ArticleBrain pathology (Zurich, Switzerland)2022
Proteomic analysis of human hippocampal subfields provides new insights into the pathogenesis of Alzheimer's disease and the role of glial cells.
Article in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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16 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- FAM134B-mediated ER-phagy degrades APP and suppresses Alzheimer's disease pathology.The EMBO journal · 2026Article
- In vivo mapping of protein-protein interactions of schizophrenia risk factors generates an interconnected disease network.Schizophrenia (Heidelberg, Germany) · 2026Article
- Subregional limbic radiomics on FDG-PET provides accurate early detection of Alzheimer's disease.BMC medical imaging · 2026Article
- Why 11β-HSD1 inhibitors show variable efficacy in Alzheimer's therapy: an APOE4-dependent HSD11B1 mechanism.Theranostics · 2026Article
- Review
- Isotope-encoded spatial biology identifies plaque-age-dependent maturation and synaptic loss in an Alzheimer's disease mouse model.Nature communications · 2025Article
- Changes in the pH value of the human brain in Alzheimer's disease pathology correlated with CD68-positive microglia: a community-based autopsy study in Beijing, China.Molecular brain · 2025Article
- GNG5 is a novel regulator of Aβ42 production in Alzheimer's disease.Cell death & disease · 2024Article
- Crosstalk Among Glial Cells in the Blood-Brain Barrier Injury After Ischemic Stroke.Molecular neurobiology · 2024Review
- CSF proteomic profiles of neurodegeneration biomarkers in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- A Holistic Analysis of Alzheimer's Disease-Associated lncRNA Communities Reveals Enhanced lncRNA-miRNA-RBP Regulatory Triad Formation Within Functionally Segregated Clusters.Journal of molecular neuroscience : MN · 2024Article
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Article
- Proteomic analysis of human hippocampal subfields provides new insights into the pathogenesis of Alzheimer's disease and the role of glial cells.Brain pathology (Zurich, Switzerland) · 2022Article
- Reduced RNA adenosine-to-inosine editing in hippocampus vasculature associated with Alzheimer's disease.Brain communications · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hippocampus and entorhinal cortex (EC), the earliest affected areas, are considered relative to early memory loss in Alzheimer's disease (AD). The hippocampus is composed of heterogeneous subfields that are affected in a different order and varying degrees during AD pathogenesis. In this study, we conducted a comprehensive proteomic analysis of the hippocampal subfields and EC region in human postmortem specimens obtained from the Chinese human brain bank. Bioinformatics analysis identified region-consistent differentially expressed proteins (DEPs) which associated with astrocytes, and region-specific DEPs which associated with oligodendrocytes and the myelin sheath. Further analysis illuminated that the region-consistent DEPs functioned as connection of region-specific DEPs. Moreover, in region-consistent DEPs, the expression level of S100A10, a marker of protective astrocytes, was increased in both aging and AD patients. Immunohistochemical analysis confirmed an increase in the number of S100A10-positive astrocytes in all hippocampal subfields and the EC region of AD patients. Dual immunofluorescence results further showed that S100A10-positive astrocytes contained apoptotic neuron debris in AD patients, suggesting that S100A10-positive astrocytes may protect brain through phagocytosis of apoptotic neurons. In region-specific DEPs, the proteome showed a specific reduction of oligodendrocytes and myelin markers in CA1, CA3, and EC regions of AD patients. Immunohistochemical analysis confirmed the loss of myelin in EC region. Above all, these results highlight the role of the glial cells in AD and provide new insights into the pathogenesis of AD and potential therapeutic strategies.
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