ArticleBrain pathology (Zurich, Switzerland)1998
Apolipoprotein E isoforms increase intracellular Ca2+ differentially through a omega-agatoxin IVa-sensitive Ca2+-channel.
Article in Brain pathology (Zurich, Switzerland), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 68 citations in OpenAlex.
- Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2025Review
- Article
- Extensive transcriptional and chromatin changes underlie astrocyte maturation in vivo and in culture.Nature communications · 2021Article
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- Reduced cortical excitatory synapse number in APOE4 mice is associated with increased calcineurin activity.Neuroreport · 2017Article
- Stem cell derived basal forebrain cholinergic neurons from Alzheimer's disease patients are more susceptible to cell death.Molecular neurodegeneration · 2014Article
- HSV-1 and Alzheimer's disease: more than a hypothesis.Frontiers in pharmacology · 2014Review
- Complex disease-associated pharmacogenetics: drug efficacy, drug safety, and confirmation of a pathogenetic hypothesis (Alzheimer's disease).The pharmacogenomics journal · 2007Review
- The endocytic receptor protein LRP also mediates neuronal calcium signaling via N-methyl-D-aspartate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Truncated apolipoprotein E (ApoE) causes increased intracellular calcium and may mediate ApoE neurotoxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Apolipoprotein E and Alzheimer's disease: molecular mechanisms and therapeutic opportunities.Journal of cellular and molecular medicineReview
- Apolipoprotein E: a major piece in the Alzheimer's disease puzzle.Journal of cellular and molecular medicineReview
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein E (apoE) is the major apolipoprotein in the brain and is known for its important role in plasticity and neurodegeneration. We show that apoE dose-dependently increases intracellular free Ca2+ in rat hippocampal astrocytes and neurons. This effect varies with isoforms in the order E4 > E3 > E2. It is insensitive to blockade of action potentials by tetrodotoxin or inhibition of binding of apoE by heparinase, by the LRP ligand lactoferrin and by low density lipoprotein. ApoE evoked Ca2+-increases are blocked in zero [Ca]o and by the Ca-channel antagonists nickel and omega-Agatoxin-IVa but not by nifedipine and omega-Conotoxin-GVIa, demonstrating an isoform-specific activation of P/Q type Ca2+-channels. This novel mechanism is discussed with respect to Alzheimer's disease, that is linked for most cases to the apoE epsilon-allelic variation (epsilon4 > epsilon3 > epsilon2).
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