ArticleAging and disease2024
P2Y1R silencing in Astrocytes Protected Neuroinflammation and Cognitive Decline in a Mouse Model of Alzheimer's Disease.
Article in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Integrated multi-omics analysis identifies potential therapeutic targets for Alzheimer's disease.Neural regeneration research · 2026Article
- Characterization of a distinct form of vimentin in the neurodegenerative brain.Acta neuropathologica communications · 2026Article
- Stage-Dependent Function of Astrocytes in Alzheimer's Disease: A Review.Neuroscience insights · 2026Review
- Role of tRNA-Derived Fragments and Their Modifications in the Pathogenesis and Treatment of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Dual inhibition of IRAK1/TAK1 signaling in astrocytes reduces accelerated mortality in human APOE4 knock-in APPswe/PSEN1dE9/P301S-Tau triple transgenic mouse model.Journal of neuroinflammation · 2025Article
- Generation and Characterization of Human iPSC-Derived Astrocytes with Potential for Modeling X-Linked Adrenoleukodystrophy Phenotypes.International journal of molecular sciences · 2025Article
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Vascular Contributions to Healthy Aging and Dementia.Aging and disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes, the major non-dividing glial cells in the central nervous system, exhibit hyperactivation in Alzheimer's disease (AD), leading to neuroinflammation and cognitive impairments. P2Y1-receptor (P2Y1R) in AD brain has been pointed out some contribution to AD pathogenesis, therefore, this study aims to elucidate how astrocytic P2Y1R affects the progression of AD and explore its potential as a new target for AD therapy. In this study, we performed the two-steps verification to assess P2Y1R inhibition in AD progression: P2Y1R-KO AD mice and AD mice treated with astrocyte-specific P2Y1R gene knockdown by using shRNAs for P2Y1R in adeno-associated virus vector. Histochemistry was conducted for the assessment of amyloid-beta accumulation, neuroinflammation and blood brain barrier function. Expression of inflammatory cytokines was evaluated by qPCR after the separation of astrocytes. Cognitive function was assessed through the Morris water maze, Y maze, and contextual fear conditioning tests. P2Y1R inhibition not only by gene knockout but also by astrocyte-specific knockdown reduced amyloid-beta accumulation, glial neuroinflammation, blood brain barrier dysfunction, and cognitive impairment in an AD mice model. Reduced neuroinflammation by astrocytic P2Y1R silencing in AD was further confirmed by the reduction of IL-6 gene expression after the separation of astrocytes from AD mouse brain, which may relate to the amelioration of blood brain barrier as well as cognitive functions. Our results clearly note that P2Y1R in astrocyte contributes to the progression of AD pathology through the acceleration of neuroinflammation, and one-time gene therapy for silencing astrocytic P2Y1R may offer a new therapeutic target for AD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.