ReviewFrontiers in aging neuroscience2014
Cognitive decline due to excess synaptic Zn(2+) signaling in the hippocampus.
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 17 papers.
What it found
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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.
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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
17 citing papers in PubMed, 42 citations in OpenAlex.
- Cell-type-specific enhancement of deviance detection by synaptic zinc in the mouse auditory cortex.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Zinc in Cognitive Impairment and Aging.Biomolecules · 2022Review
- Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status.Antioxidants (Basel, Switzerland) · 2021Article
- Association of Cigarette Smoking With Male Cognitive Impairment and Metal Ions in Cerebrospinal Fluid.Frontiers in psychiatry · 2021Article
- Structural determinants of specificity and regulation of activity in the allosteric loop network of human KLK8/neuropsin.Scientific reports · 2018Article
- Long-Term DL-3-Frontiers in aging neuroscience · 2018Article
- Differential Effects of Low- and High-dose Zinc Supplementation on Synaptic Plasticity and Neurogenesis in the Hippocampus of Control and High-fat Diet-fed Mice.Neurochemical research · 2017Article
- Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper.Behavioural brain research · 2017Article
- Article
- YXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice.Frontiers in aging neuroscience · 2017Article
- Preliminary Data on the Interaction between Some Biometals and Oxidative Stress Status in Mild Cognitive Impairment and Alzheimer's Disease Patients.Oxidative medicine and cellular longevity · 2017Article
- Recent Progress in the Understanding of Obesity: Contributions of Genome-Wide Association Studies.Current obesity reports · 2015Review
- The Zinc Ion Chelating Agent TPEN Attenuates Neuronal Death/apoptosis Caused by Hypoxia/ischemia Via Mediating the Pathophysiological Cascade Including Excitotoxicity, Oxidative Stress, and Inflammation.CNS neuroscience & therapeutics · 2015Article
- Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders.Pharmacology & therapeutics · 2015Review
- Editorial: The molecular pathology of cognitive decline: focus on metals.Frontiers in aging neuroscience · 2015Article
- Amyloid β-mediated Zn2+ influx into dentate granule cells transiently induces a short-term cognitive deficit.PloS one · 2014Article
- The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
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
No grant is acknowledged in the PubMed record.
Abstract
Zinc is an essential component of physiological brain function. Vesicular zinc is released from glutamatergic (zincergic) neuron terminals and serves as a signal factor (Zn(2) (+) signal) in both the intracellular (cytosol) compartment and the extracellular compartment. Synaptic Zn(2) (+) signaling is dynamically linked to neurotransmission and is involved in processes of synaptic plasticity such as long-term potentiation and cognitive activity. On the other hand, the activity of the hypothalamic-pituitary-adrenal (HPA) axis, i.e., glucocorticoid secretion, which can potentiate glutamatergic neuron activity, is linked to cognitive function. HPA axis activity modifies synaptic Zn(2) (+) dynamics at zincergic synapses. An increase in HPA axis activity, which occurs after exposure to stress, may induce excess intracellular Zn(2) (+) signaling in the hippocampus, followed by hippocampus-dependent memory deficit. Excessive excitation of zincergic neurons in the hippocampus can contribute to cognitive decline under stressful and/or pathological conditions. This paper provides an overview of the ``Hypothesis and Theory'' of Zn(2) (+)-mediated modification of cognitive activity.
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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.