Trial reportThe Journal of biological chemistry2012
Amyloid-β oligomers induce differential gene expression in adult human brain slices.
Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- Amyloid Precursor Protein Processing Links Female Urgency Urinary Incontinence with Alzheimer's Disease: Implications for Treatment.International journal of molecular sciences · 2026Article
- Emergence of Catalytic Activity in VRK3: Phosphoproteomic Insights into the Regulatory Network of a Former Pseudokinase.Proteomes · 2026Review
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- Imaging 3D cell cultures with optical microscopy.Nature methods · 2025Review
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Exploring the singularity of human neurons: keep calm and carry on.Frontiers in synaptic neuroscience · 2025Review
- Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions.Antioxidants (Basel, Switzerland) · 2024Review
- Synaptic proteasome is inhibited in Alzheimer's disease models and associates with memory impairment in mice.Communications biology · 2023Article
- Reduction of class I histone deacetylases ameliorates ER-mitochondria cross-talk in Alzheimer's disease.Aging cell · 2023Article
- AAV-mediated neuronal expression of an scFv antibody selective for Aβ oligomers protects synapses and rescues memory in Alzheimer models.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Article
- Differential Gene Expression in Sporadic and Genetic Forms of Alzheimer's Disease and Frontotemporal Dementia in Brain Tissue and Lymphoblastoid Cell Lines.Molecular neurobiology · 2022Article
- Modeling the Human Brain WithFrontiers in neuroscience · 2022Article
- Irisin stimulates protective signaling pathways in rat hippocampal neurons.Frontiers in cellular neuroscience · 2022Article
- Interleukin-1β mediates alterations in mitochondrial fusion/fission proteins and memory impairment induced by amyloid-β oligomers.Journal of neuroinflammation · 2021Article
- Correction of eIF2-dependent defects in brain protein synthesis, synaptic plasticity, and memory in mouse models of Alzheimer's disease.Science signaling · 2021Article
- Neural Infection by Oropouche Virus in Adult Human Brain Slices Induces an Inflammatory and Toxic Response.Frontiers in neuroscience · 2021Article
- Common Dysregulation of Innate Immunity Pathways in Human Primary Astrocytes Infected With Chikungunya, Mayaro, Oropouche, and Zika Viruses.Frontiers in cellular and infection microbiology · 2021Article
- Can Brain Health Be Supported by Vitamin D-Based Supplements? A Critical Review.Brain sciences · 2020Review
- Quinovic Acid Impedes Cholesterol Dyshomeostasis, Oxidative Stress, and Neurodegeneration in an Amyloid-Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive decline in Alzheimer disease (AD) is increasingly attributed to the neuronal impact of soluble oligomers of the amyloid-β peptide (AβOs). Current knowledge on the molecular and cellular mechanisms underlying the toxicity of AβOs stems largely from rodent-derived cell/tissue culture experiments or from transgenic models of AD, which do not necessarily recapitulate the complexity of the human disease. Here, we used DNA microarray and RT-PCR to investigate changes in transcription in adult human cortical slices exposed to sublethal doses of AβOs. The results revealed a set of 27 genes that showed consistent differential expression upon exposure of slices from three different donors to AβOs. Functional classification of differentially expressed genes revealed that AβOs impact pathways important for neuronal physiology and known to be dysregulated in AD, including vesicle trafficking, cell adhesion, actin cytoskeleton dynamics, and insulin signaling. Most genes (70%) were down-regulated by AβO treatment, suggesting a predominantly inhibitory effect on the corresponding pathways. Significantly, AβOs induced down-regulation of synaptophysin, a presynaptic vesicle membrane protein, suggesting a mechanism by which oligomers cause synapse failure. The results provide insight into early mechanisms of pathogenesis of AD and suggest that the neuronal pathways affected by AβOs may be targets for the development of novel diagnostic or therapeutic approaches.
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