ArticleMolecular neurobiology2019
Autophagy Induction by Bexarotene Promotes Mitophagy in Presenilin 1 Familial Alzheimer's Disease iPSC-Derived Neural Stem Cells.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025Review
- Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- The role of n-3-derived specialised pro-resolving mediators (SPMs) in microglial mitochondrial respiration and inflammation resolution in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Neuronal BAG3 attenuates tau hyperphosphorylation, synaptic dysfunction, and cognitive deficits induced by traumatic brain injury via the regulation of autophagy-lysosome pathway.Acta neuropathologica · 2024Article
- Alterations of human CSF and serum-based mitophagy biomarkers in the continuum of Alzheimer disease.Autophagy · 2024Article
- Mitophagy and cGAS-STING crosstalk in neuroinflammation.Acta pharmaceutica Sinica. B · 2024Review
- Article
- Promoting Alzheimer's disease research and therapy with stem cell technology.Stem cell research & therapy · 2024Review
- Mitochondrial Genome Editing: Exploring the Possible Relationship of the Atherosclerosis-Associated Mutation m.15059G>A With Defective Mitophagy.Journal of lipid and atherosclerosis · 2024Article
- Mitochondrial metabolism in neural stem cells and implications for neurodevelopmental and neurodegenerative diseases.Journal of translational medicine · 2024Review
- Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases.Biomolecules · 2023Review
- Bexarotene improves motor function after spinal cord injury in mice.Neural regeneration research · 2023Article
- The Role of Mitochondrial Dysfunction in Alzheimer's: Molecular Defects and Mitophagy-Enhancing Approaches.Life (Basel, Switzerland) · 2023Review
- Drug screening identifies tazarotene and bexarotene as therapeutic agents in multiple sulfatase deficiency.EMBO molecular medicine · 2023Article
- Cell type and sex specific mitochondrial phenotypes in iPSC derived models of Alzheimer's disease.Frontiers in molecular neuroscience · 2023Article
- Mitochondrial proteotoxicity: implications and ubiquitin-dependent quality control mechanisms.Cellular and molecular life sciences : CMLS · 2022Review
- Advances in Recapitulating Alzheimer's Disease Phenotypes Using Human Induced Pluripotent Stem Cell-Based In Vitro Models.Brain sciences · 2022Review
- The functional mechanism of bone marrow-derived mesenchymal stem cells in the treatment of animal models with Alzheimer's disease: crosstalk between autophagy and apoptosis.Stem cell research & therapy · 2022Review
- Protective effects of mitophagy enhancers against amyloid beta-induced mitochondrial and synaptic toxicities in Alzheimer disease.Human molecular genetics · 2022Article
- Mitochondrial dysfunction of induced pluripotent stem cells-based neurodegenerative disease modeling and therapeutic strategy.Frontiers in cell and developmental biology · 2022Review
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7 authors.
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Abstract
Adult neurogenesis defects have been demonstrated in the brains of Alzheimer's disease (AD) patients. The neurogenesis impairment is an early critical event in the course of familiar AD (FAD) associated with neuronal loss. It was suggested that neurologic dysfunction in AD may be caused by impaired functioning of hippocampal neural stem cells (NSCs). Multiple metabolic and structural abnormalities in neural mitochondria have long been suspected to play a critical role in AD pathophysiology. We hypothesize that the cause of such abnormalities could be defective elimination of damaged mitochondria. In the present study, we evaluated mitophagy efficacy in a cellular AD model, hiPSC-derived NSCs harboring the FAD-associated PS1 M146L mutation. We found several mitochondrial respiratory chain defects such as lower expression levels of cytochrome c oxidase (complex IV), cytochrome c reductase (complex III), succinate dehydrogenase (complex II), NADH:CoQ reductase (complex I), and also ATP synthase (complex V), most of which had been previously associated with AD. The mitochondrial network morphology and abundance in these cells was aberrant. This was associated with a marked mitophagy failure stemming from autophagy induction blockage, and deregulation of the expression of proteins involved in mitochondrial dynamics. We show that treating these cells with autophagy-stimulating drug bexarotene restored autophagy and compensated mitochondrial anomalies in PS1 M146L NSCs, by enhancing the clearance of mitochondria. Our data support the hypothesis that pharmacologically induced mitophagy enhancement is a relevant and novel therapeutic strategy for the treatment of AD.
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