ReviewCell death & disease2011
New therapeutic targets in Alzheimer's disease: brain deregulation of calcium and zinc.
Review in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 82 citations in OpenAlex.
- Neurotoxic mechanisms of cadmium in neurodegenerative diseases.Frontiers in cell and developmental biology · 2026Review
- Targeted imaging of lysosomal zinc ions with a tetrahedral DNA framework fluorescent reporter.National science review · 2024Article
- Lost in translation: Inconvenient truths on the utility of mouse models in Alzheimer's disease research.eLife · 2024Review
- High-Phytate Diets Increase Amyloid β Deposition and Apoptotic Neuronal Cell Death in a Rat Model.Nutrients · 2021Article
- Influence of Trace Elements on Neurodegenerative Diseases of The Eye-The Glaucoma Model.International journal of molecular sciences · 2021Review
- Pharmacological Inhibition of Soluble Epoxide Hydrolase as a New Therapy for Alzheimer's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Role of endolysosomes and inter-organellar signaling in brain disease.Neurobiology of disease · 2020Review
- A NeurotoxicFrontiers in molecular neuroscience · 2020Review
- Zinc transporters in Alzheimer's disease.Molecular brain · 2019Review
- Levels of Trace Elements in the Aqueous Humor of Cataract Patients Measured by the Inductively Coupled Plasma Optical Emission Spectrometry.Molecules (Basel, Switzerland) · 2019Article
- Localization of Free and Bound Metal Species through X-Ray Synchrotron Fluorescence Microscopy in the Rodent Brain and Their Relation to Behavior.Brain sciences · 2019Review
- The Pharmacology of Visual Hallucinations in Synucleinopathies.Frontiers in pharmacology · 2019Review
- Regional Distributions of Iron, Copper and Zinc and Their Relationships With Glia in a Normal Aging Mouse Model.Frontiers in aging neuroscience · 2019Article
- The SERCA2: A Gatekeeper of Neuronal Calcium Homeostasis in the Brain.Cellular and molecular neurobiology · 2018Review
- The pharmacological perturbation of brain zinc impairs BDNF-related signaling and the cognitive performances of young mice.Scientific reports · 2018Article
- Influence ofFrontiers in aging neuroscience · 2018Article
- Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper.Behavioural brain research · 2017Article
- Identification of tetrahydrocarbazoles as novel multifactorial drug candidates for treatment of Alzheimer's disease.Translational psychiatry · 2014Article
- Abnormal metal levels in the primary visual pathway of the DBA/2J mouse model of glaucoma.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2014Article
- FK506-binding protein 1b/12.6: a key to aging-related hippocampal Ca2+ dysregulation?European journal of pharmacology · 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular determinants of Alzheimer's (AD) disease are still not completely known; however, in the past two decades, a large body of evidence has indicated that an important contributing factor for the disease is the development of an unbalanced homeostasis of two signaling cations: calcium (Ca(2+)) and zinc (Zn(2+)). Both ions serve a critical role in the physiological functioning of the central nervous system, but their brain deregulation promotes amyloid-β dysmetabolism as well as tau phosphorylation. AD is also characterized by an altered glutamatergic activation, and glutamate can promote both Ca(2+) and Zn(2+) dyshomeostasis. The two cations can operate synergistically to promote the generation of free radicals that further intracellular Ca(2+) and Zn(2+) rises and set the stage for a self-perpetuating harmful loop. These phenomena can be the initial steps in the pathogenic cascade leading to AD, therefore, therapeutic interventions aiming at preventing Ca(2+) and Zn(2+) dyshomeostasis may offer a great opportunity for disease-modifying strategies.
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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.