Evidence map›Paper›PMID 29258545›Full record

ArticleJournal of neuroinflammation2017

Dendrimer-mediated delivery of N-acetyl cysteine to microglia in a mouse model of Rett syndrome.

Elizabeth Nance, Siva P Kambhampati, Elizabeth S Smith, Zhi Zhang, Fan Zhang, Sarabdeep Singh, Michael V Johnston, Rangaramanujam M Kannan, Mary E Blue, Sujatha Kannan

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
8.4field-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

65 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Inhibition of microglial glutaminase alleviates chronic stress-induced neurobehavioral and cognitive deficits.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Nano-structured strategies in combatting neurodegeneration.Frontiers in bioengineering and biotechnology · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Therapeutic potential for KCC2-targeted neurological diseases.The Japanese dental science review · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Elizabeth NanceDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Siva P KambhampatiCenter for Nanomedicine, Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Elizabeth S SmithDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Zhi ZhangDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Fan ZhangCenter for Nanomedicine, Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Sarabdeep SinghDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Michael V JohnstonHugo W. Moser Research Institute, Kennedy Krieger, Inc., Baltimore, MD, 21205, USA.
Rangaramanujam M KannanCenter for Nanomedicine, Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Mary E BlueHugo W. Moser Research Institute, Kennedy Krieger, Inc., Baltimore, MD, 21205, USA. blue@kennedykrieger.org.
Sujatha KannanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. skannan3@jhmi.edu.
Johns Hopkins Medicine · USKennedy Krieger Institute · USUniversity of Washington · US

Funding

Translational Neuroscience CoreU54HD079123 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI FATEMI, S. ALI, SCHLAGGAR, BRADLEY L · 2014 to 2019
$7.9M
Mechanisms and novel therapy in intrauterine inflammation induced brain injuryR01HD069562 · NICHD · JOHNS HOPKINS UNIVERSITY · PI KANNAN, SUJATHA · 2012 to 2016
$1.6M
Nanotherapies for the treatment of neurodevelopmental disorders.R01EB018306 · NIBIB · JOHNS HOPKINS UNIVERSITY · PI RANGARAMANUJAM, KANNAN · 2014 to 2017
$1.5M
Dendrimer therapies for treatment of Rett SyndromeR21NS100085 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BLUE, MARY E, KANNAN, SUJATHA · 2016 to 2017
$464k
Carl Zeiss AxioImager Z1 Research MicroscopeS10RR027445 · NCRR · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI BLUE, MARY E · 2010 to 2010
$139k
K+ CHANNELS IN CAROTID BODY CELLS AND GNRHF32NS010085 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SPERGEL, DANIEL J · 1995 to 1995
–
NCRR NIH HHS S10 RR027445NIBIB NIH HHS R01 EB018306NICHD NIH HHS R01 HD069562NICHD NIH HHS U54 HD079123NINDS NIH HHS F32 NS010085NINDS NIH HHS R21 NS100085
6 · The paper itself

Abstract

backgroundRett syndrome (RTT) is a pervasive developmental disorder that is progressive and has no effective cure. Immune dysregulation, oxidative stress, and excess glutamate in the brain mediated by glial dysfunction have been implicated in the pathogenesis and worsening of symptoms of RTT. In this study, we investigated a new nanotherapeutic approach to target glia for attenuation of brain inflammation/injury both in vitro and in vivo using a Mecp2-null mouse model of Rett syndrome.

methodsTo determine whether inflammation and immune dysregulation were potential targets for dendrimer-based therapeutics in RTT, we assessed the immune response of primary glial cells from Mecp2-null and wild-type (WT) mice to LPS. Using dendrimers that intrinsically target activated microglia and astrocytes, we studied N-acetyl cysteine (NAC) and dendrimer-conjugated N-acetyl cysteine (D-NAC) effects on inflammatory cytokines by PCR and multiplex assay in WT vs Mecp2-null glia. Since the cysteine-glutamate antiporter (Xc

resultsWe demonstrated that the mixed glia derived from Mecp2-null mice have an exaggerated inflammatory and oxidative stress response to LPS stimulation when compared to WT glia. Expression of Xc

conclusionsThese results suggest that delivery of drugs using dendrimer nanodevices offers a potential strategy for targeting glia and modulating oxidative stress and immune responses in RTT.

Indexed as

AcetylcysteineAnimalsBrainCytokinesDendrimersDisease Models, AnimalFree Radical ScavengersGene Expression RegulationGlutamic AcidGlutathioneLipopolysaccharidesMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLMice, TransgenicMicrogliaAcetylcysteineCytokinesDendrimersFree Radical ScavengersGlutamic AcidGlutathioneLipopolysaccharidesMecp2 protein, mouseMethyl-CpG-Binding Protein 2GlutamateMecp2-nullMicrogliaN-Acetyl cysteinePAMAM dendrimerRett syndromeSystem Xc−

Identifiers

PMID29258545
PMCPMC5735803
OpenAlexW2776148777

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.