Evidence map›Paper›PMID 39816194›Full record

Trial reportBrain communications2025

Multi-omics characterization of improved cognitive functions in Parkinson's disease patients after the combined metabolic activator treatment: a randomized, double-blinded, placebo-controlled phase II trial.

Burak Yulug, Ozlem Altay, Xiangyu Li, Lutfu Hanoglu, Seyda Cankaya, Halil A Velioglu, Simon Lam, Hong Yang, Ebru Coskun, Ezgi Idil and 18 more

Abstract readClinical Trial
In one paragraph

Trial report in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. 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

28 authors.

Burak YulugDepartment of Neurology and Neuroscience, Faculty of Medicine, Alanya Alaaddin Keykubat University, Antalya 07070, Turkey.ORCID https://orcid.org/0000-0002-9704-6173
Ozlem AltayScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.
Xiangyu LiScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.
Lutfu HanogluDepartment of Neurology, Faculty of Medicine, Istanbul Medipol University, Istanbul 34815, Turkey.
Seyda CankayaDepartment of Neurology and Neuroscience, Faculty of Medicine, Alanya Alaaddin Keykubat University, Antalya 07070, Turkey.
Halil A VeliogluDepartment of Women's and Children's Health, Karolinska Institute, Neuroimaging Lab, Stockholm 17177, Sweden.ORCID https://orcid.org/0000-0002-2306-5937
Simon LamCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London WC2R 2LS, UK.ORCID https://orcid.org/0000-0002-4476-0971
Hong YangScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.
Ebru CoskunDepartment of Neurology, Faculty of Medicine, Istanbul Medipol University, Istanbul 34815, Turkey.ORCID https://orcid.org/0000-0003-1028-6703
Ezgi IdilDepartment of Neurology and Neuroscience, Faculty of Medicine, Alanya Alaaddin Keykubat University, Antalya 07070, Turkey.
Zubeyir BayraktarogluFunctional Imaging and Cognitive-Affective Neuroscience Lab, Istanbul Medipol University, Istanbul 34815, Turkey.ORCID https://orcid.org/0000-0001-5118-4776
Rahim NogaylarDepartment of Neurology and Neuroscience, Faculty of Medicine, Alanya Alaaddin Keykubat University, Antalya 07070, Turkey.
Ahmet OzsimsekDepartment of Neurology and Neuroscience, Faculty of Medicine, Alanya Alaaddin Keykubat University, Antalya 07070, Turkey.
Serkan YildirimDepartment of Pathology, Faculty of Veterinary, Atatürk University, Erzurum 25240, Turkey.
Ismail BolatDepartment of Pathology, Faculty of Veterinary, Atatürk University, Erzurum 25240, Turkey.
Metin KilicliogluDepartment of Pathology, Faculty of Veterinary, Atatürk University, Erzurum 25240, Turkey.
Cemil BayramDepartment of Medical Pharmacology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey.
Nursena YukselDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum 25050, Turkey.
Ozlem O TozluDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum 25050, Turkey.
Muhammad ArifScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.ORCID https://orcid.org/0000-0003-2261-0881
Saeed ShoaieCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London WC2R 2LS, UK.
Ahmet HacimuftuogluDepartment of Pathology, Faculty of Veterinary, Atatürk University, Erzurum 25240, Turkey.
Cheng ZhangScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.ORCID https://orcid.org/0000-0002-3721-8586
Jens NielsenBioInnovation Institute, Copenhagen DK-2200, Denmark.ORCID https://orcid.org/0000-0002-9955-6003
Hasan TurkezDepartment of Medical Biology, Faculty of Medicine, Atatürk University, Erzurum 25240, Turkey.
Jan BorénDepartment of Molecular and Clinical Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg 41345, Sweden.
Mathias UhlénScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.
Adil MardinogluScience for Life Laboratory, KTH-Royal Institute of Technology, Stockholm 17165, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is primarily marked by mitochondrial dysfunction and metabolic abnormalities. We recently reported that the combined metabolic activators improved the immunohistochemical parameters and behavioural functions in Parkinson's disease and Alzheimer's disease animal models and the cognitive functions in Alzheimer's disease patients. These metabolic activators serve as the precursors of nicotinamide adenine dinucleotide and glutathione, and they can be used to activate mitochondrial metabolism and eventually treat mitochondrial dysfunction. Here, we designed a randomized, double-blinded, placebo-controlled phase II study in Parkinson's disease patients with 84 days combined metabolic activator administration. A single dose of combined metabolic activator contains L-serine (12.35 g),

Indexed as

combined metabolic activatorsmulti-omicsParkinson’s diseasesystems biology

Identifiers

PMID39816194
PMCPMC11733689

What OpenQuestion holds

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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.