ReviewAntioxidants & redox signaling2018
Dysregulation of Intracellular Calcium Signaling in Alzheimer's Disease.
Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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
55 citing papers in PubMed.
- Coat Color-Associated Transcriptomic Differences of Black and White Hortobágyi Racka Sheep Using the RNA-Seq Technique.Ecology and evolution · 2026Article
- Reprogramming Neuroinflammation: Mitochondrial Targets and Immune Checkpoint Inhibitors in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Compatibility of Acorus tatarinowii Schott and Polygala tenuifolia Willd. alleviate Alzheimer's disease through regulating Nos2-mediated calcium signaling pathway.Neurochemical research · 2026Article
- Tunable Chemical and Optical Control of ER-Plasma Membrane Contact Site Geometry and Dynamics with High-Fidelity Visualization.bioRxiv : the preprint server for biology · 2026Article
- The Gut-Brain Axis in Alzheimer's: From Microbiota Genetics to Stigmasterol's Neuroprotection Mechanism.Degenerative neurological and neuromuscular disease · 2026Article
- Pathological calcium influx through amyloid beta pores disrupts synaptic function.Cell calcium · 2025Article
- Identification of therapeutic targets for Alzheimer's Disease Treatment using bioinformatics and machine learning.Scientific reports · 2025Article
- Endoplasmic reticulum stress-related deficits in calcium clearance promote neuronal dysfunction that is prevented by SERCA2 gene augmentation.Cell reports. Medicine · 2024Article
- Plasma membrane curvature regulates the formation of contacts with the endoplasmic reticulum.Nature cell biology · 2024Article
- Exploration of the shared gene signatures and molecular mechanisms between Alzheimer's disease and intracranial aneurysm.Scientific reports · 2024Article
- Review
- Membrane Curvature Promotes ER-PM Contact Formation via Junctophilin-EHD Interactions.bioRxiv : the preprint server for biology · 2024Article
- Potential Use of the Cholesterol Transfer Inhibitor U18666A as a Potent Research Tool for the Study of Cholesterol Mechanisms in Neurodegenerative Disorders.Molecular neurobiology · 2024Review
- Inference of drug off-target effects on cellular signaling using interactome-based deep learning.iScience · 2024Article
- Genome-wide epistasis analysis reveals gene-gene interaction network on an intermediate endophenotype P-tau/AβScientific reports · 2024Article
- Development of capillary dysfunction in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Role of TPEN in Amyloid-βMolecular neurobiology · 2023Article
- Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach.Brain : a journal of neurology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
significanceCalcium (Ca CRITICAL ISSUES: Endoplasmic reticulum Ca FUTURE DIRECTIONS: There is a need to determine whether AD is a syndrome with one critical signaling pathway that initiates pathology, or it is a disorder with many different signaling pathways that are disrupted simultaneously or one after each other. It is necessary to validate applicability of nSOCE-activating therapy for the development of anti-AD medication. There is an experimental correlation between downregulated nSOCE and disrupted postsynaptic contacts in AD mouse models. Signaling mechanisms downstream of nSOCE which are responsible for the regulation of stability of postsynaptic contacts have to be discovered. That will bring new targets for the development of AD-preventing therapies. Antioxid. Redox Signal. 29, 1176-1188.
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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.