ArticleAntioxidants & redox signaling2011
Enhanced ROS generation mediated by Alzheimer's disease presenilin regulation of InsP3R Ca2+ signaling.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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
27 citing papers in PubMed, 52 citations in OpenAlex.
- Genetic ablation of neuronal mitochondrial calcium uptake impedes Alzheimer's disease progression.The EMBO journal · 2026Article
- Increased GABBR2 Expression on Cell Membranes Causes Increased Ca2 + Inward Flow, Associated with Cognitive Impairment in Early Alzheimer's Disease.Biochemical genetics · 2025Article
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Steady-state regulation of COPII-dependent secretory cargo sorting by inositol trisphosphate receptors, calcium, and penta EF hand proteins.The Journal of biological chemistry · 2023Article
- The Role of the Transcription Factor Nrf2 in Alzheimer's Disease: Therapeutic Opportunities.Biomolecules · 2023Review
- Potential oxidative stress related targets of mitochondria-focused therapy of PTSD.Frontiers in physiology · 2023Review
- Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.European review for medical and pharmacological sciences · 2022Review
- Hyperphosphorylated Human Tau Accumulates at the Synapse, Localizing on Synaptic Mitochondrial Outer Membranes and Disrupting Respiration in a Mouse Model of Tauopathy.Frontiers in molecular neuroscience · 2022Article
- Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.Biomedicines · 2021Review
- Alzheimer's disease-causing presenilin-1 mutations have deleterious effects on mitochondrial function.Theranostics · 2021Article
- Interrelation between ROS and CaRedox biology · 2020Review
- Allium roseum L. extract inhibits amyloid beta aggregation and toxicity involved in Alzheimer's disease.PloS one · 2020Article
- Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Interactions of Mitochondria/Metabolism and Calcium Regulation in Alzheimer's Disease: A Calcinist Point of View.Neurochemical research · 2017Review
- Emerging pathways driving early synaptic pathology in Alzheimer's disease.Biochemical and biophysical research communications · 2017Review
- ROS and intracellular ion channels.Cell calcium · 2016Review
- Calcium-Sensing Receptors of Human Neural Cells Play Crucial Roles in Alzheimer's Disease.Frontiers in physiology · 2016Review
- Redox regulation of store-operated Ca2+ entry.Antioxidants & redox signaling · 2014Review
- Calcium regulation of neural rhythms, memory and Alzheimer's disease.The Journal of physiology · 2014Review
- The very many faces of presenilins and the γ-secretase complex.Protoplasma · 2013Review
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 at 1 institution in 1 country.
Funding
Abstract
Familial Alzheimer's disease (FAD) is caused by mutations in amyloid precursor protein and presenilins (PS1, PS2). Many FAD-linked PS mutations affect intracellular calcium (Ca(2+)) homeostasis by proximal mechanisms independent of amyloid production by dramatically enhancing gating of the inositol trisphosphate receptor (InsP(3)R) intracellular Ca(2+) release channel by a gain-of-function effect that mirrors genetics of FAD and is independent of secretase activity. Electrophysiological recordings of InsP(3)R in FAD patient B cells, cortical neurons of asymptomatic PS1-AD mice, and other cells revealed they have higher occupancy in a high open probability burst mode, resulting in enhanced Ca(2+) signaling. Exaggerated Ca(2+) signaling through this mechanism results in enhanced generation of reactive oxygen species, believed to be an important component in AD pathogenesis. Exaggerated Ca(2+) signaling through InsP(3)R-PS interaction is a disease specific and robust proximal mechanism in AD that may contribute to the pathology of AD by enhanced generation of reactive oxygen species.
Indexed as
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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.