ArticleASN neuro2011
Early astrocytic atrophy in the entorhinal cortex of a triple transgenic animal model of Alzheimer's disease.
Article in ASN neuro, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed.
- Entorhinal Astrocyte Transplants Restore Spatial Exploration and Alleviate Amyloid-Beta Pathology in Alzheimer's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Perisynaptic Astrocytic Processes as Communication Hubs and Early Sites of Dysfunction.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026Review
- Glial and Neuronal Alzheimer's Disease-Related Alterations Reproduced in Human Induced Pluripotent Stem Cells With Presenilin-1 Mutation.Research square · 2026Article
- Frequency-Specific Transcranial Photobiomodulation Elicits Complementary Glial Mechanisms for Neurovascular Protection and Amyloid Clearance in Alzheimer Disease.Cyborg and bionic systems (Washington, D.C.) · 2026Article
- Cocaine affects astrocyte iNOS expression.Brain research · 2026Article
- Stage-Dependent Function of Astrocytes in Alzheimer's Disease: A Review.Neuroscience insights · 2026Review
- Rescue of protein dyshomeostasis in hippocampal astrocytes from an Alzheimer's disease mouse model by stabilizing ER-mitochondrial interactions at a 20 nm distance.Alzheimer's research & therapy · 2025Article
- Article
- Revealing and Characterizing Astrocytic Atrophy in an Animal Model of Depression.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Long-Term Treatment with Fluoroethylnormemantine (FENM) Alleviated Memory Deficits, Amyloid Pathology, and Microglial Reaction in APP/PS1 Mice.ACS pharmacology & translational science · 2024Article
- Differential Glial Response and Neurodegenerative Patterns in CA1, CA3, and DG Hippocampal Regions of 5XFAD Mice.International journal of molecular sciences · 2024Article
- Revisiting astrocytic calcium signaling in the brain.Fundamental research · 2024Review
- Alzheimer's Disease, Obesity, and Type 2 Diabetes: Focus on Common Neuroglial Dysfunctions (Critical Review and New Data on Human Brain and Models).Brain sciences · 2024Review
- Cholecystokinin B receptor agonists alleviates anterograde amnesia in cholecystokinin-deficient and aged Alzheimer's disease mice.Alzheimer's research & therapy · 2024Article
- Epileptiform activity in brain organoids derived from patient with Glucose Transporter 1 Deficiency Syndrome.Frontiers in neuroscience · 2024Article
- Intracerebral inoculation of healthy non-transgenic rats with a single aliquot of oligomeric amyloid-β (1-42) profoundly and progressively alters brain function throughout life.Frontiers in aging neuroscience · 2024Article
- Impairment of entorhinal cortex network activity in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Amyloid precursor protein induces reactive astrogliosis.bioRxiv : the preprint server for biology · 2023Article
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Electroacupuncture prevents astrocyte atrophy to alleviate depression.Cell death & disease · 2023Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The EC (entorhinal cortex) is fundamental for cognitive and mnesic functions. Thus damage to this area appears as a key element in the progression of AD (Alzheimer's disease), resulting in memory deficits arising from neuronal and synaptic alterations as well as glial malfunction. In this paper, we have performed an in-depth analysis of astroglial morphology in the EC by measuring the surface and volume of the GFAP (glial fibrillary acidic protein) profiles in a triple transgenic mouse model of AD [3xTg-AD (triple transgenic mice of AD)]. We found significant reduction in both the surface and volume of GFAP-labelled profiles in 3xTg-AD animals from very early ages (1 month) when compared with non-Tg (non-transgenic) controls (48 and 54%, reduction respectively), which was sustained for up to 12 months (33 and 45% reduction respectively). The appearance of Aβ (amyloid β-peptide) depositions at 12 months of age did not trigger astroglial hypertrophy; nor did it result in the close association of astrocytes with senile plaques. Our results suggest that the AD progressive cognitive deterioration can be associated with an early reduction of astrocytic arborization and shrinkage of the astroglial domain, which may affect synaptic connectivity within the EC and between the EC and other brain regions. In addition, the EC seems to be particularly vulnerable to AD pathology because of the absence of evident astrogliosis in response to Aβ accumulation. Thus we can consider that targeting astroglial atrophy may represent a therapeutic strategy which might slow down the progression of AD.
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