Evidence map›Paper›PMID 31799735›Full record

ArticleGlia2020

Ablation of reactive astrocytes exacerbates disease pathology in a model of Alzheimer's disease.

Loukia Katsouri, Amy M Birch, Alexander W J Renziehausen, Carolin Zach, Yahyah Aman, Hannah Steeds, Angela Bonsu, Emily O C Palmer, Nazanin Mirzaei, Miriam Ries and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Review
  3. Amyloid-Frontiers in neuroscience · 2026
    Review
  4. Heterogeneity of Astrocyte Reactivity.Annual review of neuroscience · 2025
    Review
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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

11 authors at 1 institution in 1 country.

Loukia KatsouriDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.ORCID 0000-0003-0186-6116
Amy M BirchDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Alexander W J RenziehausenDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Carolin ZachDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Yahyah AmanDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Hannah SteedsDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Angela BonsuDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Emily O C PalmerDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Nazanin MirzaeiDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Miriam RiesDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.
Magdalena SastreDepartment of Brain Sciences, Imperial College London, Hammersmith Hospital, London, UK.ORCID 0000-0001-8931-6316
Hammersmith Hospital · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

The role of astrocytes in the progression of Alzheimer's disease (AD) remains poorly understood. We assessed the consequences of ablating astrocytic proliferation in 9 months old double transgenic APP23/GFAP-TK mice. Treatment of these mice with the antiviral agent ganciclovir conditionally ablates proliferating reactive astrocytes. The loss of proliferating astrocytes resulted in significantly increased levels of monomeric amyloid-β (Aβ) in brain homogenates, associated with reduced enzymatic degradation and clearance mechanisms. In addition, our data revealed exacerbated memory deficits in mice lacking proliferating astrocytes concomitant with decreased levels of synaptic markers and higher expression of pro-inflammatory cytokines. Our data suggest that loss of reactive astrocytes in AD aggravates amyloid pathology and memory loss, possibly via disruption of amyloid clearance and enhanced neuroinflammation.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAstrocytesCell ProliferationDisease Models, AnimalDisease ProgressionGlial Fibrillary Acidic ProteinInflammationMemory, Short-TermMiceMice, TransgenicSpatial MemoryAmyloid beta-Protein PrecursorGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseastrocyteAβglial fibrillary acidic protein (GFAP)inflammationsynapses

Identifiers

PMID31799735
PMCPMC7383629
OpenAlexW2993940957

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.