ArticleActa neuropathologica communications2017
Oligomeric amyloid-beta induces MAPK-mediated activation of brain cytosolic and calcium-independent phospholipase A
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 70 citations in OpenAlex.
- Circulating lipids are related to longitudinal changes of ATN biomarkers for Alzheimer's disease.Molecular psychiatry · 2026Article
- A perspective: PLA2G4A as drug target for vascular inflammation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Evidence for cPLA2 activation in Alzheimer's disease synaptic pathology.Acta neuropathologica communications · 2026Article
- Development of potent, selective cPLAnpj drug discovery · 2026Article
- Membrane-associated estrogen receptor α prevents the amyloid β-induced suppression of GIRK channel activity in hippocampal neurons from female mice.Biology of sex differences · 2025Article
- Microglia-specific regulation of lipid metabolism in Alzheimer's disease revealed by microglial depletion in 5xFAD Mice.Nature communications · 2025Article
- Polyamine biosynthesis dysregulation in Alzheimer's disease and Down syndrome cellular models.bioRxiv : the preprint server for biology · 2025Article
- Development of Calcium-Dependent Phospholipase A2 Inhibitors to Target Cellular Senescence and Oxidative Stress in Neurodegenerative Diseases.Antioxidants & redox signaling · 2024Review
- Effects of APOE4 on omega-3 brain metabolism across the lifespan.Trends in endocrinology and metabolism: TEM · 2024Review
- Changes in lipid metabolism track with the progression of neurofibrillary pathology in tauopathies.Journal of neuroinflammation · 2024Article
- Mitochondrial oxidative damage reprograms lipid metabolism of renal tubular epithelial cells in the diabetic kidney.Cellular and molecular life sciences : CMLS · 2024Article
- Brain areas lipidomics in female transgenic mouse model of Alzheimer's disease.Scientific reports · 2024Article
- The assembly of the Mitochondrial Complex I Assembly complex uncovers a redox pathway coordination.Nature communications · 2023Article
- The Phospholipase A2 Superfamily: Structure, Isozymes, Catalysis, Physiologic and Pathologic Roles.International journal of molecular sciences · 2023Review
- Uncovering mechanisms of brain inflammation in Alzheimer's disease with APOE4: Application of single cell-type lipidomics.Annals of the New York Academy of Sciences · 2022Review
- Increased Expression and Activity of Brain Cortical cPLA2 Due to Chronic Lipopolysaccharide Administration in Mouse Model of Familial Alzheimer's Disease.Pharmaceutics · 2022Article
- Article
- Calcium-dependent cytosolic phospholipase AMolecular neurodegeneration · 2022Article
- Rapid identification of plasmalogen molecular species using targeted multiplexed selected reaction monitoring mass spectrometry.Journal of mass spectrometry and advances in the clinical lab · 2021Article
- Age-related changes in brain phospholipids and bioactive lipids in the APP knock-in mouse model of Alzheimer's disease.Acta neuropathologica communications · 2021Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is histopathologically characterized by the build-up of fibrillar amyloid beta (Aβ) in the form of amyloid plaques and the development of intraneuronal neurofibrillary tangles consisting of aggregated hyperphosphorylated Tau. Although amyloid fibrils were originally considered responsible for AD pathogenesis, recent convincing evidence strongly implicates soluble oligomeric Aβ as the primary neurotoxic species driving disease progression. A third largely ignored pathological hallmark, originally described by Alois Alzheimer, is the presence of "adipose inclusions", suggestive of aberrant lipid metabolism. The molecular mechanisms underlying these "lipoid granules", as well as their potential link to soluble and/or fibrillar Aβ remain largely unknown. Seeking to better-understand these conundrums, we took advantage of the powerful technology of multidimensional mass spectrometry-based shotgun lipidomics and an AD transgenic mouse model overexpressing mutant amyloid precursor protein (APP E693Δ-Osaka-), where AD-like pathology and neurodegeneration occur as a consequence of oligomeric Aβ accumulation in the absence of amyloid plaques. Our results revealed for the first time that APP overexpression and oligomeric Aβ accumulation lead to an additive global accumulation of nonesterified polyunsaturated fatty acids (PUFAs) independently of amyloid plaques. Furthermore, we revealed that this accumulation is mediated by an increase in phospholipase A
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