ArticleJournal of neuroinflammation2020
Characterization of astrocytes throughout life in wildtype and APP/PS1 mice after early-life stress exposure.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- Early-life adversity in rodents: Experimental design is of the essence.Neurobiology of stress · 2026Article
- Loss of ovarian hormones is detrimental in early disease stages of mouse models of Alzheimer's disease and multi-etiology dementia.Biology of sex differences · 2025Article
- Early-life stress sensitizes response to future stress: Evidence and mechanisms.Neurobiology of stress · 2025Review
- Neuron-Astrocyte Interactions in Aging and Alzheimer's Disease: Dysregulation of Amyloid Precursor Protein.Ageing & longevity · 2025Article
- Probing the roles of developmentally active neurons, in early-life adversity induced disruptions of adult behaviors.Frontiers in neuroscience · 2025Review
- The Dual Role of Amyloid Beta-Peptide in Oxidative Stress and Inflammation: Unveiling Their Connections in Alzheimer's Disease Etiopathology.Antioxidants (Basel, Switzerland) · 2024Review
- Early-life stress and amyloidosis in mice share pathogenic pathways involving synaptic mitochondria and lipid metabolism.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Early resource scarcity causes cortical astrocyte enlargement and sex-specific changes in the orbitofrontal cortex transcriptome in adult rats.Neurobiology of stress · 2024Article
- Developmental and adult stress: effects of steroids and neurosteroids.Stress (Amsterdam, Netherlands) · 2024Review
- Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology.Acta neuropathologica communications · 2023Article
- Early life adversity as a risk factor for cognitive impairment and Alzheimer's disease.Translational neurodegeneration · 2023Review
- Early-life stress lastingly impacts microglial transcriptome and function under basal and immune-challenged conditions.Translational psychiatry · 2022Article
- Early Life Events and Maturation of the Dentate Gyrus: Implications for Neurons and Glial Cells.International journal of molecular sciences · 2022Review
- Early-life stress does not alter spatial memory performance, hippocampal neurogenesis, neuroinflammation, or telomere length in 20-month-old male mice.Neurobiology of stress · 2021Article
- Article
- Behavioral Deficits in Mice with Postnatal Disruption ofCerebral cortex communications · 2021Article
- Long-Term Impact of Early-Life Stress on Hippocampal Plasticity: Spotlight on Astrocytes.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEarly-life stress (ES) is an emerging risk factor for later life development of Alzheimer's disease (AD). We have previously shown that ES modulates amyloid-beta pathology and the microglial response to it in the APPswe/PS1dE9 mouse model. Because astrocytes are key players in the pathogenesis of AD, we studied here if and how ES affects astrocytes in wildtype (WT) and APP/PS1 mice and how these relate to the previously reported amyloid pathology and microglial profile.
methodsWe induced ES by limiting nesting and bedding material from postnatal days (P) 2-9. We studied in WT mice (at P9, P30, and 6 months) and in APP/PS1 mice (at 4 and 10 months) (i) GFAP coverage, cell density, and complexity in hippocampus (HPC) and entorhinal cortex (EC); (ii) hippocampal gene expression of astrocyte markers; and (iii) the relationship between astrocyte, microglia, and amyloid markers.
resultsIn WT mice, ES increased GFAP coverage in HPC subregions at P9 and decreased it at 10 months. APP/PS1 mice at 10 months exhibited both individual cell as well as clustered GFAP signals. APP/PS1 mice when compared to WT exhibited reduced total GFAP coverage in HPC, which is increased in the EC, while coverage of the clustered GFAP signal in the HPC was increased and accompanied by increased expression of several astrocytic genes. While measured astrocytic parameters in APP/PS1 mice appear not be further modulated by ES, analyzing these in the context of ES-induced alterations to amyloid pathology and microglial shows alterations at both 4 and 10 months of age.
conclusionsOur data suggest that ES leads to alterations to the astrocytic response to amyloid-β pathology.
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