Evidence map›Paper›PMID 41160288›Full record

ReviewMolecular biology reports2025

Potential of Benfotiamine in the treatment of neuropsychological disorders.

Alireza Motamedzadeh, Yousef Karimzad, Felora Ferdosi, Fatemeh Nabavizadeh, Fatemeh Rahmati-Dehkordi, Ehsan Dadgostar, Michael Aschner, Atie Validad, Benyamin Kazemi, Omid Reza Tamtaji

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Alireza MotamedzadehDepartment of Internal Medicine, Faculty of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
Yousef KarimzadDepartment of Physical Medicine and Rehabilitation, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Felora FerdosiDepartment of Radiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Fatemeh NabavizadehElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Fatemeh Rahmati-DehkordiStudents' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Ehsan DadgostarBehavioral Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Atie ValidadDepartment of Anesthesiology, Birjand University of Medical Sciences, Birjand, South Khorasan, Iran. pooh199069@yahoo.com.
Benyamin KazemiDepartment of Neurosurgery, School of Medicine, Firoozgar Hospital, Iran University of Medical Sciences, Tehran, Iran. Benyamiin.kazemi@gmail.com.
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 disorders pose significant health challenges. Current drug therapies are often inadequate, highlighting the urgent need for new and effective treatments. Thiamine deficiency has been implicated in the pathophysiology of various neuropsychiatric disorders. In this context, benfotiamine, a synthetic thiamine derivative, has gained increasing attention for its potential therapeutic effects across a range of neuropsychiatric conditions. Emerging evidence supports the neuroprotective effects of benfotiamine, which are mediated through its modulation of diverse cellular and molecular pathways, i.e., Tau phosphorylation, amyloid β, oxidative stress, neuroinflammation, as well as synaptic plasticity via the glycogen synthase kinase-3β (GSK3β) signaling pathway. In this narrative review, we provide a comprehensive overview of the cellular and molecular pathways modulated by benfotiamine in the context of neuropsychiatric disorders. Specifically, we highlight its effects on oxidative stress, inflammatory signaling, mitochondrial function, glucose metabolism, and advanced glycation end-product (AGE) formation, all of which contribute to its neuroprotective and potentially therapeutic properties.

Indexed as

Mental DisordersNeuroprotective AgentsThiamineAnimalsHumansOxidative StressSignal TransductionThiamine DeficiencybenphothiamineNeuroprotective AgentsThiamineAlzheimer’s diseaseBenfotiamineMemoryNeuropsychiatric 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.