Evidence map›Paper›PMID 30661205›Full record

ArticleMolecular neurobiology2019

Recovery of Olfactory Function After Excitotoxic Lesion of the Olfactory Bulbs Is Associated with Increases in Bulbar SIRT1 and SIRT4 Expressions.

Concepció Marin, Cristobal Langdon, Isam Alobid, Mireya Fuentes, Mercè Bonastre, Joaquim Mullol

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Olfactory Dysfunction and Cognitive Decline: Are They Related?Current allergy and asthma reports · 2025
    Review
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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 3 institutions in 2 countries.

Concepció MarinINGENIO, IRCE, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS-CELLEX, Rosselló 149-153, 08036, Barcelona, Catalonia, Spain. cmarin@clinic.cat.ORCID http://orcid.org/0000-0001-8478-7477
Cristobal LangdonCentre for Biomedical Investigation in Respiratory Diseases (CIBERES), Barcelona, Spain.
Isam AlobidCentre for Biomedical Investigation in Respiratory Diseases (CIBERES), Barcelona, Spain.
Mireya FuentesINGENIO, IRCE, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS-CELLEX, Rosselló 149-153, 08036, Barcelona, Catalonia, Spain.
Mercè BonastreINGENIO, IRCE, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS-CELLEX, Rosselló 149-153, 08036, Barcelona, Catalonia, Spain.
Joaquim MullolINGENIO, IRCE, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), IDIBAPS-CELLEX, Rosselló 149-153, 08036, Barcelona, Catalonia, Spain. jmullol@clinic.cat.
Centro de Investigación Biomédica en Red de Enfermedades Respiratorias · ESCentre for Biomedical Network Research on Rare Diseases · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ES

Funding

Fundació la Marató de TV3 110610
6 · The paper itself

Abstract

Excitotoxicity consists in a cascade of intracellular events initiated by an excessive release of glutamate and hyperactivation of glutamatergic receptors that is involved in several pathologies, including traumatic brain injury and neurodegenerative diseases such as Parkinson's disease. Both disorders are a common cause of olfactory dysfunction. We previously reported a role for glutamate excitotoxicity in olfactory dysfunction showing an olfactory deficit 1 week after lesion and a spontaneous recovery 2 weeks after excitotoxicity lesion of the olfactory bulbs (OBs). The olfactory dysfunction recovery was associated with an increase in subventricular zone neurogenesis and an increase in the OB glomerular dopaminergic interneurons. However, the underlying molecular mechanisms involved in the OB dopaminergic differentiation and olfactory recovery are still unknown. To investigate the role of silent information regulator family proteins sirtuins (SIRTs), a family of NAD+-dependent histone deacetylases, on the olfactory function recovery, we examined the OB SIRT (SIRT1, SIRT2, and SIRT4) expressions after OB excitotoxic lesions in rodents. N-methyl-D-aspartate (NMDA) OB administration induced a decrease in the number of correct choices in the discrimination tests 1 week after lesions (p < 0.01) and a spontaneous recovery of the olfactory deficit 2 weeks after lesions (p < 0.01) associated with an increase in OB SIRT1 and SIRT4 expression. Our results point out for the first time the association between recovery of olfactory function and the increase in bulbar SIRT1 and SIRT4 expression suggesting a role for these SIRTs in the pathophysiology of recovery of loss of smell.

Indexed as

SmellAnimalsMaleNeurotoxinsN-MethylaspartateOlfactory BulbRats, Sprague-DawleySirtuin 1SirtuinsNeurotoxinsN-MethylaspartateSIRT5 protein, ratSirtuin 1SirtuinsDopamineExcitotoxicityNeurogenesisOlfactionParkinson’s diseaseSirtuinsTraumatic brain injury

Identifiers

PMID30661205
OpenAlexW2909279232

What OpenQuestion holds

Textmetadata
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.