Evidence map›Paper›PMID 25482048›Full record

ArticleMolecular neurobiology2016

Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis.

Savina Apolloni, Paola Fabbrizio, Chiara Parisi, Susanna Amadio, Cinzia Volonté

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 69 citations in OpenAlex.

  1. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Histamine and Microglia.Current topics in behavioral neurosciences · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Drug Repurposing: A Network-based Approach to Amyotrophic Lateral Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  18. Review
  19. Review
  20. Article
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 3 institutions in 1 country.

Savina ApolloniCellular Biology and Neurobiology Institute, CNR, Via del Fosso di Fiorano, 65, 00143, Rome, Italy.
Paola FabbrizioDivision Experimental Neuroscience, Santa Lucia Foundation, IRCCS,, Via del Fosso di Fiorano, 65, Rome, 00143, Italy.
Chiara ParisiCellular Biology and Neurobiology Institute, CNR, Via del Fosso di Fiorano, 65, 00143, Rome, Italy.
Susanna AmadioDivision Experimental Neuroscience, Santa Lucia Foundation, IRCCS,, Via del Fosso di Fiorano, 65, Rome, 00143, Italy.
Cinzia VolontéCellular Biology and Neurobiology Institute, CNR, Via del Fosso di Fiorano, 65, 00143, Rome, Italy. cinzia.volonte@cnr.it.
Istituti di Ricovero e Cura a Carattere Scientifico · ITFondazione Santa Lucia · ITInstitute of Cell Biology and Neurobiology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the Cu(2+)/Zn(2+) superoxide dismutase 1 (SOD1) gene underlie 14-23 % of familial and 1-7 % of sporadic cases of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease characterized by a specific loss of motor neurons in the brain and spinal cord. Neuroinflammation and oxidative stress are emerging as key players in the pathogenesis of ALS, thus justifying the interest in glial cells and particularly microglia, in addition to motor neurons, as novel therapeutic approaches against ALS. Recently, histamine was proven to participate in the pathogenesis of neuroinflammatory and neurodegenerative diseases, and particularly, microglia was shown to be sensitive to the histamine challenge mainly through histamine H1 receptors. Clemastine is a first-generation and CNS-penetrant H1 receptor antagonist considered as a safe antihistamine compound that was shown to possess immune suppressive properties. In order to investigate if clemastine might find promising application in the treatment of ALS, in this work, we tested its action in the SOD1(G93A) mouse model which is extensively used in ALS preclinical studies. We demonstrated that chronic clemastine administration in SOD1(G93A) mice reduces microgliosis, modulates microglia-related inflammatory genes, and enhances motor neuron survival. Moreover, in vitro, clemastine is able to modify several activation parameters of SOD1(G93A) microglia, and particularly CD68 and arginase-1 expression, as well as phospho-ERK1/2 and NADPH oxidase 2 levels. Being clemastine a drug already employed in clinical practice, our results strongly encourage its further exploitation as a candidate for preclinical trials and a new modulator of neuroinflammation in ALS.

Indexed as

Disease Models, AnimalAmyotrophic Lateral SclerosisAnimalsAnti-Inflammatory AgentsCells, CulturedClemastineFemaleHumansMiceMice, Inbred C57BLMice, TransgenicMicrogliaNeuroprotectionPhenotypeSuperoxide DismutaseAnti-Inflammatory AgentsClemastineSOD1 G93A proteinSuperoxide DismutaseHistamine H1 receptorM1/M2 phenotypeMicrogliaMotor neuronP2X7

Identifiers

PMID25482048
OpenAlexW2042108426

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.