Evidence map›Paper›PMID 24374328›Full record

ArticleNeuroscience2014

Effects of sustained proNGF blockade on attentional capacities in aged rats with compromised cholinergic system.

B Yegla, V Parikh

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Mental disorders, functional impairment, and nerve growth factor.Psychology research and behavior management · 2017
    Article
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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

2 authors at 1 institution in 1 country.

B YeglaDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States.
V ParikhDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States. Electronic address: vinay.parikh@temple.edu.
Temple University · US

Funding

Cholinergic and cognitive decline in response to TrkA knockdown using RNAiR03AG029592 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARIKH, VINAY · 2008 to 2009
$129k
NIA NIH HHS AG0292592NIA NIH HHS R03 AG029592
6 · The paper itself

Abstract

Disruption in nerve growth factor (NGF) signaling via tropomyosin-related kinase A (trkA) receptors compromises the integrity of the basal forebrain (BF) cholinergic system, yielding cognitive, specifically attentional, impairments in Alzheimer's disease (AD). Although normal aging is considered a risk factor for AD, the mechanisms underlying the selective vulnerability of the aging cholinergic system to trkA disruption is not clear. The levels of proNGF, a proneurotrophin that possesses higher affinity for p75 receptors, increase in aging. The present study was designed to test the hypothesis that cholinergic and attentional dysfunction in aged rats with reduced BF trkA receptors occurs due to the overactivation of endogenous proNGF signaling. We employed a viral vector that produced trkA shRNA to suppress trkA receptors in the corticopetal cholinergic neurons of aged rats. BF trkA suppression impaired animals' performance on signal trials in both the sustained attention task (SAT) and the cognitively taxing distractor version of SAT (dSAT) and these deficits were normalized by chronic intracerebroventricular administration of proNGF antibody. Moreover, depolarization-evoked acetylcholine (ACh) release and the density of cortical cholinergic fibers were partially restored in these animals. However, SAT/dSAT scores reflecting overall performance did not improve following proNGF blockade in trkA knockdown rats due to impaired performance in non-signal trials. Sustained proNGF blockade alone did not alter baseline attentional performance but produced moderate impairments during challenging conditions. Collectively, our findings indicate that barring proNGF-p75 signaling may exert some beneficial effects on attentional capacities specifically when BF trkA signaling is abrogated. However, endogenous proNGF may also possess neurotrophic effects and blockade of this proneurotrophin may not completely ameliorate attentional impairments in AD and potentially hinder performance during periods of high cognitive load in normal aging.

Indexed as

AcetylcholineAgingAnimalsAntibodiesAttentionCholine O-AcetyltransferaseCholinergic NeuronsConditioning, OperantGene Knockdown TechniquesMaleNerve Growth FactorProsencephalonRatsRats, WistarReceptor, trkARNA, Small InterferingAcetylcholineAntibodiesCholine O-AcetyltransferaseNerve Growth FactorReceptor, trkARNA, Small InterferingacetylcholineagingAlzheimer’s diseaseattentionproNGF

Identifiers

PMID24374328
PMCPMC3945974
OpenAlexW2031102771

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.