ArticleMolecular neurobiology2013
Amyloid β peptides promote autophagy-dependent differentiation of mouse neural stem cells: Aβ-mediated neural differentiation.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Neurogenesis Is Increased in Human Neural Stem Cells by Aβ40 Peptide.International journal of molecular sciences · 2022Article
- Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084 and DMT, on Neurogenesis and Neuroinflammation in an AβInternational journal of molecular sciences · 2022Article
- Article
- Oligomeric and Fibrillar Species of Aβ42 Diversely Affect Human Neural Stem Cells.International journal of molecular sciences · 2021Article
- Alternative Targets to Fight Alzheimer's Disease: Focus on Astrocytes.Biomolecules · 2021Review
- Stereological Changes in Microvascular Parameters in Hippocampus of a Transgenic Rat Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Article
- Aβ40 Oligomers Promote Survival and Early Neuronal Differentiation of Dentate Gyrus-Isolated Precursor Cells Through Activation of the Akt Signaling Pathway.Neurotoxicity research · 2020Article
- Diet-dependent gut microbiota impacts on adult neurogenesis through mitochondrial stress modulation.Brain communications · 2020Article
- Physiological and pathological effects of amyloid-β species in neural stem cell biology.Neural regeneration research · 2019Review
- Physiological effects of amyloid precursor protein and its derivatives on neural stem cell biology and signaling pathways involved.Neural regeneration research · 2019Article
- Aβ42 Peptide Promotes Proliferation and Gliogenesis in Human Neural Stem Cells.Molecular neurobiology · 2019Article
- Amyloid β Peptide Compromises Neural Stem Cell Fate by Irreversibly Disturbing Mitochondrial Oxidative State and Blocking Mitochondrial Biogenesis and Dynamics.Molecular neurobiology · 2019Article
- Role of Amyloid Precursor Protein (APP) and Its Derivatives in the Biology and Cell Fate Specification of Neural Stem Cells.Molecular neurobiology · 2018Review
- Effects of Acetylcholine on β-Amyloid-Induced cPLA2 Activation in the TB Neuroectodermal Cell Line: Implications for the Pathogenesis of Alzheimer's Disease.Cellular and molecular neurobiology · 2018Article
- Journey to the Center of the Fetal Brain: Environmental Exposures and Autophagy.Frontiers in cellular neuroscience · 2018Review
- Huperzine A protects neural stem cells against Aβ-induced apoptosis in a neural stem cells and microglia co-culture system.International journal of clinical and experimental pathology · 2015Article
- PI3K/AKT/mTOR/p70S6K Pathway Is Involved in Aβ25-35-Induced Autophagy.BioMed research international · 2015Article
- MicroRNA-34a Modulates Neural Stem Cell Differentiation by Regulating Expression of Synaptic and Autophagic Proteins.Molecular neurobiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although regarded as neurotoxic, amyloid β (Aβ) peptides may also mediate a wide range of nonpathogenic processes. Autophagy has been implicated in Aβ-mediated effects, although its precise function in neural differentiation remains unknown. Here, we addressed the role of different Aβ fragments in neural stem cell (NSC) proliferation and differentiation, and investigated whether autophagy is involved in Aβ-induced alterations of neural fate. Our results demonstrate that neuronal and glial-specific protein markers are significantly induced by both Aβ1-40 and Aβ1-42. However, Aβ1-40 preferentially enhances neurogenesis of NSCs, as determined by βIII-tubulin, NeuN, and MAP2 neuronal marker immunoreactivity, while Aβ1-42 appears to favor gliogenesis. In contrast, Aβ25-35 does not influence NSC fate. The effect of Aβ1-40 on neurogenesis is partially dependent on its role in NSC self-renewal as both S-phase of the cell cycle and BrdU labeling were markedly increased. Nevertheless, Aβ1-40 resulted also in increased Tuj1 promoter activity. Autophagy, assessed by conversion of endogenous LC3-I/II, fluorescence of pGFP-LC3-transfected cells, and Atg9 protein levels, was evident in both Aβ1-40- and Aβ1-42-treated NSCs, independently of reactive oxygen species production and apoptosis. Finally, inhibition of autophagy by pharmacologic means abrogated Aβ-induced lineage-specific protein markers. These results support distinct roles for different Aβ peptides in NSC fate decision and underline the importance of autophagy control of this process.
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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.