Evidence map›Paper›PMID 22731394›Full record

ArticleJournal of neurochemistry2012

3,6'-Dithiothalidomide, a new TNF-α synthesis inhibitor, attenuates the effect of Aβ1-42 intracerebroventricular injection on hippocampal neurogenesis and memory deficit.

Isabella Russo, Luca Caracciolo, David Tweedie, Sang-Ho Choi, Nigel H Greig, Sergio Barlati, Francesca Bosetti

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-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

33 citing papers in PubMed, 63 citations in OpenAlex.

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  9. Immunomodulatory drugs alleviate l-dopa-induced dyskinesia in a rat model of Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2019
    Article
  10. Protective Effects of 1-Methylnicotinamide on AβJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  11. Intranasal Losartan Decreases Perivascular Beta Amyloid, Inflammation, and the Decline of Neurogenesis in Hypertensive Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Isabella RussoMolecular Neuroscience Unit, Brain Physiology and Metabolism Section, National Institute on Aging, NIH, Bethesda, MD, USA.
Luca Caracciolo
David Tweedie
Sang-Ho Choi
Nigel H Greig
Sergio Barlati
Francesca Bosetti
National Institutes of Health · USUniversity of Brescia · IT

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Role of cyclooxygenases in neuroinflammationZIAAG000425 · NIA · NATIONAL INSTITUTE ON AGING · PI BOSETTI, FRANCESCA · 2009 to 2010
$682k
Intramural NIH HHS ZIA AG000425
6 · The paper itself

Abstract

Evidence indicates altered neurogenesis in neurodegenerative diseases associated with inflammation, including Alzheimer's disease (AD). Neuroinflammation and its propagation have a critical role in the degeneration of hippocampal neurons, cognitive impairment, and altered neurogenesis. Particularly, tumor necrosis factor (TNF)-α plays a central role in initiating and regulating the cytokine cascade during an inflammatory response and is up-regulated in brain of AD patients. In this study, we investigated the effects of a novel thalidomide-based TNF-α lowering drug, 3,6'-dithiothalidomide, on hippocampal progenitor cell proliferation, neurogenesis and, memory tasks after intracerebroventricular injection of β-amyloid (Aß)(1-42) peptide. Seven days after Aβ(1-42) injection, a significant proliferation of hippocampal progenitor cells and memory impairment were evident. Four weeks after Aβ(1-42) peptide injection, elevated numbers of surviving 5-bromo-2'-deoxyuridine cells and newly formed neurons were detected. Treatment with 3,6'-dithiothalidomide attenuated these Aβ(1-42) provoked effects. Our data indicate that although treatment with 3,6'-dithiothalidomide in part attenuated the increase in hippocampal neurogenesis caused by Aβ(1-42) -induced neuroinflammation, the drug prevented memory deficits associated with increased numbers of activated microglial cells and inflammatory response. Therefore, 3,6'-dithiothalidomide treatment likely reduced neuronal tissue damage induced by neuroinflammation following Aβ(1-42) injection. Understanding the modulation of neurogenesis, and its relationship with memory function could open new therapeutic interventions for AD and other neurodegenerative disorders with an inflammatory component.

Indexed as

Amyloid beta-PeptidesAnimalsDisease Models, AnimalHippocampusInjections, IntraventricularMaleMemory DisordersMiceMice, Inbred C57BLNeurogenesisPeptide FragmentsThalidomideTumor Necrosis Factor-alpha3,6'-dithiothalidomideAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsThalidomideTumor Necrosis Factor-alpha

Identifiers

PMID22731394
PMCPMC4608365
OpenAlexW1622028638

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.