Evidence map›Paper›PMID 38173014›Full record

ArticleTranslational neurodegeneration2024

Nanotechnology for microglial targeting and inhibition of neuroinflammation underlying Alzheimer's pathology.

Hoda M Gebril, Aravind Aryasomayajula, Mariana Reis Nogueira de Lima, Kathryn E Uhrich, Prabhas V Moghe

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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  5. Theranostic Nanoparticles for Fluorosensitive Visualization and Inhibition of Amyloid Beta-Induced Neuroinflammation.Particle & particle systems characterization : measurement and description of particle properties and behavior in powders and other disperse systems · 2026
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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

5 authors at 2 institutions in 1 country.

Hoda M GebrilDepartment of Biomedical Engineering, Rutgers University, 599 Taylor Rd., Piscataway, NJ, 08854, USA. hoda.gebril@rutgers.edu.ORCID 0000-0001-5797-9406
Aravind AryasomayajulaDepartment of Biomedical Engineering, Rutgers University, 599 Taylor Rd., Piscataway, NJ, 08854, USA.
Mariana Reis Nogueira de LimaDepartment of Chemistry, University of California, 501 Big Springs Rd., Riverside, CA, 92507, USA.
Kathryn E UhrichDepartment of Chemistry, University of California, 501 Big Springs Rd., Riverside, CA, 92507, USA.
Prabhas V MogheDepartment of Biomedical Engineering, Rutgers University, 599 Taylor Rd., Piscataway, NJ, 08854, USA. moghe@rutgers.edu.
Rutgers, The State University of New Jersey · USUniversity of California, Riverside · US

Funding

Microglial-Targeted Nanotherapeutics for Inhibition of Alpha-Synuclein Aggregation and Inflammation in Neurodegenerative DiseasesR21AG060024 · NIA · RUTGERS, THE STATE UNIV OF N.J. · PI MOGHE, PRABHAS V, PANG, ZHIPING P. · 2018 to 2019
$435k
NIA NIH HHS R21 AG060024
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is considered to have a multifactorial etiology. The hallmark of AD is progressive neurodegeneration, which is characterized by the deepening loss of memory and a high mortality rate in the elderly. The neurodegeneration in AD is believed to be exacerbated following the intercoupled cascades of extracellular amyloid beta (Aβ) plaques, uncontrolled microglial activation, and neuroinflammation. Current therapies for AD are mostly designed to target the symptoms, with limited ability to address the mechanistic triggers for the disease. In this study, we report a novel nanotechnology based on microglial scavenger receptor (SR)-targeting amphiphilic nanoparticles (NPs) for the convergent alleviation of fibril Aβ (fAβ) burden, microglial modulation, and neuroprotection.

methodsWe designed a nanotechnology approach to regulate the SR-mediated intracellular fAβ trafficking within microglia. We synthesized SR-targeting sugar-based amphiphilic macromolecules (AM) and used them as a bioactive shell to fabricate serum-stable AM-NPs via flash nanoprecipitation. Using electron microscopy, in vitro approaches, ELISA, and confocal microscopy, we investigated the effect of AM-NPs on Aβ fibrilization, fAβ-mediated microglial inflammation, and neurotoxicity in BV2 microglia and SH-SY5Y neuroblastoma cell lines.

resultsAM-NPs interrupted Aβ fibrilization, attenuated fAβ microglial internalization via targeting the fAβ-specific SRs, arrested the fAβ-mediated microglial activation and pro-inflammatory response, and accelerated lysosomal degradation of intracellular fAβ. Moreover, AM-NPs counteracted the microglial-mediated neurotoxicity after exposure to fAβ.

conclusionsThe AM-NP nanotechnology presents a multifactorial strategy to target pathological Aβ aggregation and arrest the fAβ-mediated pathological progression in microglia and neurons.

Indexed as

Alzheimer DiseaseNeuroblastomaAgedAmyloid beta-PeptidesHumansMicrogliaNeuroinflammatory DiseasesAmyloid beta-PeptidesAlzheimer’s diseaseAmphiphilic nanoparticleFibril amyloid betaMicrogliaNeuroinflammationScavenger receptor

Identifiers

PMID38173014
PMCPMC10765804
OpenAlexW4390562078

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.