ArticleFrontiers in molecular neuroscience2013
Role of endoplasmic reticulum Ca2+ signaling in the pathogenesis of Alzheimer disease.
Article in Frontiers in molecular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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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Who cites it
52 citing papers in PubMed, 106 citations in OpenAlex.
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- A Review on the Pathophysiology of Alzheimer's Disease.Current protein & peptide science · 2026Review
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Unraveling the Vicious Cycle: Oxidative Stress and Neurotoxicity in Neurodegenerative Diseases.FASEB bioAdvances · 2025Review
- Article
- DeepGAMI: deep biologically guided auxiliary learning for multimodal integration and imputation to improve genotype-phenotype prediction.Genome medicine · 2023Article
- Implication of the cooking oil-peroxidation product "hydroxynonenal" for Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Biomolecular Markers of Brain Aging.Advances in experimental medicine and biology · 2023Article
- Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer's and other neurodegenerative diseases.Alzheimer's research & therapy · 2022Article
- Upregulated CaCells · 2022Article
- Cytoskeleton Protein EB3 Contributes to Dendritic Spines Enlargement and Enhances Their Resilience to Toxic Effects of Beta-Amyloid.International journal of molecular sciences · 2022Article
- Review
- The role of Bcl-2 proteins in modulating neuronal CaBiochimica et biophysica acta. Molecular cell research · 2021Review
- Enhancing calmodulin binding to ryanodine receptor is crucial to limit neuronal cell loss in Alzheimer disease.Scientific reports · 2021Article
- Selective linkage of mitochondrial enzymes to intracellular calcium stores differs between human-induced pluripotent stem cells, neural stem cells, and neurons.Journal of neurochemistry · 2021Article
- Mitochondria-associated membranes (MAMs): a potential therapeutic target for treating Alzheimer's disease.Clinical science (London, England : 1979) · 2021Review
- Reassessment of Pioglitazone for Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Evolutionary History of Alzheimer Disease-Causing Protein Family Presenilins with Pathological Implications.Journal of molecular evolution · 2020Article
- Sex-specific features of spine densities in the hippocampus.Scientific reports · 2020Article
- Transgenic Mice Overexpressing HumanInternational journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Alzheimer disease (AD) is a major threat of twenty-first century that is responsible for the majority of dementia in the elderly. Development of effective AD-preventing therapies are the top priority tasks for neuroscience research. Amyloid hypothesis of AD is a dominant idea in the field, but so far all amyloid-targeting therapies have failed in clinical trials. In addition to amyloid accumulation, there are consistent reports of abnormal calcium signaling in AD neurons. AD neurons exhibit enhanced intracellular calcium (Ca(2) (+)) liberation from the endoplasmic reticulum (ER) and reduced store-operated Ca(2) (+) entry (SOC). These changes occur primarily as a result of ER Ca(2) (+) overload. We argue that normalization of intracellular Ca(2) (+) homeostasis could be a strategy for development of effective disease-modifying therapies. The current review summarizes recent data about changes in ER Ca(2) (+) signaling in AD. Ca(2) (+) channels that are discussed in the current review include: inositol trisphosphate receptors, ryanodine receptors, presenilins as ER Ca(2) (+) leak channels, and neuronal SOC channels. We discuss how function of these channels is altered in AD and how important are resulting Ca(2) (+) signaling changes for AD pathogenesis.
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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.