Evidence map›Paper›PMID 27498053›Full record

ArticleNeurobiology of aging2016

The neurotrophin receptor p75 mediates gp120-induced loss of synaptic spines in aging mice.

Alessia Bachis, Erin Wenzel, Allyssia Boelk, Jodi Becker, Italo Mocchetti

Abstract read
In one paragraph

Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

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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 3 institutions in 1 country.

Alessia BachisLaboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
Erin WenzelLaboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA; Department of Pharmacology, Georgetown University Medical Center, Washington, DC, USA.
Allyssia BoelkLaboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
Jodi BeckerCenter for Cancer Research, National Cancer Institute, Frederick, MD, USA.
Italo MocchettiLaboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA. Electronic address: moccheti@georgetown.edu.
Georgetown University · USCenter for Cancer Research · USGeorgetown University Medical Center · US

Funding

Role of proBNDF and p75NTR in HIV-mediated Axonal/Dendritic DegenerationR01NS079172 · NINDS · GEORGETOWN UNIVERSITY · PI Italo Mocchetti · 2012 to 2026
$7.0M
Cellular and molecular mechanisms of gp120 neurotoxicityR21NS074916 · NINDS · GEORGETOWN UNIVERSITY · PI MOCCHETTI, ITALO · 2011 to 2012
$426k
NINDS NIH HHS R01 NS079172NINDS NIH HHS R21 NS074916
6 · The paper itself

Abstract

Human immunodeficiency virus 1 and its envelope protein gp120 reduce synaptodendritic complexity. However, the mechanisms contributing to this pathological feature are still not understood. The proneurotrophin brain-derived neurotrophic factor promotes synaptic simplification through the activation of the p75 neurotrophin receptor (p75NTR). Here, we have used gp120 transgenic (gp120tg) mice to investigate whether p75NTR has a role in gp120-mediated neurotoxicity. Old (∼10 months) gp120tg mice exhibited an increase in proneurotrophin brain-derived neurotrophic factor levels in the hippocampus as well as a decrease in the number of dendritic spines when compared to age-matched wild type. These effects were not observed in 3- or 6-month-old mice. To test if the reduction in spine density and morphology is caused by the activation of p75NTR, we crossed gp120tg mice with p75NTR null mice. We found that deletion of only 1 copy of the p75NTR gene in gp120tg mice is sufficient to normalize the number of hippocampal spines, strongly suggesting that the neurotoxic effect of gp120 is mediated by p75NTR. These data indicate that p75NTR antagonists could provide an adjunct therapy against synaptic simplification caused by human immunodeficiency virus 1.

Indexed as

AgingAnimalsBrain-Derived Neurotrophic FactorDendritic SpinesHippocampusHIV-1HIV Envelope Protein gp120HIV InfectionsHumansMaleMice, Inbred C57BLMice, TransgenicMolecular Targeted TherapyNeurocognitive DisordersReceptor, Nerve Growth FactorSynapsesBrain-Derived Neurotrophic FactorHIV Envelope Protein gp120Receptor, Nerve Growth FactorAgingHippocampusHIVp75NTRproBDNFTrkB

Identifiers

PMID27498053
PMCPMC5264514
OpenAlexW2466192218

What OpenQuestion holds

Textmetadata
LicenceTDM
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.