ArticleScientific reports2018
Activated forms of astrocytes with higher GLT-1 expression are associated with cognitive normal subjects with Alzheimer pathology in human brain.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 4 of them syntheses that pooled it.
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Who cites it
67 citing papers in PubMed, 4 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- The glutamatergic system in Alzheimer's disease: a systematic review with meta-analysis.Molecular psychiatry · 2024Pooled it
- Systematic review of human post-mortem immunohistochemical studies and bioinformatics analyses unveil the complexity of astrocyte reaction in Alzheimer's disease.Neuropathology and applied neurobiology · 2022Pooled it
- The Role of Astrocytes in Synapse Loss in Alzheimer's Disease: A Systematic Review.Frontiers in cellular neuroscience · 2022Pooled it
- EAAT2 as a therapeutic research target in Alzheimer's disease: A systematic review.Frontiers in neuroscience · 2022Pooled it
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Single-nucleus atlas provides insights into changes in the evolution of the pig hippocampus.BMC biology · 2026Article
- P2X7 receptor-dependent microglia-astrocyte coupling in Alzheimer's disease: from eATP sensing to synaptic and proteostatic failure.Frontiers in aging neuroscience · 2026Review
- Differential impact of manganese on glutamate clearance, electroencephalography, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Functional Specificity of Astrocyte Subtypes in Alzheimer's Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data.Molecular neurobiology · 2025Article
- Tau pathology in the dorsal raphe may be a prodromal indicator of Alzheimer's disease.Molecular psychiatry · 2025Article
- Comparative epigenetics of domestic animals: focusing on DNA accessibility and its impact on gene regulation and traits.Journal of veterinary science · 2025Review
- Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer's disease.Nature neuroscience · 2024Article
- Sexual dimorphism, altered hippocampal glutamatergic neurotransmission, and cognitive impairment in APP knock-in mice.Journal of Alzheimer's disease : JAD · 2024Article
- PS1/gamma-secretase acts as rogue chaperone of glutamate transporter EAAT2/GLT-1 in Alzheimer's disease.Acta neuropathologica communications · 2024Article
- Article
- The concept of resilience to Alzheimer's Disease: current definitions and cellular and molecular mechanisms.Molecular neurodegeneration · 2024Review
- Unlocking the therapeutic potential of P2X7 receptor: a comprehensive review of its role in neurodegenerative disorders.Frontiers in pharmacology · 2024Review
- Astrocyte-Neuron Interactions in Alzheimer's Disease.Advances in neurobiology · 2024Review
- Music compensates for altered gene expression in age-related cognitive disorders.Scientific reports · 2023Article
- PS1/gamma-secretase acts as rogue chaperone of glutamate transporter EAAT2/GLT-1 in Alzheimer's disease.Research square · 2023Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the cognitive impairment in Alzheimer's disease (AD) is believed to be caused by amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs), several postmortem studies have reported cognitive normal subjects with AD brain pathology. As the mechanism underlying these discrepancies has not been clarified, we focused the neuroprotective role of astrocytes. After examining 47 donated brains, we classified brains into 3 groups, no AD pathology with no dementia (N-N), AD pathology with no dementia (AD-N), and AD pathology with dementia (AD-D), which represented 41%, 21%, and 38% of brains, respectively. No differences were found in the accumulation of Aβ plaques or NFTs in the entorhinal cortex (EC) between AD-N and AD-D. Number of neurons and synaptic density were increased in AD-N compared to those in AD-D. The astrocytes in AD-N possessed longer or thicker processes, while those in AD-D possessed shorter or thinner processes in layer I/II of the EC. Astrocytes in all layers of the EC in AD-N showed enhanced GLT-1 expression in comparison to those in AD-D. Therefore these activated forms of astrocytes with increased GLT-1 expression may exert beneficial roles in preserving cognitive function, even in the presence of Aβ and NFTs.
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