Evidence map›Paper›PMID 24732467›Full record

ArticlePloS one2014

IGF2 ameliorates amyloidosis, increases cholinergic marker expression and raises BMP9 and neurotrophin levels in the hippocampus of the APPswePS1dE9 Alzheimer's disease model mice.

Tiffany J Mellott, Sarah M Pender, Rebecca M Burke, Erika A Langley, Jan Krzysztof Blusztajn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 94 citations in OpenAlex.

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  6. The IGF System and Aging.Endocrine reviews · 2025
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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 1 institution in 1 country.

Tiffany J MellottDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Sarah M PenderDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Rebecca M BurkeDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Erika A LangleyDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Jan Krzysztof BlusztajnDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
Boston University · US

Funding

THE BALTIMORE LONGITUDINAL STUDY OF HUMAN AGINGZ01AG000015 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 1985 to 2008
$11.4M
Juvenile trophic factors for the prevention and treatment of hippocampal agingR01AG032709 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF · 2008 to 2010
$1.1M
Intramural NIH HHS Z01 AG000015NIA NIH HHS AG032709NIA NIH HHS R01 AG032709NIA NIH HHS T32 AG00015
6 · The paper itself

Abstract

The development of an effective therapy for Alzheimer's disease (AD) is a major challenge to biomedical sciences. Because much of early AD pathophysiology includes hippocampal abnormalities, a viable treatment strategy might be to use trophic factors that support hippocampal integrity and function. IGF2 is an attractive candidate as it acts in the hippocampus to enhance memory consolidation, stimulate adult neurogenesis and upregulate cholinergic marker expression and acetylcholine (ACh) release. We performed a seven-day intracerebroventricular infusion of IGF2 in transgenic APPswe.PS1dE9 AD model mice that express green fluorescent protein in cholinergic neurons (APP.PS1/CHGFP) and in wild type WT/CHGFP littermates at 6 months of age representing early AD-like disease. IGF2 reduced the number of hippocampal Aβ40- and Aβ42-positive amyloid plaques in APP.PS1/CHGFP mice. Moreover, IGF2 increased hippocampal protein levels of the ACh-synthesizing enzyme, choline acetyltransferase in both WT/CHGFP and APP.PS1/CHGFP mice. The latter effect was likely mediated by increased protein expression of the cholinergic differentiating factor, BMP9, observed in IGF2-treated mice as compared to controls. IGF2 also increased the protein levels of hippocampal NGF, BDNF, NT3 and IGF1 and of doublecortin, a marker of neurogenesis. These data show that IGF2 administration is effective in reversing and preventing several pathophysiologic processes associated with AD and suggest that IGF2 may constitute a therapeutic target for AD.

Indexed as

Activin Receptors, Type IActivin Receptors, Type IIAlzheimer DiseaseAmyloid beta-PeptidesAmyloidosisAnimalsBiomarkersCholine O-AcetyltransferaseCholinergic NeuronsDisease Models, AnimalDoublecortin Domain ProteinsGlial Fibrillary Acidic ProteinGliosisGrowth Differentiation Factor 2HippocampusHumansActivin Receptors, Type IActivin Receptors, Type IIAcvrl1 protein, mouseAmyloid beta-PeptidesBiomarkersCholine O-AcetyltransferaseDoublecortin Domain ProteinsGlial Fibrillary Acidic ProteinGrowth Differentiation Factor 2Insulin-Like Growth Factor IIMicrotubule-Associated ProteinsNerve Growth FactorsNeuropeptides

Identifiers

PMID24732467
PMCPMC3986048
OpenAlexW2094105781

What OpenQuestion holds

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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.