ArticleFrontiers in aging neuroscience2013
Zinc homeostasis and neurodegenerative disorders.
Article in Frontiers in aging neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 2 of them syntheses that pooled it.
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Who cites it
122 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.
- Pooled it
- Decreased circulating Zinc levels in Parkinson's disease: a meta-analysis study.Scientific reports · 2017Pooled it
- Molecular Imaging of In Vivo Zinc Distribution Using Nuclear and Magnetic Resonance Imaging.Chemical & biomedical imaging · 2026Review
- Zinc-mediated lysosomal activation by 1H10 enhances autophagy and attenuates tau pathology in Alzheimer's disease models.Molecular brain · 2026Article
- Identification of Alzheimer's disease subtypes and biomarkers from human multi-omics data using subspace merging algorithm.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Approximate size and preliminary composition of the low-mass zinc pool in the cytosol of Saccharomyces cerevisiae.The Journal of biological chemistry · 2026Article
- Synthesis, Radiochemistry, and Preclinical Assessment of the First GPR39 PET Imaging Agent.Journal of medicinal chemistry · 2026Article
- Redox-Controlled Chalcogen Bonding as a Modulator of ZnClJournal of the American Chemical Society · 2026Article
- The Impact of Zinc on Cellular Dynamics, Brain Function, and its Therapeutic Potential in Neuronal Regeneration.Molecular neurobiology · 2026Review
- Article
- Copper regulates the expression of immune genes in microglial cells in vitro.Immunobiology · 2025Article
- Zinc Oxide Nanoparticles Attenuated Neurochemical and Histopathological Alterations Associated with Aluminium Chloride Intoxication in Rats.Biological trace element research · 2025Article
- Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.Signal transduction and targeted therapy · 2025Review
- Proteomics analysis in rats reveals convergent mechanisms between major depressive disorder and dietary zinc deficiency.Pharmacological reports : PR · 2025Article
- Predicting cellular adaptation proteins dependent on eIF2α regulation under stress conditions: Physiological and pathophysiological implications in neuronal function.Computational and structural biotechnology journal · 2025Article
- Drugs with glutamate-based mechanisms of action in psychiatry.Pharmacological reports : PR · 2024Review
- Review
- Graph-guided Bayesian Factor Model for Integrative Analysis of Multi-modal Data with Noisy Network Information.Statistics in biosciences · 2024Article
- Changes of Target Essential Trace Elements in Multiple Sclerosis: A Systematic Review and Meta-Analysis.Biomedicines · 2024Review
- Neurochemical Research of LOXBlock-1 and ZnSOBiological trace element research · 2024Article
62 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc is an essential trace element, whose importance to the function of the central nervous system (CNS) is increasingly being appreciated. Alterations in zinc dyshomeostasis has been suggested as a key factor in the development of several neuropsychiatric disorders. In the CNS, zinc occurs in two forms: the first being tightly bound to proteins and, secondly, the free, cytoplasmic, or extracellular form found in presynaptic vesicles. Under normal conditions, zinc released from the synaptic vesicles modulates both ionotropic and metabotropic post-synaptic receptors. While under clinical conditions such as traumatic brain injury, stroke or epilepsy, the excess influx of zinc into neurons has been found to result in neurotoxicity and damage to postsynaptic neurons. On the other hand, a growing body of evidence suggests that a deficiency, rather than an excess, of zinc leads to an increased risk for the development of neurological disorders. Indeed, zinc deficiency has been shown to affect neurogenesis and increase neuronal apoptosis, which can lead to learning and memory deficits. Altered zinc homeostasis is also suggested as a risk factor for depression, Alzheimer's disease (AD), aging, and other neurodegenerative disorders. Under normal CNS physiology, homeostatic controls are put in place to avoid the accumulation of excess zinc or its deficiency. This cellular zinc homeostasis results from the actions of a coordinated regulation effected by different proteins involved in the uptake, excretion and intracellular storage/trafficking of zinc. These proteins include membranous transporters (ZnT and Zip) and metallothioneins (MT) which control intracellular zinc levels. Interestingly, alterations in ZnT and MT have been recently reported in both aging and AD. This paper provides an overview of both clinical and experimental evidence that implicates a dysfunction in zinc homeostasis in the pathophysiology of depression, AD, and aging.
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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.