ArticleCellular and molecular life sciences : CMLS2019
Link between the unfolded protein response and dysregulation of mitochondrial bioenergetics in Alzheimer's disease.
Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Genome-wide association studies of Alzheimer's disease and related disorders stratified by sex, onset age, and Apolipoprotein E genotype reveal novel risk loci in African Americans.Alzheimer's research & therapy · 2025Article
- Tracing mitochondrial marks of neuronal aging in iPSCs-derived neurons and directly converted neurons.Communications biology · 2025Article
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- Caspases in Alzheimer's Disease: Mechanism of Activation, Role, and Potential Treatment.Molecular neurobiology · 2024Review
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- Dual roles of UPRJournal of molecular medicine (Berlin, Germany) · 2023Review
- Using Drosophila to identify naturally occurring genetic modifiers of amyloid beta 42- and tau-induced toxicity.G3 (Bethesda, Md.) · 2023Article
- Sirtuins at the Crossroads between Mitochondrial Quality Control and Neurodegenerative Diseases: Structure, Regulation, Modifications, and Modulators.Aging and disease · 2023Review
- Energy Crisis Links to Autophagy and Ferroptosis in Alzheimer's Disease: Current Evidence and Future Avenues.Current neuropharmacology · 2023Article
- Redox Active α-Lipoic Acid Differentially Improves Mitochondrial Dysfunction in a Cellular Model of Alzheimer and Its Control Cells.International journal of molecular sciences · 2022Article
- Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022Review
- Deciphering therapeutic options for neurodegenerative diseases: insights from SIRT1.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Curcumin prevents Alzheimer's disease progression by upregulating JMJD3.American journal of translational research · 2022Article
- Inorganic Polyphosphate, Mitochondria, and Neurodegeneration.Progress in molecular and subcellular biology · 2022Article
- Amyloid-Driven Tau Accumulation on Mitochondria Potentially Leads to Cognitive Deterioration in Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Effects of Urolithin A on Mitochondrial Parameters in a Cellular Model of Early Alzheimer Disease.International journal of molecular sciences · 2021Article
- Article
- Epileptic Mechanisms Shared by Alzheimer's Disease: Viewed via the Unique Lens of Genetic Epilepsy.International journal of molecular sciences · 2021Review
- Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer's disease mouse model.Communications biology · 2021Article
- Curcumin slows the progression of Alzheimer's disease by modulating mitochondrial stress responses via JMJD3-H3K27me3-BDNF axis.American journal of translational research · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder affecting more than 47.5 million people worldwide. Metabolic impairments are common hallmarks of AD, and amyloid-β (Aβ) peptide and hyperphosphorylated tau protein-the two foremost histopathological signs of AD-have been implicated in mitochondrial dysfunction. Many neurodegenerative disorders, including AD, show excessive amounts of mis-/unfolded proteins leading to an activation of the unfolded protein response (UPR). In the present study, we aimed to characterize the link between ER stress and bioenergetics defects under normal condition (human SH-SY5Y neuroblastoma cells: control cells) or under pathological AD condition [SH-SY5Y cells overexpressing either the human amyloid precursor protein (APP) or mutant tau (P301L)]. More specifically, we measured UPR gene expression, cell viability, and bioenergetics parameters, such as ATP production and mitochondrial membrane potential (MMP) in basal condition and after an induced ER stress by thapsigargin. We detected highly activated UPR and dysregulated bioenergetics in basal condition in both AD cellular models. Strikingly, acute-induced ER stress increased the activity of the UPR in both AD cellular models, leading to up-regulation of apoptotic pathways, and further dysregulated mitochondrial function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.