ReviewFrontiers in aging neuroscience2014
The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Inverse Association Between Serum Uric Acid Levels and Alzheimer's Disease Risk.Molecular neurobiology · 2016Pooled it
- Pioneering next-generation bioactive materials for endodontics: Insights of mitochondrial biology.Bioactive materials · 2026Article
- Zinc increases stress granule formation by promoting RNA condensation.Cell reports · 2026Article
- Zinc-mediated lysosomal activation by 1H10 enhances autophagy and attenuates tau pathology in Alzheimer's disease models.Molecular brain · 2026Article
- ZnbioRxiv : the preprint server for biology · 2026Article
- Zinc and Copper Metallic Instability: Investigating Altered Metal Functionality in both Human and Animal Studies.Biological trace element research · 2026Review
- Zinc as a master regulator of intracellular organelle homeostasis.Experimental & molecular medicine · 2026Review
- Mass spectrometry analysis of young and aged mice and human Alzheimer's disease with Lewy body pathology using on-slide tissue digestion.Analytical and bioanalytical chemistry · 2026Article
- Zinc-Mediated Lysosomal Destabilization Links Mitochondrial Damage to Neuronal Death in a Cellular MPPJournal of neurochemistry · 2026Article
- In Situ Biomineralization Enhances Mitochondrial Transplantation to Differentiating Osteoclast Precursors for Suppressing Cancer-Induced Osteolysis.Research (Washington, D.C.) · 2026Article
- ZnJournal of the American Chemical Society · 2025Article
- A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma.Communications biology · 2025Article
- Functional characterization of genes encoding cadmium pumping PMicrobiology spectrum · 2023Article
- Role of TPEN in Amyloid-βMolecular neurobiology · 2023Article
- Metallothionein I/II Expression and Metal Ion Levels in Correlation with Amyloid Beta Deposits in the Aged Feline Brain.Brain sciences · 2023Article
- The Devastating Effects of Sleep Deprivation on Memory: Lessons from Rodent Models.Clocks & sleep · 2023Review
- miRNAs and Stem Cells as Promising Diagnostic and Therapeutic Targets for Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Multifunctional role of zinc in human health: an update.EXCLI journal · 2023Review
- Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.Biomedicines · 2022Review
- Nanomaterials alleviating redox stress in neurological diseases: mechanisms and applications.Journal of nanobiotechnology · 2022Review
12 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 1 institution in 1 country.
Funding
Abstract
Brain aging is marked by structural, chemical, and genetic changes leading to cognitive decline and impaired neural functioning. Further, aging itself is also a risk factor for a number of neurodegenerative disorders, most notably Alzheimer's disease (AD). Many of the pathological changes associated with aging and aging-related disorders have been attributed in part to increased and unregulated production of reactive oxygen species (ROS) in the brain. ROS are produced as a physiological byproduct of various cellular processes, and are normally detoxified by enzymes and antioxidants to help maintain neuronal homeostasis. However, cellular injury can cause excessive ROS production, triggering a state of oxidative stress that can lead to neuronal cell death. ROS and intracellular zinc are intimately related, as ROS production can lead to oxidation of proteins that normally bind the metal, thereby causing the liberation of zinc in cytoplasmic compartments. Similarly, not only can zinc impair mitochondrial function, leading to excess ROS production, but it can also activate a variety of extra-mitochondrial ROS-generating signaling cascades. As such, numerous accounts of oxidative neuronal injury by ROS-producing sources appear to also require zinc. We suggest that zinc deregulation is a common, perhaps ubiquitous component of injurious oxidative processes in neurons. This review summarizes current findings on zinc dyshomeostasis-driven signaling cascades in oxidative stress and age-related neurodegeneration, with a focus on AD, in order to highlight the critical role of the intracellular liberation of the metal during oxidative neuronal injury.
Indexed as
Identifiers
What OpenQuestion holds
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.