Evidence map›Paper›PMID 41152868›Full record

ArticleJournal of neuroinflammation2025

TSPO contributes to neuropathology and cognitive deficits in Alzheimer's disease.

Kelly Ceyzériat, Aurélien M Badina, Laurene Abjean, Léa Meyer, Farha Bouteldja, Marta Balkota, Quentin Amossé, Oriane Prudhomme, Ryan J Middleton, Guo-Jun Liu and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

19 authors.

Kelly CeyzériatCIBM Center for Biomedical Imaging, Geneva, Switzerland.
Aurélien M BadinaDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Laurene AbjeanDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Léa MeyerDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Farha BouteldjaDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Marta BalkotaDepartment of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Quentin AmosséDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Oriane PrudhommeDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Ryan J MiddletonAustralian Nuclear Science and Technology Organisation (ANSTO), Sydney, Australia.
Guo-Jun LiuAustralian Nuclear Science and Technology Organisation (ANSTO), Sydney, Australia.
Richard B BanatiAustralian Nuclear Science and Technology Organisation (ANSTO), Sydney, Australia.
Thomas ZilliFaculty of Biomedical Sciences, Università Della Svizzera Italiana, Lugano, Switzerland.
Aurelien LathuiliereDepartment of Rehabilitation and Geriatrics, Memory Center, Geneva University Hospital and University of Geneva, Geneva, Switzerland.
David OwenDepartment of Brain Sciences, Imperial College London, London, UK.
Pierre MaechlerDepartment of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Valentina GaribottoDiagnostic Department, Division of Nuclear Medicine, University Hospitals and University of Geneva, Geneva, Switzerland.
Stergios TsartsalisDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Philippe MilletDepartment of Psychiatry, University of Geneva, Geneva, Switzerland.
Benjamin B TournierDepartment of Psychiatry, University of Geneva, Geneva, Switzerland. benjamin.tournier@hug.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 18kDa translocator protein (TSPO) is increased in neurodegenerative diseases. In Alzheimer's disease (AD) animal models, TSPO's upregulation is detected first in astrocytes, then in microglia. However, the role of TSPO in the pathophysiology and symptoms characteristic of the disease remains unknown. In the human postmortem hippocampus, we show here that TSPO correlated positively with reactive astrocyte-associated genes and negatively with genes involved in glycolytic pathways. In addition, we observed that TSPO deletion in 3 × TgAD mice reversed the reduction in glucose uptake and reduced astrocyte reactivity. We observed a decrease of poorly and highly aggregated forms of Tau (-44% and -82%, respectively) and Aβ42 (-25% and -95%, respectively) at 9 months of age. In 5 × FAD mice, we confirmed the association between TSPO, astrocyte reactivity and Aβ. Functionally, Tau over-expression in the hippocampus induced a memory decline in WT animals, prevented in TSPO

Indexed as

Alzheimer DiseaseCognition DisordersReceptors, GABAAgedAmyloid beta-PeptidesAnimalsAstrocytesDisease Models, AnimalFemaleHippocampusHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAmyloid beta-PeptidesBzrp protein, mouseReceptors, GABAtau ProteinsTSPO protein, human3 × TgADAlzheimer’s diseaseAstrocytesHippocampusTSPO

Identifiers

PMID41152868
PMCPMC12570730

What OpenQuestion holds

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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.