Evidence map›Paper›PMID 22059533›Full record

ArticleBiochemistry2011

Induction of methionine-sulfoxide reductases protects neurons from amyloid β-protein insults in vitro and in vivo.

Jackob Moskovitz, Panchanan Maiti, Dahabada H J Lopes, Derek B Oien, Aida Attar, Tingyu Liu, Shivina Mittal, Jane Hayes, Gal Bitan

Abstract read
In one paragraph

Article in Biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

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  10. Aβ truncated species: Implications for brain clearance mechanisms and amyloid plaque deposition.Biochimica et biophysica acta. Molecular basis of disease · 2018
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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

9 authors at 2 institutions in 1 country.

Jackob MoskovitzDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, Kansas 66045, United States.
Panchanan Maiti
Dahabada H J Lopes
Derek B Oien
Aida Attar
Tingyu Liu
Shivina Mittal
Jane Hayes
Gal Bitan
University of California, Los Angeles · USUniversity of Kansas · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BURNS, JEFFREY MURRAY · 2011 to 2020
$16.6M
PROTEIN CHEMISTRY COREP01AG027818 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEPLOW, DAVID B. · 2006 to 2010
$7.6M
A novel method to identify methionine-oxidized proteinsR03AG027363 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI MOSKOVITZ, JACKOB · 2007 to 2008
$113k
NIA NIH HHS AG027363NIA NIH HHS AG027818NIA NIH HHS P01 AG027818NIA NIH HHS P30 AG035982NIA NIH HHS R03 AG027363
6 · The paper itself

Abstract

Self-assembly of amyloid β-protein (Aβ) into toxic oligomers and fibrillar polymers is believed to cause Alzheimer's disease (AD). In the AD brain, a high percentage of Aβ contains Met-sulfoxide at position 35, though the role this modification plays in AD is not clear. Oxidation of Met(35) to sulfoxide has been reported to decrease the extent of Aβ assembly and neurotoxicity, whereas surprisingly, oxidation of Met(35) to sulfone yields a toxicity similar to that of unoxidized Aβ. We hypothesized that the lower toxicity of Aβ-sulfoxide might result not only from structural alteration of the C-terminal region but also from activation of methionine-sulfoxide reductase (Msr), an important component of the cellular antioxidant system. Supporting this hypothesis, we found that the low toxicity of Aβ-sulfoxide correlated with induction of Msr activity. In agreement with these observations, in MsrA(-/-) mice the difference in toxicity between native Aβ and Aβ-sulfoxide was essentially eliminated. Subsequently, we found that treatment with N-acetyl-Met-sulfoxide could induce Msr activity and protect neuronal cells from Aβ toxicity. In addition, we measured Msr activity in a double-transgenic mouse model of AD and found that it was increased significantly relative to that of nontransgenic mice. Immunization with a novel Met-sulfoxide-rich antigen for 6 months led to antibody production, decreased Msr activity, and lowered hippocampal plaque burden. The data suggest an important neuroprotective role for the Msr system in the AD brain, which may lead to development of new therapeutic approaches for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCells, CulturedDisease Models, AnimalEnzyme ActivationFemaleHippocampusMethionineMethionine Sulfoxide ReductasesMiceMice, Inbred C57BLMice, TransgenicNeuronsNeuroprotective AgentsOxidation-ReductionAmyloid beta-PeptidesMethioninemethionine sulfoxideMethionine Sulfoxide ReductasesN-acetylmethionine sulfoxideNeuroprotective Agents

Identifiers

PMID22059533
PMCPMC3235361
OpenAlexW2020964350

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.