ArticleBiochimica et biophysica acta2013
Lysophosphatidic acid induces increased BACE1 expression and Aβ formation.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Protein Kinase C-delta (PKCδ) in Neurodegeneration and Cerebral Ischemia: Molecular Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Islet Amyloid Polypeptide Modelled to Simulate Diabetes Co-Oligomerized with β-Amyloid 1-42 Reproducing the Pathological Cascade of Alzheimer's Disease in Human Cerebral Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Liraglutide attenuates aluminum chloride-induced Alzheimer's disease in rats by modulating the oxLDL/LPA/LPAR1 pathway.Communications biology · 2026Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Unraveling the Role of Autotaxin and Lysophosphatidic Acid in Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Potential.International journal of molecular sciences · 2025Review
- Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease.MethodsX · 2022Review
- Modulation of Neurolipid Signaling and Specific Lipid Species in the Triple Transgenic Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Dual Role of Lysophosphatidic Acid Receptor 2 (LPAFrontiers in cellular neuroscience · 2021Article
- Modulation of Brain Hyperexcitability: Potential New Therapeutic Approaches in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Plasmalogens, platelet-activating factor and beyond - Ether lipids in signaling and neurodegeneration.Neurobiology of disease · 2020Review
- Association of lysophosphatidic acids with cerebrospinal fluid biomarkers and progression to Alzheimer's disease.Alzheimer's research & therapy · 2020Article
- Pleotropic Roles of Autotaxin in the Nervous System Present Opportunities for the Development of Novel Therapeutics for Neurological Diseases.Molecular neurobiology · 2020Review
- Lysophospholipids and Their G-Coupled Protein Signaling in Alzheimer's Disease: From Physiological Performance to Pathological Impairment.Frontiers in molecular neuroscience · 2020Article
- The Novel Perspectives of Adipokines on Brain Health.International journal of molecular sciences · 2019Review
- An Updated Review of Lysophosphatidylcholine Metabolism in Human Diseases.International journal of molecular sciences · 2019Review
- Autotaxin⁻Lysophosphatidic Acid Signaling in Alzheimer's Disease.International journal of molecular sciences · 2018Review
- Membrane-Associated Effects of Glucocorticoid on BACE1 Upregulation and Aβ Generation: Involvement of Lipid Raft-Mediated CREB Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- TNF-α regulates the proteolytic degradation of ST6Gal-1 and endothelial cell-cell junctions through upregulating expression of BACE1.Scientific reports · 2017Article
- Blood-based metabolic signatures in Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2017Article
- Hyperglycemia Increases the Production of Amyloid Beta-Peptide Leading to Decreased Endothelial Tight Junction.CNS neuroscience & therapeutics · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The abnormal production and accumulation of β-amyloid peptide (Aβ), which is produced from amyloid precursor protein (APP) by the sequential actions of β-secretase and γ-secretase, are thought to be the initial causative events in the development of Alzheimer's disease (AD). Accumulating evidence suggests that vascular factors play an important role in the pathogenesis of AD. Specifically, studies have suggested that one vascular factor in particular, oxidized low density lipoprotein (oxLDL), may play an important role in regulating Aβ formation in AD. However, the mechanism by which oxLDL modulates Aβ formation remains elusive. In this study, we report several new findings that provide biochemical evidence suggesting that the cardiovascular risk factor oxLDL may contribute to Alzheimer's disease by increasing Aβ production. First, we found that lysophosphatidic acid (LPA), the most bioactive component of oxLDL induces increased production of Aβ. Second, our data strongly indicate that LPA induces increased Aβ production via upregulating β-secretase expression. Third, our data strongly support the notion that different isoforms of protein kinase C (PKC) may play different roles in regulating APP processing. Specifically, most PKC members, such as PKCα, PKCβ, and PKCε, are implicated in regulating α-secretase-mediated APP processing; however, PKCδ, a member of the novel PKC subfamily, is involved in LPA-induced upregulation of β-secretase expression and Aβ production. These findings may contribute to a better understanding of the mechanisms by which the cardiovascular risk factor oxLDL is involved in Alzheimer's disease.
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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.