Evidence map›Paper›PMID 36449279›Full record

ReviewEssays in biochemistry2023

Astrocyte adaptation in Alzheimer's disease: a focus on astrocytic P2X7R.

Paula Beltran-Lobo, Matthew J Reid, Maria Jimenez-Sanchez, Alexei Verkhratsky, Beatriz G Perez-Nievas, Wendy Noble

Open access · hybridFull text readReview
In one paragraph

Review in Essays in biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 25 citations in OpenAlex.

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  15. P2XBrain, behavior, and immunity · 2023
    Article
  16. Review
  17. The P2X7 Receptor, a Multifaceted Receptor in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 4 countries.

Paula Beltran-LoboDepartment of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 5 Cutcombe Road, London, SE5 9RX, U.K.
Matthew J ReidDepartment of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 5 Cutcombe Road, London, SE5 9RX, U.K.
Maria Jimenez-SanchezDepartment of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 5 Cutcombe Road, London, SE5 9RX, U.K.
Alexei VerkhratskyFaculty of Biology, Medicine and Health, The University of Manchester, Manchester, U.K.
Beatriz G Perez-NievasDepartment of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 5 Cutcombe Road, London, SE5 9RX, U.K.
Wendy NobleDepartment of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, 5 Cutcombe Road, London, SE5 9RX, U.K.ORCID 0000-0002-7898-4295
King's College London · GBManchester Academic Health Science Centre · GB

Funding

Medical Research Council MR/N022696/1Medical Research Council MR/V036947/1
6 · The paper itself

Abstract

Astrocytes are key homeostatic and defensive cells of the central nervous system (CNS). They undertake numerous functions during development and in adulthood to support and protect the brain through finely regulated communication with other cellular elements of the nervous tissue. In Alzheimer's disease (AD), astrocytes undergo heterogeneous morphological, molecular and functional alterations represented by reactive remodelling, asthenia and loss of function. Reactive astrocytes closely associate with amyloid β (Aβ) plaques and neurofibrillary tangles in advanced AD. The specific contribution of astrocytes to AD could potentially evolve along the disease process and includes alterations in their signalling, interactions with pathological protein aggregates, metabolic and synaptic impairments. In this review, we focus on the purinergic receptor, P2X7R, and discuss the evidence that P2X7R activation contributes to altered astrocyte functions in AD. Expression of P2X7R is increased in AD brain relative to non-demented controls, and animal studies have shown that P2X7R antagonism improves cognitive and synaptic impairments in models of amyloidosis and tauopathy. While P2X7R activation can induce inflammatory signalling pathways, particularly in microglia, we focus here specifically on the contributions of astrocytic P2X7R to synaptic changes and protein aggregate clearance in AD, highlighting cell-specific roles of this purinoceptor activation that could be targeted to slow disease progression.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesBrainSignal TransductionAmyloid beta-PeptidesAlzheimers diseaseastrocytesp2x7synapsestau proteins

Identifiers

PMID36449279
PMCPMC10011405
OpenAlexW4310460300

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read1
Read underepoch 390

Registered trials

None linked

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.