Evidence map›Paper›PMID 39891787›Full record

ReviewMetabolic brain disease2025

The effects of ursodeoxycholic acid on Parkinson's disease, a mechanistic review of the recent evidence.

Seyed Mehrad Razavi, Niusha Esmaealzadeh, Mazyar Ataei, Nadia Afshari, Moloud Saleh, Yasaman Amini, Sadaf Hasrati, Fatemeh Ghazizadeh Hashemi, Abolghasem Mortazavi, Leila Mohaghegh Shalmani and 1 more

Abstract readReview
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In one paragraph

Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Emerging Roles of Bile Acids in Neuroinflammation.International journal of molecular sciences · 2025
    Review
  10. 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.

Seyed Mehrad RazaviDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Niusha EsmaealzadehDepartment of Traditional Pharmacy, School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mazyar AtaeiDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Nadia AfshariDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Moloud SalehDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Yasaman AminiDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Sadaf HasratiDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Fatemeh Ghazizadeh HashemiPsychosomatic Research Center, Imam Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Abolghasem MortazaviDepartment of Neurosurgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Leila Mohaghegh ShalmaniDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. leila_mohaghegh@yahoo.com.
Amir Hossein AbdolghaffariDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. amirhosein172@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionParkinson`s disease stands as the second-most widespread neurodegenerative disorder. Parkinson`s disease is relentless in progression and irreversible in nature, for which there is no cure. Therapies are only used to attenuate motor symptoms. As Parkinson`s disease is primarily defined by degeneration of dopaminergic neurons in the substantia nigra, and considering that neuroinflammation and mitochondrial dysfunction in these neurons are key factors contributing to disease progression, alternative therapies should aim to preserve healthy mitochondria. Method. Eligible studies on the effect of Ursodeoxycholic acid (UDCA) on Parkinson`s disease were collected from PubMed, Google Scholar, Scopus, Web of Science and Cochrane library for clinical, in-vivo, and in-vitro studies. Result. UDCA and its taurine conjugate (TUDCA), which are endogenous bile acids, have exhibited neuroprotective potential in various neurological conditions, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, in both animal experimental models and clinical investigations. This is attributed to three significant properties, in addition to their capability to cross the blood-brain barrier. First, their anti-inflammatory properties are manifested through the reduction of significant inflammatory factors such as tumor necrosis factor-α, interleukin 1β and other related elements. Second, their antioxidant property is marked by an increase in the expression of superoxide dismuthase, glutathione peroxidase and other antioxidant enzymes. The third property is the antiapoptotic activity, characterized by decreased caspase-3 activity and lower expression of pro-apoptotic Bax in the striatum. Conclusion. Based on this comprehensive review, UDCA and TUDCA have the potential to be considered as a therapeutic agent in the management of the Parkinson's disease.

Indexed as

Neuroprotective AgentsParkinson DiseaseUrsodeoxycholic AcidAnimalsHumansNeuroprotective AgentsUrsodeoxycholic AcidBile acids, pharmacologyNeurodegenerative diseasesParkinson’s diseaseTauroursodeoxycholic acidUrsodeoxycholic acid

Identifiers

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Registered trials

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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.