derived astrocytes, presumably through autophagy upregulation.
“these compounds are sufficient to reduce TARDBPM337V-associated toxicity in iPSC-derived astrocytes [357], presumably through autophagy upregulation.”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [357]
10-NCP and related compounds are capable of inducing neuronal autophagy through an MTOR- and AKT-independent signaling cascade.
“10-NCP and related compounds are also capable of inducing neuronal autophagy through an MTOR- and AKT-independent signaling cascade [357,384].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [357]
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Self-citation
- Authors
- Barmada, S. J., Serio, A., Arjun, A., Bilican, B., Daub, A., Ando, D. M., Tsvetkov, A., Pleiss, M., Li, X., Peisach, D., Shaw, C., Chandran, S., & Finkbeiner, S.
- Affiliations
- Gladstone Institutes (US)
- MRC Centre for Regenerative Medicine (GB)
- University of Michigan (US)
- King's College London (GB)
- Corresponding author
- Finkbeiner, Steven
- ORCID
- Venue
- Nature Chemical Biology
- Published
- 2014-06-29
- Volume
- 10
- Issue
- 8
- Pages
- 677-685
- ISSN
- 1552-4450 (ISSN-L)
- 1552-4469
- PMC
- PMC4106236
- OpenAlex
- W1999522052
- Cited by
- 431
- References
- 50
- Citations by year
- 2026: 26 · 2025: 26 · 2024: 24 · 2023: 28 · 2022: 26 · 2021: 56 · 2020: 52 · 2019: 42 · 2018: 42 · 2017: 36 · 2016: 26 · 2015: 39 · 2014: 7
- FWCI
- 23.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Chemical Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Gladstone Institutes
- Motor Neurone Disease Association (CHANDRAN/MAR10/982-797)
- National Institutes of Health (1c06rr018928-01)
- National Institute of Mental Health (U01MH105035, U01 MH1050135)
- National Institute of Neurological Disorders and Stroke (U24NS078370, K08NS072233, R01NS039074, R01NS083390, R43NS081844)
- National Center for Research Resources (C06-RR-018928)
- Robert Packard Center for ALS Research, Johns Hopkins University
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- autophagy, TDP-43, amyotrophic lateral sclerosis, frontotemporal dementia, protein turnover, neurodegeneration, stem cell-derived neurons, astrocytes, neurotoxicity
- MeSH terms
- Amino Acid Sequence, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Autophagy, Cell Survival, Cells, Cultured, DNA-Binding Proteins, Fluphenazine, Half-Life, Humans, Methotrimeprazine, Microtubule-Associated Proteins, Molecular Sequence Data, Mutation, Neurons, Stem Cells, Reproducibility of Results, Mice, Rats, Small Molecule Libraries, Induced Pluripotent Stem Cells, Single-Cell Analysis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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