Evidence map›Paper›PMID 21471641›Full record

ArticleJournal of Alzheimer's disease : JAD2011

Endogenous galanin protects mouse hippocampal neurons against amyloid toxicity in vitro via activation of galanin receptor-2.

Caroline R Elliott-Hunt, Fiona E Holmes, Dean M Hartley, Sylvia Perez, Elliott J Mufson, David Wynick

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  18. Maximizing neuroprotection: where do we stand?Therapeutics and clinical risk management · 2012
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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

6 authors at 2 institutions in 2 countries.

Caroline R Elliott-HuntSchools of Physiology and Pharmacology and Clinical Sciences, University of Bristol, Bristol, UK.
Fiona E Holmes
Dean M Hartley
Sylvia Perez
Elliott J Mufson
David Wynick
Rush University Medical Center · USUniversity of Bristol · GB

Funding

TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI IKONOMOVIC, MILOS D · 1997 to 2024
$39.7M
Tau Truncation & Conformation In Alzheimer's Disease ProgressionP01AG009466 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BINDER, LESTER IRVIN · 1991 to 2012
$14.3M
GALANIN IN ALZHEIMER'S DISEASER01AG010668 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI MUFSON, ELLIOTT JAY · 1991 to 2011
$4.1M
Cellular and Molecular Medial Temporal Lobe Pathology in Elderly PreMCI subjectsR01AG043375 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI GINSBERG, STEPHEN D, MUFSON, ELLIOTT JAY · 2013 to 2017
$3.6M
Medical Research Council G0300028Medical Research Council G1000863NIA NIH HHS AG10668NIA NIH HHS P01 AG009466NIA NIH HHS P01 AG014449NIA NIH HHS R01 AG010668NIA NIH HHS R01 AG043375Wellcome Trust 081485
6 · The paper itself

Abstract

Expression of the neuropeptide galanin is known to be upregulated in the brain of patients with Alzheimer's disease (AD). We and others have shown that galanin plays a neuroprotective role in a number of excitotoxic injury paradigms, mediated by activation of the second galanin receptor subtype (GAL2). In the present study, we investigated whether galanin/GAL2 plays a similar protective role against amyloid-β(Aβ) toxicity. Here we report that galanin or the GAL2/3-specific peptide agonist Gal2-11, both equally protect primary dispersed mouse wildtype (WT) neonatal hippocampal neurons from 250 nM Aβ1-42 toxicity in a dose dependent manner. The amount of Aβ1-42 induced cell death was significantly greater in mice with loss-of-function mutations in galanin (Gal-KO) or GAL2 (GAL2-MUT) compared to strain-matched WT controls. Conversely, cell death was significantly reduced in galanin over-expressing (Gal-OE) transgenic mice compared to strain-matched WT controls. Exogenous galanin or Gal2-11 rescued the deficits in the Gal-KO but not the GAL2-MUT cultures, confirming that the protective effects of endogenous or exogenous galanin are mediated by activation of GAL2. Despite the high levels of endogenous galanin in the Gal-OE cultures, the addition of exogenous 100 nM or 50 nM galanin or 100 nM Gal2-11 further significantly reduced cell death, implying that GAL2-mediated neuroprotection is not at maximum in the Gal-OE mice. These data further support the hypothesis that galanin over-expression in AD is a neuroprotective response and imply that the development of a drug-like GAL2 agonist might reduce the progression of symptoms in patients with AD.

Indexed as

Amyloid beta-PeptidesAnalysis of VarianceAnimalsAnimals, NewbornCell DeathCells, CulturedDose-Response Relationship, DrugGalaninGlutamic AcidHippocampusMiceMice, TransgenicNeuronsPeptide FragmentsReceptor, Galanin, Type 2Amyloid beta-Peptidesamyloid beta-protein (1-42)Galaningalanin (2-11)-amideGlutamic AcidPeptide FragmentsReceptor, Galanin, Type 2

Identifiers

PMID21471641
PMCPMC3145121
OpenAlexW1750403914

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.