The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Pharmacological targeting of GSK-3 and NRF2 provides neuroprotection in a preclinical model of tauopathy
Open accessAbstract
Tauopathies are a group of neurodegenerative disorders where TAU protein is presented as aggregates or is abnormally phosphorylated, leading to alterations of axonal transport, neuronal death and neuroinflammation. Currently, there is no treatment to slow progression of these diseases. Here, we have investigated whether dimethyl fumarate (DMF), an inducer of the transcription factor NRF2, could mitigate tauopathy in a mouse model. The signaling pathways modulated by DMF were also studied in mouse embryonic fibroblast (MEFs) from wild type or KEAP1-deficient mice. The effect of DMF on neurodegeneration, astrocyte and microglial activation was examined in Nrf2+/+ and Nrf2−/− mice stereotaxically injected in the right hippocampus with an adeno-associated vector expressing human TAUP301L and treated daily with DMF (100 mg/kg, i.g) during three weeks. DMF induces the NRF2 transcriptional through a mechanism that involves KEAP1 but also PI3K/AKT/GSK-3-dependent pathways. DMF modulates GSK-3β activity in mouse hippocampi. Furthermore, DMF modulates TAU phosphorylation, neuronal impairment measured by calbindin-D28K and BDNF expression, and inflammatory processes involved in astrogliosis, microgliosis and pro-inflammatory cytokines production. This study reveals neuroprotective effects of DMF beyond disruption of the KEAP1/NRF2 axis by inhibiting GSK3 in a mouse model of tauopathy. Our results support repurposing of this drug for treatment of these diseases.
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Cites
Synapse Loss and Microglial Activation Precede Tangles in a P301S Tauopathy Mouse Model
Yoshiyama, Y., Higuchi, M., Zhang, B., Huang, S.-M., Iwata, N., Saido, T. C., Maeda, J., Suhara, T., Trojanowski, J. Q., & Lee, V. M.-Y. (2007) · Neuron · doi:10.1016/j.neuron.2007.01.010 · Cited by 2,208
Rada, P., Rojo, A. I., Chowdhry, S., McMahon, M., Hayes, J. D., & Cuadrado, A. (2011) · Molecular and Cellular Biology · doi:10.1128/mcb.01204-10 · Cited by 759 · cited 2×
“β-TrCP leads to Cullin-1/Rbx1mediated NRF2 ubiquitination and its subsequent degradation [8].”
BackgroundSelf-citationNrf2 reduces levels of phosphorylated tau protein by inducing autophagy adaptor protein NDP52
Jo, C., Gundemir, S., Pritchard, S., Jin, Y. N., Rahman, I., & Johnson, G. V. W. (2014) · Nature Communications · doi:10.1038/ncomms4496 · Cited by 323
Sanchez-Guajardo, V., Febbraro, F., Kirik, D., & Romero-Ramos, M. (2010) · PLoS ONE · doi:10.1371/journal.pone.0008784 · Cited by 256
GSK‐3 in Neurodegenerative Diseases
Lei, P., Ayton, S., Bush, A. I., & Adlard, P. A. (2011) · International Journal of Alzheimer’s Disease · doi:10.4061/2011/189246 · Cited by 177
López González, I., Garcia-Esparcia, P., Llorens, F., & Ferrer, I. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17020206 · Cited by 101
Cited by
Castro-Sánchez, S., García-Yagüe, Á. J., Kügler, S., & Lastres-Becker, I. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101118 · Cited by 76
Self-citationCuadrado, A., Cazalla, E., Bach, A., Bathish, B., Naidu, S. D., DeNicola, G. M., Dinkova-Kostova, A. T., Fernández-Ginés, R., Grochot-Przeczek, A., Hayes, J. D., et al. (2025) · Redox Biology · doi:10.1016/j.redox.2025.103569 · Cited by 28
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Metadata
- Authors
- Cuadrado, A., Kügler, S., & Lastres-Becker, I.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2018-04
- Volume
- 14
- Pages
- 522-534
- ISSN
- 2213-2317 (ISSN-L)
- OpenAlex
- W2767982908
- Cited by
- 179
- References
- 6
- FWCI
- 10.99
- Type
- journal article
- Language
- en
- Open access
- gold
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