Evidence map›Paper›PMID 39730671›Full record

ArticleScientific reports2024

Partial microglial depletion and repopulation exert subtle but differential effects on amyloid pathology at different disease stages.

L H D Le, M K O'Banion, A K Majewska

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. 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

3 authors.

L H D LeDepartment of Neuroscience, Del Monte Institute for Neuroscience, University of Rochester, Rochester, NY, USA.ORCID 0000-0002-2762-7044
M K O'BanionDepartment of Neuroscience, Del Monte Institute for Neuroscience, University of Rochester, Rochester, NY, USA.ORCID 0000-0003-1246-3363
A K MajewskaDepartment of Neuroscience, Del Monte Institute for Neuroscience, University of Rochester, Rochester, NY, USA. ania_majewska@urmc.rochester.edu.ORCID 0000-0002-2167-6849

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 1985 to 2026
$42.8M
The role of hyaluronan in longevity and cancer resistance of longest-lived rodentP01AG047200 · NIA · UNIVERSITY OF ROCHESTER · PI Andrei Seluanov · 2014 to 2026
$36.9M
Mechanisms that regulate microglial dynamics in the context of plasticity (Supplement)R01NS114480 · NINDS · UNIVERSITY OF ROCHESTER · PI MAJEWSKA, ANNA K · 2020 to 2024
$2.2M
AD supplement to NIH R01 NS114480Alzheimer's Association AARG-NTF-19-619116NIA NIH HHS P01 AG047200NIEHS NIH HHS P30 ES001247NINDS NIH HHS R01 NS114480University of Rochester Goodman awardUniversity of Rochester Medical Center Del Monte Institute for Neuroscience Pilot Program
6 · The paper itself

Abstract

Colony-stimulating factor-1-receptor (CSF1R) inhibitors have been widely used to rapidly deplete microglia from the brain, allowing the remaining microglia population to self-renew and repopulate. These new-born microglia are thought to be "rejuvenated" and have been shown to be beneficial in several disease contexts and in normal aging. Their role in Alzheimer's disease (AD) is thus of great interest as they represent a potential disease-modifying therapy. Here, we explored the differential effects of microglial depletion and repopulation during amyloid pathology progression using 5xFAD mice. We utilized the CSF1R inhibitor PLX3397 to induce microglial self-renewal and tracked microglia-plaque dynamics with in vivo imaging. We observed transient improvement in plaque burden on different timescales depending on the animal's age. While the improvement in plaque burden did not persist in any age group, renewing microglia during mid- to late-pathology might still be beneficial as we observed a potential improvement in microglial sensitivity to noradrenergic signaling. Altogether, our findings provide further insights into the therapeutic potential of microglial renewal in AD.

Indexed as

Alzheimer DiseaseMice, TransgenicMicrogliaPlaque, AmyloidReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAminopyridinesAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalDisease ProgressionMicePyrrolesAminopyridinesAmyloid beta-PeptidesCsf1r protein, mousepexidartinibPyrrolesReceptors, Granulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID39730671
PMCPMC11680822

What OpenQuestion holds

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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.