ReviewNature reviews. Neurology2017
ER stress and the unfolded protein response in neurodegeneration.
Review in Nature reviews. Neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 565 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
565 citing papers in PubMed, 1 synthesis or guideline pooled it, 985 citations in OpenAlex.
- Evaluation of Cell-Specific Alterations in Alzheimer's Disease and Relevance of In Vitro Models.Genes · 2023Pooled it
- DNL343 and Disease Progression in Amyotrophic Lateral Sclerosis: A Randomized Clinical Trial.JAMA network open · 2026Trial
- Organelle-anchored translation factories: the roles of neuronal RNA-binding protein condensates in organizing local protein synthesis in neurological diseases.Protein & cell · 2026Review
- Cross-disease protein aggregate interactions in neurodegeneration: from molecular mechanisms to therapeutic strategies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- L-carnitine modulates molecular responses associated with inflammation, endoplasmic reticulum stress, and neurotrophic signaling in cerebral cortex of neonatal GcdhMetabolic brain disease · 2026Article
- Vitamin B6 Modifies Tau-Induced Cellular Stress- and Proteostasis-Related Responses.Journal of fungi (Basel, Switzerland) · 2026Article
- ER-to-Golgi transport machinery promotes the excessive cargo-triggered unfolded protein response in C. elegans.PLoS genetics · 2026Article
- Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Phase separation in neurodegenerative disorders: a metabolic perspective on protein aggregation and therapeutic targeting.Translational neurodegeneration · 2026Review
- Region Specific miRNA-mRNA Networks in Gray and White Matter Lesions of Progressive Multiple Sclerosis.Annals of clinical and translational neurology · 2026Article
- Article
- CT1812 Attenuates Surgery-Induced Cognitive Impairment and Modulates TMEM97- and PGRMC1-Associated Hippocampal Stress Responses in Aged Mice.Neurochemical research · 2026Article
- Sex-specific trajectories of nonlinear immune aging at single-cell level.Nature communications · 2026Article
- Pathological depositions in human disease: converging mechanisms in atherosclerosis, Alzheimer's disease, and related disorders.Molecular biomedicine · 2026Review
- An ER stress-responsive RNA rheostat for programmable gene and mRNA therapies.Cell chemical biology · 2026Article
- Exercise-Mediated Modulation of the NLRP3 Inflammasome in Aging and Neurodegenerative Diseases: Mechanisms, Microglial Crosstalk, and Translational Perspectives.Molecular neurobiology · 2026Review
- Calreticulin as a stress-responsive integrator of ER proteostasis, calcium homeostasis, and immune clearance.Molecular biology reports · 2026Review
- Review
- Molecular mechanisms underlaying fluoride-induced neurotoxicity: interplay of antioxidants and endoplasmic reticulum stress-mediated apoptotic pathways in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Aberrant GRP78 Phase Transition Sustains Endothelial IRE1α Signaling and Drives Blood-Brain Barrier Failure in Cerebral Amyloid Angiopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
505 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical manifestation of neurodegenerative diseases is initiated by the selective alteration in the functionality of distinct neuronal populations. The pathology of many neurodegenerative diseases includes accumulation of misfolded proteins in the brain. In physiological conditions, the proteostasis network maintains normal protein folding, trafficking and degradation; alterations in this network - particularly disturbances to the function of endoplasmic reticulum (ER) - are thought to contribute to abnormal protein aggregation. ER stress triggers a signalling reaction known as the unfolded protein response (UPR), which induces adaptive programmes that improve protein folding and promote quality control mechanisms and degradative pathways or can activate apoptosis when damage is irreversible. In this Review, we discuss the latest advances in defining the functional contribution of ER stress to brain diseases, including novel evidence that relates the UPR to synaptic function, which has implications for cognition and memory. A complex concept is emerging wherein the consequences of ER stress can differ drastically depending on the disease context and the UPR signalling pathway that is altered. Strategies to target specific components of the UPR using small molecules and gene therapy are in development, and promise interesting avenues for future interventions to delay or stop neurodegeneration.
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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.