ArticlePloS one2020
Optical induction of autophagy via Transcription factor EB (TFEB) reduces pathological tau in neurons.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- The deubiquitinase OTULIN regulates tau expression and RNA metabolism in neurons.Genomic psychiatry : advancing science from genes to society · 2025Article
- Transcriptional regulation of autophagy and its implications in human disease.Cell death and differentiation · 2023Review
- Upregulation of the ESCRT pathway and multivesicular bodies accelerates degradation of proteins associated with neurodegeneration.Autophagy reports · 2023Article
- MEK1/2 inhibition rescues neurodegeneration by TFEB-mediated activation of autophagic lysosomal function in a model of Alzheimer's Disease.Molecular psychiatry · 2022Article
- Single-nucleus chromatin accessibility profiling highlights distinct astrocyte signatures in progressive supranuclear palsy and corticobasal degeneration.Acta neuropathologica · 2022Article
- Optophysiology: Illuminating cell physiology with optogenetics.Physiological reviews · 2022Review
- The emergence of molecular systems neuroscience.Molecular brain · 2022Review
- Retromer regulates the lysosomal clearance of MAPT/tau.Autophagy · 2021Article
- Autophagy and Tau Protein.International journal of molecular sciences · 2021Review
- Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis.Neurobiology of disease · 2021Review
- Steering Molecular Activity with Optogenetics: Recent Advances and Perspectives.Advanced biology · 2021Review
- Therapeutic Potential of Vital Transcription Factors in Alzheimer's and Parkinson's Disease With Particular Emphasis on Transcription Factor EB Mediated Autophagy.Frontiers in neuroscience · 2021Review
- Degradation and Transmission of Tau by Autophagic-Endolysosomal Networks and Potential Therapeutic Targets for Tauopathy.Frontiers in molecular neuroscience · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pathological accumulation of microtubule associated protein tau in neurons is a major neuropathological hallmark of Alzheimer's disease (AD) and related tauopathies. Several attempts have been made to promote clearance of pathological tau (p-Tau) from neurons. Transcription factor EB (TFEB) has shown to clear p-Tau from neurons via autophagy. However, sustained TFEB activation and autophagy can create burden on cellular bioenergetics and can be deleterious. Here, we modified previously described two-plasmid systems of Light Activated Protein (LAP) from bacterial transcription factor-EL222 and Light Responsive Element (LRE) to encode TFEB. Upon blue-light (465 nm) illumination, the conformation changes in LAP induced LRE-driven expression of TFEB, its nuclear entry, TFEB-mediated expression of autophagy-lysosomal genes and clearance of p-Tau from neuronal cells and AD patient-derived human iPSC-neurons. Turning the blue-light off reversed the expression of TFEB-target genes and attenuated p-Tau clearance. Together, these results suggest that optically regulated TFEB expression unlocks the potential of opto-therapeutics to treat AD and other dementias.
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Registered trials
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