Evidence map›Paper›PMID 38918332›Full record

ReviewNeurochemical research2024

Therapeutic Potential of Fingolimod on Psychological Symptoms and Cognitive Function in Neuropsychiatric and Neurological Disorders.

Fatemeh Rahmati-Dehkordi, Hadi Khanifar, Nazanin Najari, Zeinab Tamtaji, Abdolkarim Talebi Taheri, Michael Aschner, Mehdi Shafiee Ardestani, Hamed Mirzaei, Ehsan Dadgostar, Fatemeh Nabavizadeh and 1 more

Abstract readReview
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In one paragraph

Review in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

11 authors.

Fatemeh Rahmati-DehkordiElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Hadi KhanifarDepartment of Internal Medicine, Shahre-kord University of Medical Sciences, Shahre-kord, Iran.
Nazanin NajariBehavioral Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Zeinab TamtajiStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran.
Abdolkarim Talebi TaheriStudents' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Mehdi Shafiee ArdestaniDepartment of Radio Pharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Hamed MirzaeiResearch Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran.
Ehsan DadgostarBehavioral Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. ehsandadgostar71@gmail.com.
Fatemeh NabavizadehElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Nabavizadeh@tums.ac.ir.
Omid Reza TamtajiElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. tamtaji.or@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropsychiatric and neurological disorders pose a significant global health burden, highlighting the need for innovative therapeutic approaches. Fingolimod (FTY720), a common drug to treat multiple sclerosis, has shown promising efficacy against various neuropsychiatric and neurological disorders. Fingolimod exerts its neuroprotective effects by targeting multiple cellular and molecular processes, such as apoptosis, oxidative stress, neuroinflammation, and autophagy. By modulating Sphingosine-1-Phosphate Receptor activity, a key regulator of immune cell trafficking and neuronal function, it also affects synaptic activity and strengthens memory formation. In the hippocampus, fingolimod decreases glutamate levels and increases GABA levels, suggesting a potential role in modulating synaptic transmission and neuronal excitability. Taken together, fingolimod has emerged as a promising neuroprotective agent for neuropsychiatric and neurological disorders. Its broad spectrum of cellular and molecular effects, including the modulation of apoptosis, oxidative stress, neuroinflammation, autophagy, and synaptic plasticity, provides a comprehensive therapeutic approach for these debilitating conditions. Further research is warranted to fully elucidate the mechanisms of action of fingolimod and optimize its use in the treatment of neuropsychiatric and neurological disorders.

Indexed as

Fingolimod HydrochlorideNervous System DiseasesNeuroprotective AgentsAnimalsCognitionHumansMental DisordersOxidative StressSphingosine 1 Phosphate Receptor ModulatorsFingolimod HydrochlorideNeuroprotective AgentsSphingosine 1 Phosphate Receptor ModulatorsDepressionFingolimodMemoryNeuropsychiatric Disorders

Identifiers

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.