Evidence map›Paper›PMID 37873302›Full record

ArticlebioRxiv : the preprint server for biology2023

C5aR1 signaling promotes region and age dependent synaptic pruning in models of Alzheimer's Disease.

Angela Gomez-Arboledas, Maria I Fonseca, Enikö Kramar, Shu-Hui Chu, Nicole Schartz, Purnika Selvan, Marcelo A Wood, Andrea J Tenner

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Angela Gomez-ArboledasDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
Maria I FonsecaDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
Enikö KramarDepartment of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697, USA.
Shu-Hui ChuDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
Nicole SchartzDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
Purnika SelvanDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
Marcelo A WoodDepartment of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697, USA.
Andrea J TennerDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA.
University of California, Irvine · US

Funding

UC Irvine MODEL-ADU54AG054349 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI FRANK M LAFERLA · 2017 to 2026
$71.9M
Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
Uncover Strategies Used By Biological SystemsP50GM076516 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI NIE, QING · 2007 to 2016
$25.1M
Investigating the interface of epigenetics and metabolism underlying memory formation in the adult, aging, and AD brainR01AG076835 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI Marcelo Andres Wood · 2022 to 2026
$3.6M
Defining the Mechanistic Link between C5aR1 signaling and cognitive loss in Alzheimer's diseasesR01AG060148 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI MORTAZAVI, SEYED ALI, TENNER, ANDREA JOAN · 2018 to 2021
$2.6M
Modulating Polarization of Glial Cells in AD mouse models by a Complement Receptor AntagonistR21AG061746 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI TENNER, ANDREA JOAN · 2019 to 2020
$425k
NCI NIH HHS P30 CA062203NIA NIH HHS R01 AG060148NIA NIH HHS R01 AG076835NIA NIH HHS R21 AG061746NIA NIH HHS U54 AG054349NIGMS NIH HHS P50 GM076516
6 · The paper itself

Abstract

introductionSynaptic loss is a hallmark of Alzheimer's disease (AD) that correlates with cognitive decline in AD patients. Complement-mediated synaptic pruning has been associated with this excessive loss of synapses in AD. Here, we investigated the effect of C5aR1 inhibition on microglial and astroglial synaptic pruning in two mouse models of AD.

methodsA combination of super-resolution and confocal and tridimensional image reconstruction was used to assess the effect of genetic ablation or pharmacological inhibition of C5aR1 on the Arctic48 and Tg2576 models of AD.

resultsGenetic ablation or pharmacological inhibition of C5aR1 rescues the excessive pre-synaptic pruning and synaptic loss in an age and region dependent fashion in two mouse models of AD, which correlates with improved long-term potentiation (LTP). DISCUSSION: Reduction of excessive synaptic pruning is an additional beneficial outcome of the suppression of C5a-C5aR1 signaling, further supporting its potential as an effective targeted therapy to treat AD.

Indexed as

Alzheimer’s diseaseC1qC5aR1microgliasynaptic pruning

Identifiers

PMID37873302
PMCPMC10592845
OpenAlexW4387244553

What OpenQuestion holds

Textmetadata
LicenceCC BY-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.