ArticleInternational journal of medical sciences2015
Astrocytes protect neurons from Aβ1-42 peptide-induced neurotoxicity increasing TFAM and PGC-1 and decreasing PPAR-γ and SIRT-1.
Article in International journal of medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
- Production, Mechanisms, and Therapeutic Strategies of Tryptophan Metabolites in CNS Diseases.Molecular neurobiology · 2025Review
- Neutrophils-astrocyte interactions in central nervous system inflammation.Cell death & disease · 2025Review
- Exploring fatty acid metabolism in Alzheimer's disease: the key role of CPT1A.Scientific reports · 2024Article
- Different amyloid β42 preparations induce different cell death pathways in the model of SH-SY5Y neuroblastoma cells.Cellular & molecular biology letters · 2024Article
- Tryptophan Metabolism in Alzheimer's Disease with the Involvement of Microglia and Astrocyte Crosstalk and Gut-Brain Axis.Aging and disease · 2024Review
- Glioprotective Effects of Sulforaphane in Hypothalamus: Focus on Aging Brain.Neurochemical research · 2024Article
- Research progress of SREBP and its role in the pathogenesis of autoimmune rheumatic diseases.Frontiers in immunology · 2024Review
- A Comprehensive Review on Potential Molecular Drug Targets for the Management of Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024Review
- miR-6076 targets BCL6 in SH-SY5Y cells to regulate amyloid-β-induced neuronal damage.Journal of cellular and molecular medicine · 2023Article
- Side-Chain Immune Oxysterols Induce Neuroinflammation by Activating Microglia.International journal of molecular sciences · 2023Article
- Effect of Antioxidant Supplementation on NET Formation Induced by LPS In Vitro; the Roles of Vitamins E and C, Glutathione, and N-acetyl Cysteine.International journal of molecular sciences · 2023Article
- Functions of Astrocytes under Normal Conditions and after a Brain Disease.International journal of molecular sciences · 2023Review
- Profiling and Cellular Analyses of Obesity-Related circRNAs in Neurons and Glia under Obesity-like In Vitro Conditions.International journal of molecular sciences · 2023Article
- Astrocytic MicroRNAs and Transcription Factors in Alzheimer's Disease and Therapeutic Interventions.Cells · 2022Review
- SIRT1 inactivation switches reactive astrocytes to an antiinflammatory phenotype in CNS autoimmunity.The Journal of clinical investigation · 2022Article
- Metabolic Regulation of Glia and Their Neuroinflammatory Role in Alzheimer's Disease.Cellular and molecular neurobiology · 2022Review
- Alteration of Mitochondrial DNA Copy Number and Increased Expression Levels of Mitochondrial Dynamics-Related Genes in Sjögren's Syndrome.Biomedicines · 2022Article
- Facilitation of Insulin Effects by Ranolazine in Astrocytes in Primary Culture.International journal of molecular sciences · 2022Article
- RETRACTED: Activating SIRT-1 Signalling with the Mitochondrial-CoQ10 Activator Solanesol Improves Neurobehavioral and Neurochemical Defects in Ouabain-Induced Experimental Model of Bipolar Disorder.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Garlic oil alleviates high triglyceride levels in alcohol-exposed rats by inhibiting liver oxidative stress and regulating the intestinal barrier and intestinal flora.Food science & nutrition · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) and mitochondrial transcription factor A (TFAM), protecting mitochondria against Aβ1-42-induced damage and promoting mitochondrial biogenesis. In summary our data suggest that astrocytes may have a key role in protecting neurons, increasing neural viability and mitochondrial biogenesis, acquiring better oxidative stress protection and perhaps modulating inflammatory processes against Aβ1-42 toxic peptide. This might be a sign of a complex epigenetic process in Alzheimer's disease development.
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